Summary
The 2024 U.S. Medical Eligibility Criteria for Contraceptive Use (U.S. MEC) comprises recommendations for the use of specific contraceptive methods by persons who have certain characteristics or medical conditions. These recommendations for health care providers were updated by CDC after review of the scientific evidence and a meeting with national experts in Atlanta, Georgia, during January 25–27, 2023. The information in this report replaces the 2016 U.S. MEC (CDC. U.S. Medical Eligibility Criteria for Contraceptive Use, 2016. MMWR 2016:65[No. RR-3]:1–103). Notable updates include 1) the addition of recommendations for persons with chronic kidney disease; 2) revisions to the recommendations for persons with certain characteristics or medical conditions (i.e., breastfeeding, postpartum, postabortion, obesity, surgery, deep venous thrombosis or pulmonary embolism with or without anticoagulant therapy, thrombophilia, superficial venous thrombosis, valvular heart disease, peripartum cardiomyopathy, systemic lupus erythematosus, high risk for HIV infection, cirrhosis, liver tumor, sickle cell disease, solid organ transplantation, and drug interactions with antiretrovirals used for prevention or treatment of HIV infection); and 3) inclusion of new contraceptive methods, including new doses or formulations of combined oral contraceptives, contraceptive patches, vaginal rings, progestin-only pills, levonorgestrel intrauterine devices, and vaginal pH modulator. The recommendations in this report are intended to serve as a source of evidence-based clinical practice guidance for health care providers. The goals of these recommendations are to remove unnecessary medical barriers to accessing and using contraception and to support the provision of person-centered contraceptive counseling and services in a noncoercive manner. Health care providers should always consider the individual clinical circumstances of each person seeking contraceptive services. This report is not intended to be a substitute for professional medical advice for individual patients; when needed, patients should seek advice from their health care providers about contraceptive use.
Introduction
U.S. Medical Eligibility Criteria for Contraceptive Use, 2024 (U.S. MEC) provides recommendations for health care providers for safe use of contraceptive methods for persons who have certain characteristics or medical conditions within the framework of removing unnecessary medical barriers to accessing and using contraception. U.S. MEC is a companion document to U.S. Selected Practice Recommendations for Contraceptive Use, 2024 (U.S. SPR) (1), which provides recommendations for health care providers that address provision of contraceptive methods and management of side effects and issues related to contraceptive method use (2). Both U.S. MEC and U.S. SPR were adapted from global guidance developed by the World Health Organization (WHO) (3,4). WHO intended for the global guidance to be used by local or national policymakers, family planning program managers, and the scientific community as a reference when they develop family planning guidance at the country or program level (3). CDC first published U.S. MEC in 2010, after a formal process during 2008–2010 to adapt the global guidance for use in the United States, which included rigorous identification and critical appraisal of the scientific evidence through systematic reviews and input from national experts on how to translate that evidence into recommendations for U.S. health care providers (5); a subsequent update was published in 2016 (6).
U.S. MEC and U.S. SPR recommendations are components of quality contraceptive services and can be used in conjunction with other guidance documents such as Providing Quality Family Planning Services: Recommendations of CDC and the U.S. Office of Population Affairs, which provides recommendations for the content and delivery of services related to preventing or for achieving pregnancy (7–9). Evidence-based guidance can support health care providers when providing person-centered counseling and contraceptive services, including assisting persons in selecting and using contraceptive methods safely and effectively.
Equitable access to the full range of contraceptive methods for all those seeking care is an essential component of high-quality sexual and reproductive health care. Contraceptive services should be offered in a noncoercive manner that supports a person’s values, goals, and reproductive autonomy through a shared decision-making process with health care providers (10–14). Because of the history of and ongoing forced sterilization and reproductive coercion in the United States among persons of racial and ethnic minority groups, persons with disabilities, and other groups that have been marginalized, it is important that persons can select the method that best meets their needs to promote reproductive autonomy (10–12).
This report replaces the 2016 version of U.S. MEC (6) with new and revised recommendations, on the basis of new evidence and input from experts. This updated document uses gender-inclusive language throughout. However, when summarizing published evidence that describes study populations by specific genders, the wording of the primary studies has been maintained for accuracy. A summary of new and revised recommendations from the 2016 U.S. MEC is provided (Appendix A). Notable updates include
addition of recommendations for persons with chronic kidney disease, specifically those with nephrotic syndrome, those receiving hemodialysis, and those receiving peritoneal dialysis;
revisions to recommendations for persons with certain characteristics or medical conditions (i.e., breastfeeding, postpartum, postabortion, obesity, surgery, history of deep venous thrombosis or pulmonary embolism with or without anticoagulant therapy, thrombophilia, superficial venous thrombosis, valvular heart disease, peripartum cardiomyopathy, systemic lupus erythematosus, cirrhosis, liver tumor, sickle cell disease, and solid organ transplantation);
revisions to recommendations for persons at high risk for HIV infection (this recommendation was developed and published in 2020) (15);
revisions to recommendations for drug interactions with antiretrovirals to include prevention in addition to treatment for HIV infection (this recommendation was developed and published in 2020) (15); and
inclusion of additional contraceptive methods, including new doses or formulations of combined oral contraceptives (COCs), contraceptive patches, vaginal rings, progestin-only pills (POPs), levonorgestrel intrauterine devices (LNG-IUDs), and vaginal pH modulator.
U.S. MEC recommendations are meant to serve as a source of evidence-based clinical guidance for health care providers and can support the provision of person-centered contraceptive counseling and services in a noncoercive manner. Health care providers should always consider the individual clinical circumstances of each person seeking contraceptive services. This report is not intended to be a substitute for professional medical advice for individual patients; when needed, patients should seek advice from their health care providers about contraceptive use.
Methods
Since publication of the 2016 U.S. MEC, CDC has monitored the literature for new evidence relevant to the recommendations through the WHO/CDC Continuous Identification of Research Evidence (CIRE) system (16). This system identifies new evidence as it is published and allows WHO and CDC to update systematic reviews and facilitate updates to recommendations as new evidence warrants. Automated searches are run in PubMed weekly, and the results are reviewed. Abstracts that meet specific criteria are added to the web-based CIRE system, which facilitates coordination and peer review of systematic reviews for both WHO and CDC. For this update, CDC reviewed all existing recommendations in the 2016 U.S. MEC for new evidence identified by CIRE that had the potential to lead to a changed recommendation. To obtain comments from the public about revisions to CDC’s contraception recommendations (U.S. MEC and U.S. SPR), CDC published a notice in the Federal Register (86 FR 46703) on August 19, 2021, requesting public comment on content to consider for revision or addition to the recommendations and how to improve the implementation of the guidance documents (17). The comment period closed on October 18, 2021. CDC received 46 submissions from the general public, including private persons, professional organizations, academic institutions, and industry. CDC reviewed each of the submissions and carefully considered them when revising the recommendations.
During January 21, 25, and 26, 2022, CDC held virtual scoping meetings that included 27 participants with expertise in contraception, adolescent health, and thrombosis, as well as representatives from partner organizations, to solicit their individual input on the scope for updating both the 2016 U.S. MEC and 2016 U.S. SPR. The 27 invited participants represented various types of health care providers and health care provider organizations. Lists of participants and potential conflicts of interests are provided at the end of this report. Meeting participants discussed topics to be addressed in the update of U.S. MEC on the basis of the presentation of new evidence published since 2016 (identified through the CIRE system), submissions received through the Federal Register notice, and feedback CDC received from other sources (e.g., health care providers and others through e-mail, public inquiry, and questions received at conferences). CDC identified multiple topics to consider when updating the guidance, including revision of existing recommendations for certain characteristics or medical conditions (postpartum, postabortion, obesity, anticoagulant therapy, known thrombogenic mutations, viral hepatitis, cirrhosis, liver tumors, sickle cell disease, and solid organ transplantation), addition of recommendations for new characteristics or medical conditions (chronic kidney disease and antiphospholipid syndrome), and addition of recommendations for new contraceptive methods (including new formulations of COCs, contraceptive patches, vaginal rings, POPs, LNG-IUDs, and vaginal pH modulator). CDC determined that all other recommendations in the 2016 U.S. MEC were up to date and consistent with the existing body of evidence for that recommendation.
In preparation for a subsequent expert meeting held during January 25–27, 2023, to review the scientific evidence for potential recommendations, CDC staff members and other invited authors conducted systematic reviews for each of the topics being considered. The purpose of these systematic reviews was to identify direct and indirect evidence about the safety of contraceptive method use by persons with selected characteristics or medical conditions (e.g., risk for disease progression or other adverse health effects in persons with chronic kidney disease who use combined hormonal contraceptives [CHCs]). Person-centered outcomes that might represent contraceptive users’ values and preferences (e.g., method continuation and patient satisfaction) were considered where relevant and available for each of the systematic reviews. Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines were followed for reporting systematic reviews (18). The Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach was used to assess the certainty of the evidence (19,20). Certainty of evidence was rated as high, moderate, low, or very low depending on criteria including study design, risk for bias, indirectness, imprecision, and inconsistency. Outcomes evaluated in randomized clinical trials (RCTs) are considered to have high certainty of evidence and those in observational studies to have low certainty; these ratings are adjusted according to the previously mentioned criteria. When direct evidence was limited or not available, indirect evidence (e.g., evidence on proxy outcomes or among healthy persons) and theoretical issues were considered. Reviews are referenced and cited throughout this report; the full reviews will be submitted to peer-reviewed journals and will contain the details of each review, including the systematic review question, literature search protocol (registered in https://www.crd.york.ac.uk/PROSPERO), inclusion and exclusion criteria, evidence tables, and quality assessments. Brief summaries of the evidence and GRADE tables are included (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). CDC staff members continued to monitor new evidence identified through the CIRE system during the preparation for the January 2023 meeting.
In addition to the preparation of the systematic reviews, CDC included patient perspectives in the guideline update process to better consider how the resulting updated recommendations could meet patient preferences and needs. Consideration of patient perspectives can center discussions on the evidence in a person-centered care model, can support inclusion of patient perspectives along with provider perspectives on the evidence, and has the potential to shape recommendations (14,21,22). In November and December 2022, listening sessions were held with a different group of 18 participants, representing themselves or patient advocacy organizations, who provided perspectives from patient populations such as youths; lesbian, gay, bisexual, transgender, queer, and intersex (LGBTQI+) persons; persons with disabilities; and persons with chronic medical conditions. The goal of the listening sessions was to gather insights about participants’ experiences, values, preferences, and information needs related to contraceptive choice and decision-making.
During January 25–27, 2023, in Atlanta, Georgia, CDC held a meeting with 40 participants who were invited to provide their individual perspectives on the scientific evidence presented and the implications for practice for U.S. MEC. Thirty-eight participants represented a wide range of expertise in contraception provision, research, and reproductive justice and included obstetricians and gynecologists, pediatricians, family physicians, internal medicine physicians, nurse practitioners, epidemiologists, and others with research and clinical practice expertise in contraceptive safety, effectiveness, and management. Two participants were patient representatives who provided their individual perspectives on the topics discussed throughout the meeting. Six additional participants with expertise relevant to specific topics on the meeting agenda provided information and participated in the discussion on their topic of expertise only (e.g., an expert in kidney disease was asked to provide general information about the condition and to assist in interpreting the evidence and any theoretical concerns on the use of contraceptive methods in persons with the condition). During the meeting, a summary of the information from the patient listening sessions was presented, and the two patient representatives presented information on their individual experiences and perspectives related to receipt of contraceptive services. The evidence from the systematic review for each topic was presented, including direct evidence and any indirect evidence or theoretical concerns. Meeting participants provided their individual perspectives on topics discussed throughout the meeting and on using the evidence to develop recommendations that would meet the needs of U.S. health care providers and the patients they serve. Participants also provided feedback on the certainty of evidence, the balance of benefits and harms, and values and preferences. Areas of research that need additional investigation also were considered during the meeting. Lists of participants and potential conflicts of interest are provided at the end of this report.
After the January 2023 meeting, CDC determined the recommendations in this report, taking into consideration the individual perspectives provided by the meeting participants. Feedback also was received from a group of four external reviewers, composed of health care providers and researchers who had not participated in the scoping or update meetings. These external reviewers were asked to provide comments on the accuracy, feasibility, and clarity of the recommendations.
Keeping Guidance Up to Date
As with any evidence-based guidance document, a key challenge is keeping the recommendations up to date as new scientific evidence becomes available. Working with WHO, CDC uses the CIRE system to ensure that WHO and CDC guidance is based on the best available evidence and that a mechanism is in place to update guidance when new evidence becomes available (16). CDC will continue to work with WHO to identify and assess all new relevant evidence and determine whether changes in the recommendations are warranted. CDC will completely review U.S. MEC periodically. Updates to the guidance will published in CDC’s Morbidity and Mortality Weekly Report (MMWR) and posted on the CDC website (https://www.cdc.gov/contraception/hcp/contraceptive-guidance).
As part of the process to update these recommendations, CDC identifies gaps in the evidence for the recommendations considered. Evidence is often limited on the safety of contraceptive methods among persons with certain characteristics or medical conditions. Generalizability of the published evidence to all persons seeking contraceptive services presents a challenge because of biases about who might be included in studies on contraceptive safety. New, high-quality research on contraception that addresses priority research gaps inclusive of diverse populations can further strengthen these recommendations and improve clinical practice.
How to Use This Document
The recommendations in this report are intended to help health care providers determine the safe use of contraceptive methods among persons with certain characteristics and medical conditions. Providers can use the information in these recommendations during contraceptive counseling with patients. The tables include recommendations for the use of contraceptive methods by persons with certain characteristics or medical conditions. Each condition is defined as representing either a person’s characteristics (e.g., age or postpartum status) or a known medical condition (e.g., diabetes or hypertension). The recommendations refer to contraceptive methods being used for contraceptive purposes; the recommendations do not consider the use of contraceptive methods for treatment of medical conditions because the eligibility criteria in these situations might differ. The conditions affecting eligibility for the use of each contraceptive method are classified into one of four categories (Box 1).
BOX 1. Categories of medical eligibility criteria for contraceptive use.
U.S. MEC 1 = A condition for which there is no restriction for the use of the contraceptive method
U.S. MEC 2 = A condition for which the advantages of using the method generally outweigh the theoretical or proven risks
U.S. MEC 3 = A condition for which the theoretical or proven risks usually outweigh the advantages of using the method
U.S. MEC 4 = A condition that represents an unacceptable health risk if the contraceptive method is used
Abbreviation: U.S. MEC = U.S. Medical Eligibility Criteria for Contraceptive Use.
Contraceptive Decision-Making
CDC acknowledges the paramount importance of personal autonomy in contraceptive decision-making. This is critically important because of the context of historical and ongoing contraceptive coercion and reproductive mistreatment in the United States, especially among communities that have been marginalized, including human rights violations such as forced sterilization and enrollment in contraceptive trials without informed consent (10–12). Coercive practices in the health care system can include provider bias for certain contraceptive methods over a patient’s reproductive goals and preferences, lack of person-centered counseling and support, and policies or incentives for uptake of certain contraceptive methods (11). For health care providers and the settings in which they work, it is important to acknowledge the structural systems that drive inequities (e.g., discrimination because of race, ethnicity, disability, sex, gender, and sexual orientation), work to mitigate harmful impacts, and recognize that provider bias (unconscious or explicit) might affect contraceptive counseling and provision of services (12). All persons seeking contraceptive care need access to appropriate counseling and services that support the person’s values, goals, and reproductive autonomy (10–14). Health care providers can support the contraceptive needs of all persons by using a person-centered framework and recognizing the many factors that influence individual decision-making about contraception (10,12,14).
The U.S. MEC and U.S. SPR recommendations can be used to support a person’s contraceptive decision-making (Box 2). Persons should have equitable access to the full range of contraceptive methods and be given the information they need for contraceptive decision-making in a noncoercive manner. Patient-centeredness has been defined by the Institute of Medicine as “providing care that is respectful of and responsive to individual patient preferences, needs, and values and ensuring that patient values guide all clinical decisions” (23). Shared decision-making and person-centered approaches to providing health care recognize the expertise of both the medical provider and the patient (10,12,23).
BOX 2. Using the U.S. Medical Eligibility Criteria for Contraceptive Use and U.S. Selected Practice Recommendations for Contraceptive Use recommendations to support contraceptive decision-making.
CDC acknowledges the paramount importance of personal autonomy in contraceptive decision-making.
Persons should have equitable access to the full range of contraceptive methods.
Contraceptive services should be offered in a noncoercive manner that honors a person’s values, goals, and reproductive autonomy.
Shared decision-making and person-centered approaches recognize the expertise of both the health care provider and the person.
-
A person-centered approach to contraceptive decision-making
º prioritizes a person’s preferences and reproductive autonomy rather than a singular focus on pregnancy prevention,
º respects the person as the main decision-maker in contraceptive decisions, and
º includes respecting the decision not to use contraception or to discontinue contraceptive method use.
U.S. MEC and U.S. SPR recommendations can be used by health care providers to support persons in contraceptive decision-making.
U.S. MEC and U.S. SPR recommendations can be used by health care providers to remove unnecessary medical barriers to accessing and using contraception.
Abbreviations: U.S. MEC = U.S. Medical Eligibility Criteria for Contraceptive Use; U.S. SPR = U.S. Selected Practice Recommendations for Contraceptive Use.
Health care providers should always consider the individual clinical and social factors of each person seeking contraceptive services and discuss reproductive desires, expectations, preferences, and priorities regarding contraception. A person might consider and prioritize many elements when choosing an acceptable contraceptive method, such as safety, effectiveness (24), availability (including accessibility and affordability), side effects, user control, reversibility, and ease of removal or discontinuation. In addition, a person’s health risks associated with pregnancy and access to comprehensive health care services should be considered in these discussions. A person-centered approach to contraceptive decision-making prioritizes a person’s preferences and reproductive autonomy rather than a singular focus on pregnancy prevention and respects the person as the main decision-maker in contraceptive decisions, including the decision not to use contraception or to discontinue contraceptive method use (12,25). Voluntary informed choice of contraceptive methods is an essential guiding principle, and contraceptive counseling, where applicable, might be an important contributor to the successful use of contraceptive methods. Key resources provide additional information on person-centered contraceptive counseling and care (7,10,12,26).
Using U.S. MEC Categories in Practice
Health care providers can use the eligibility categories when assessing the safety of contraceptive method use for persons with certain characteristics or medical conditions. Category 1 comprises conditions for which no restrictions exist for use of the contraceptive method. However, category 1 does not imply that the method is the most appropriate choice for a person, who might be prioritizing other factors when considering contraception. Classification of a method or condition as category 2 indicates the method generally can be used, with additional discussion about risks and benefits, and careful follow-up might be required. For a method or condition classified as category 3, use of that method usually is not recommended unless other more appropriate methods are not available or acceptable. The severity of the condition and the availability, practicality, and acceptability of alternative methods should be considered, and careful follow-up is required. Hence, provision of a contraceptive method to a person with a condition classified as category 3 requires careful clinical judgment and might warrant additional counseling, consultation, or follow-up. Category 4 comprises conditions that represent an unacceptable health risk if the method is used. For example, a person who smokes and is aged <35 years generally can use COCs (category 2). However, for a person aged ≥35 years who smokes <15 cigarettes per day, the use of COCs usually is not recommended unless other methods are not available or acceptable (category 3). A person aged ≥35 years who smokes ≥15 cigarettes per day should not use COCs because of unacceptable health risks, primarily the risk for myocardial infarction and stroke (category 4). The implementation of this clinical guidance might vary within different health systems, clinics, or settings. For example, in certain settings, category 3 might mean that a special consultation is warranted. Health departments and medical societies or organizations can provide information on implementation through additional guidance or clinical protocols.
The recommendations address medical eligibility criteria for the initiation and continued use of all contraceptive methods evaluated. The issue of medical eligibility criteria for continuation of a contraceptive method is clinically relevant whenever a medical condition develops or worsens during use of a contraceptive method. When the categories differ for initiation and continuation, these differences are noted. When different initiation and continuation recommendations are not given, the category is the same for initiation and continuation of use.
On the basis of this classification system, the eligibility criteria for initiating and continuing use of a specific contraceptive method are presented in tables (Appendices A, B, C, D, E, and J). In these tables, the first column indicates the condition. Multiple conditions are divided into subconditions to differentiate between varying condition types or severity. The next columns provide classifications of the condition for initiation, continuation, or both into categories 1, 2, 3, or 4 for specific contraceptive methods. For certain conditions, the last column further clarifies the numeric category in cases where the numeric classification does not adequately capture the recommendation. These clarifications are considered a necessary element of the recommendation. The last column also summarizes the evidence for the recommendation if evidence exists. The recommendations for which no evidence is cited might be based on information from sources other than systematic reviews and might take into account individual perspectives from either the WHO or U.S. expert meetings in which these recommendations were developed. For certain recommendations, comments in the third column can provide additional rationale or other information about the recommendation. Information provided along with the numeric recommendation (i.e., clarifications, evidence, and comments) is additional detail that providers can use as part of their counseling and referrals, as needed.
U.S. MEC recommendations comprise one aspect of contraceptive counseling. All persons should be counseled about the full range of contraceptive options for which they are medically eligible. Voluntary informed choice of contraceptive methods is an essential guiding principle of these recommendations, and person-centered contraceptive counseling can help to ensure a person’s contraceptive needs are met successfully.
Recommendations for Use of Contraceptive Methods
The classifications for whether persons with certain characteristics or medical conditions can safely use specific contraceptive methods are provided for intrauterine devices (IUDs), including the copper IUD (Cu-IUD) and LNG-IUD (Appendix B); progestin-only contraceptives (POCs), including progestin-only implants, depot medroxyprogesterone acetate injections, and POPs (Appendix C); CHCs, including COCs, combined transdermal patches, and combined vaginal rings (Appendix D); barrier contraceptive methods, including external (male) and internal (female) condoms, spermicides and vaginal pH modulator, and diaphragm with spermicide or cervical cap with spermicide (Appendix E); fertility awareness–based methods (Appendix F); lactational amenorrhea method (Appendix G); coitus interruptus (Appendix H); permanent contraception, including tubal surgery and vasectomy (Appendix I); and emergency contraception, including emergency use of the Cu-IUD and emergency contraceptive pills (Appendix J). A table at the end of this report summarizes the classifications for the hormonal and intrauterine methods (Appendix K).
Prevention of Sexually Transmitted Infections
All patients, regardless of contraceptive choice, should be counseled about the use of condoms and the risk for sexually transmitted infections (STIs), including HIV infection (27). Most contraceptive methods, such as hormonal methods, IUDs, and permanent contraception do not protect against STIs, including HIV infection. Consistent and correct use of external (male) latex condoms reduces the risk for STIs, including HIV infection (27). Although evidence is limited, use of internal (female) condoms can provide protection from acquisition and transmission of STIs (27). Patients also should be counseled that pre-exposure prophylaxis (PrEP), when taken as prescribed, is highly effective for preventing HIV infection (28). Additional information about prevention and treatment of STIs is available from CDC’s Sexually Transmitted Infections Treatment Guidelines (https://www.cdc.gov/std/treatment-guidelines/default.htm) (27), and information on PrEP for prevention of HIV infection is available from the U.S. Public Health Service’s Preexposure Prophylaxis for the Prevention of HIV Infection in the United States — 2021 Update: A Clinical Practice Guideline (https://www.cdc.gov/hiv/pdf/risk/prep/cdc-hiv-prep-guidelines-2021.pdf) (28).
Pregnancy and Increased Health Risk
Discussion of health risks associated with pregnancy is an important aspect of contraceptive counseling. For persons with certain medical conditions, pregnancy poses increased health risks. Conditions included in U.S. MEC that are associated with increased risk for adverse health events as a result of pregnancy are identified throughout the document (Box 3). This is not a comprehensive list of all conditions that could lead to adverse events during pregnancy. Certain medical conditions included in U.S. MEC recommendations also are treated with teratogenic drugs, which could have adverse effects when used during pregnancy. When applying U.S. MEC classifications during person-centered counseling, health care providers should discuss the risks of a particular contraceptive method as well as the health risks associated with pregnancy. Even though permanent contraception and long-acting, reversible contraceptive methods are highly effective, persons should be provided with the full range of contraceptive options and supported in their autonomous decisions about pregnancy planning and contraceptive choices. Discussions about pregnancy should include reviewing access to comprehensive health care services and subspecialists for a high-risk pregnancy (29).
BOX 3. Conditions included in U.S. Medical Eligibility Criteria for Contraceptive Use associated with increased risk for adverse health events as a result of pregnancy*.
Breast cancer
Chronic kidney disease: with current nephrotic syndrome, receiving hemodialysis, or receiving peritoneal dialysis
Complicated valvular heart disease
Cystic fibrosis
Decompensated cirrhosis
Deep venous thrombosis/pulmonary embolism
Diabetes: insulin dependent; with nephropathy, retinopathy, or neuropathy or other vascular disease; or of >20 years’ duration
Endometrial cancer
Epilepsy
Gestational trophoblastic disease
Hepatocellular adenoma and malignant liver tumors (hepatocellular carcinoma)
History of bariatric surgery within the past 2 years
HIV infection: not clinically well or not receiving antiretroviral therapy
Hypertension (systolic ≥160 mm Hg or diastolic ≥100 mm Hg)
Ischemic heart disease
Ovarian cancer
Peripartum cardiomyopathy
Schistosomiasis with fibrosis of the liver
Sickle cell disease
Solid organ transplantation within the past 2 years
Stroke
Systemic lupus erythematosus
Thrombophilia (e.g., factor V Leiden mutation; prothrombin gene mutation; protein S, protein C, and antithrombin deficiencies; or antiphospholipid syndrome)
Tuberculosis
* Even though permanent contraception and long-acting, reversible contraceptive methods are highly effective, persons should be provided with the full range of contraceptive options and supported in their autonomous decisions about pregnancy planning and contraceptive choices. Discussions about pregnancy should include reviewing access to comprehensive health care services and subspecialists for a high-risk pregnancy.
Acknowledgments
Contraception and Fertility Care Unit, Department of Sexual and Reproductive Health and Research, World Health Organization; CommunicateHealth.
Acknowledgments
U.S. Medical Eligibility Criteria for Contraceptive Use and U.S. Selected Practice Recommendations for Contraceptive Use Meeting Participants
CDC Guideline Development Group for U.S. Medical Eligibility Criteria for Contraceptive Use and U.S. Selected Practice Recommendations for Contraceptive Use
Anna Brittain, Megan Cohen, Kathryn Curtis, Kendra Hatfield-Timajchy, Katherine Kortsmit, Antoinette Nguyen, Emily Snyder, Naomi Tepper, Maura Whiteman, Lauren Zapata, CDC, Atlanta, Georgia.
Invited Meeting Participants, January 21, 2022, Virtual
Diana Blithe, National Institute of Child Health and Human Development, Bethesda, Maryland; Mary Cushman, University of Vermont, Burlington, Vermont; Alison Edelman, Oregon Health & Science University, Portland, Oregon; Mary Lyn Gaffield, Department of Sexual and Reproductive Health and Research, World Health Organization, Geneva, Switzerland; Andra James, Duke University Medical Center, Durham, North Carolina; Andrew Kaunitz, University of Florida, Jacksonville, Florida; Kathryn Lindley, Washington University Center for Women’s Heart Disease, St. Louis, Missouri; Chelsea Morroni, United Kingdom Faculty of Sexual and Reproductive Healthcare, Edinburgh, Scotland; Lydia Pecker, Johns Hopkins University School of Medicine, Baltimore, Maryland; Sarah Prager, University of Washington, Seattle, Washington; Michael Streiff, Johns Hopkins University School of Medicine, Baltimore, Maryland; Bethany Samuelson Bannow, Oregon Health & Science University, Portland, Oregon; Angeline Ti, Wellstar Atlanta, Atlanta, Georgia; Carolyn Westhoff, Columbia University, New York, New York.
Conflicts of interest for invited meeting participants, January 21, 2022, virtual: Michael Streiff, consultation for Bayer, Janssen, Pfizer, and Portola, recipient of grants to support research from Boehringer Ingelheim, Janssen, Novo Nordisk, Portola, Sanofi, Tremeau pharmaceuticals, conducted lectures for Bayer, Pfizer, and Portola; Alison Edelman, consultant for American College of Obstetricians and Gynecologists (ACOG), supports medical eligibility criteria activities for World Health Organization, Oregon Health & Science University receives research funding from Merck and HRA Pharma; Andrew Kaunitz, University of Florida College of Medicine receives financial support for clinical trials sponsored by Merck and Mithra; Carolyn Westhoff, editor of Contraception, consultant for Merck and Bayer, member of a number of data safety and monitoring boards for overseeing phase 4 Food and Drug Administration–mandated studies of new contraceptives, Columbia University receives research funding for clinical trials for each new contraceptive discussed.
CDC Subject Matter Experts and Attendees, January 21, 2022, Virtual
Wanda Barfield, Brook Belay, Elizabeth Clark, Shanna Cox, Suzanne Folger, Sarah Foster, Craig Hooper, Jessica Rodenhizer, Tanvi Suresh, Angela Thompson-Paul, Lee Warner, CDC, Atlanta, Georgia.
Invited Meeting Participants, January 25–26, 2022, Virtual
Elise Berlan, American Academy of Pediatrics and Nationwide Children’s Hospital, Columbus, Ohio; Sonya Borrero, University of Pittsburgh, Pittsburgh, Pennsylvania; Anitra Beasley Brod, Society of Family Planning and Baylor College of Medicine, Houston, Texas; Nicole Chaisson, American Academy of Family Physicians and University of Minnesota, Minneapolis, Minnesota; Alison Edelman, Oregon Health & Science University, Portland, Oregon; Mary Lyn Gaffield, Department of Sexual and Reproductive Health and Research, World Health Organization, Geneva, Switzerland; Emily Godfrey, University of Washington, Seattle, Washington; June Gupta, Planned Parenthood Federation of America, New York, New York; Samantha Hyacinth, Reproductive Health Access Project, New York, New York; Jessica Marcella, Office of Population Affairs, U.S. Department of Health and Human Services, Washington, DC; Chelsea Morroni, United Kingdom Faculty of Sexual and Reproductive Healthcare, Edinburgh, Scotland; Latoya Patterson, National Medical Association and Duke University, Durham, North Carolina; Sarah Prager, University of Washington, Seattle, Washington; Sarah Romer, Office of Population Affairs, U.S. Department of Health and Human Services, Washington, DC; Lisa Stern, Coalition to Expand Contraceptive Access, Sacramento, California; Maria Trent, Society for Adolescent Health and Medicine and Johns Hopkins University School of Medicine, Baltimore, Maryland; Nisha Verma, American College of Obstetricians and Gynecologists, Washington, DC; Carolyn Westhoff, Columbia University, New York, New York.
Conflicts of interest for invited meeting participants, January 25–26, 2022, virtual: Elise Berlan, Nexplanon clinical trainer for Merck/Organon, received research funding from Merck/Organon; Nicole Chaisson, Nexplanon trainer for Organon; Alison Edelman, consultant for American College of Obstetricians and Gynecologists (ACOG), supports medical eligibility criteria activities for World Health Organization, Oregon Health & Science University receives research funding from Merck and HRA Pharma; Carolyn Westhoff, editor of Contraception, consultant for Merck and Bayer, member of a number of data safety and monitoring boards for overseeing phase 4 Food and Drug Administration–mandated studies of new contraceptives, Columbia University receives research funding for clinical trials for each new contraceptive discussed.
CDC Subject Matter Experts and Attendees, January 25–26, 2022, Virtual
Wanda Barfield, Elizabeth Clark, Shanna Cox, Suzanne Folger, Sarah Foster, Jennifer Nelson, Jessica Rodenhizer, Tanvi Suresh, Lee Warner, CDC, Atlanta, Georgia.
Systematic Review Presenters, January 25–27, 2023, Atlanta, Georgia
Courtney Baker, Megan Cohen, Kathryn Curtis, Emma Halper, Katherine Kortsmit, Antoinette Nguyen, Emily Snyder, Naomi Tepper, Lauren Zapata, CDC, Atlanta, Georgia.
Invited Meeting Participants, January 25–27, 2023, Atlanta, Georgia
Amy Lansky, CDC, Atlanta, Georgia (Chair); Elise Berlan, American Academy of Pediatrics and Nationwide Children’s Hospital, Columbus, Ohio; Diana Blithe, National Institute of Child Health and Human Development, Bethesda, Maryland; Sonya Borrero, Office of Population Affairs, U.S. Department of Health and Human Services and University of Pittsburgh, Pittsburgh, Pennsylvania; Kristyn Brandi, American College of Obstetricians and Gynecologists, Washington, DC; Anitra Beasley Brod, Society of Family Planning and Baylor College of Medicine, Houston, Texas; Anna Burgner, Vanderbilt University, Nashville, Tennessee; Nicole Chaisson, American Academy of Family Physicians and University of Minnesota, Minneapolis, Minnesota; Mitchell Creinin, University of California-Davis, Davis, California; Mary Cushman, University of Vermont, Burlington, Vermont; Ann Dude, Society for Maternal-Fetal Medicine and University of North Carolina, Chapel Hill, North Carolina; Alison Edelman, Oregon Health & Science University, Portland, Oregon; Mary Lyn Gaffield, World Health Organization, Geneva, Switzerland; Emily Godfrey, University of Washington, Seattle, Washington; Ashira Greenberg, Patient Advocate and Sexual Health Educator, New York, New York; Edith Guilbert, Institut National de Santé Publique du Québec, Quebec City, Quebec; June Gupta, Planned Parenthood Federation of America, New York, New York; Sadia Haider, Rush University, Chicago, Illinois; Andra James, Duke University, Durham, North Carolina; Paritosh Kaul, Society for Adolescent Health and Medicine and Medical College of Wisconsin, Milwaukee, Wisconsin; Andrew Kaunitz, University of Florida, Jacksonville, Florida; Nancy Kidula, World Health Organization, Geneva, Switzerland; Sari Kives, North American Society for Pediatric and Adolescent Gynecology and University of Toronto Hospital for Sick Children, Toronto, Ontario; David Klein, Uniformed Services University, Travis Air Force Base, Fairfield, California; Anandi Kotak, Food and Drug Administration, Washington, DC; Aaron Lazorwitz, University of Colorado, Boulder, Colorado; Yvonne Malloy, National Hispanic Medical Association, Washington, DC; Monica McLemore, University of Washington, Seattle, Washington; Isabel Morgan, National Birth Equity Collaborative, New Orleans, Louisiana; Chelsea Morroni, United Kingdom Faculty of Sexual and Reproductive Healthcare, Edinburgh, Scotland; Brian Nguyen, University of Southern California, Los Angeles, California; Juno Obedin-Maliver, World Professional Association for Transgender Health and Stanford University, Palo Alto, California; Tina Pattara-Lau, Indian Health Service, Phoenix, Arizona; Lydia Pecker, Johns Hopkins University School of Medicine, Baltimore, Maryland; Michael Policar, University of California-San Francisco, San Francisco, California; Elisabeth Quint, University of Michigan, Ann Arbor, Michigan; Mia Robinson, Patient Advocate and Sickle Cell Awareness 365, Atlanta, Georgia; Sarah Romer, Office of Population Affairs, U.S. Department of Health and Human Services, Washington, DC; Monika Sarkar, University of California-San Francisco, San Francisco, California; Maria Small, National Medical Association and Duke University, Durham, North Carolina; Lisa Stern, Coalition to Expand Contraceptive Access, Sacramento, California; Michael Streiff, Johns Hopkins University School of Medicine, Baltimore, Maryland; Ivana Thompson, Physicians for Reproductive Health and University of Washington, Seattle, Washington; Angeline Ti, Reproductive Health Access Project and Wellstar Health System, Inc., Atlanta, Georgia; Carolyn Westhoff, Columbia University, New York, New York; Katharine White, Boston University School of Medicine, Boston, Massachusetts; Tracey Wilkinson, Indiana University, Bloomington, Indiana.
Conflicts of interest for invited meeting participants, January 25–27, 2023, Atlanta, Georgia: Elise Berlan, Nexplanon clinical trainer for Merck/Organon; Nicole Chaisson, Nexplanon clinical trainer for Merck/Organon; Mitchell Creinin, received honorarium from Gedeon Richter, Mayne, and Organon, served on advisory board for Gedeon Richter, GlaxoSmithKline, OLIC, and Organon, consulted for Danco, Estetra SRL, FHI360, Mayne, and Medicines360, University of California-Davis, receives contraceptive research funding from Chemo Research SL, Evofem, Medicines360, Merck, Sebela, and National Institutes of Health National Institute of Child Health and Human Development; Alison Edelman, receives travel reimbursement from American College of Obstetricians and Gynecologists, World Health Organization, CDC, and Gynuity for committee activities, receives royalties from Up to Date, Inc., Oregon Health & Science University receives research funding from Oregon Health & Science University Foundation, Merck, HRA Pharma, Bill & Melinda Gates Foundation, and National Institutes of Health; Emily Godfrey, works with Organon and received honoraria as Nexplanon trainer; Andrew Kaunitz, consultant to Mithra, University of Florida receives research support from Bayer, Merck, Mithra, and Mylan; Aaron Lazorwitz, receives research support from Organon for investigator-initiated research with the etonogestrel contraceptive implant; Yvanna Marlin-Guanga, employed under CommunicateHealth, contractor for U.S. Medical Eligibility Criteria for Contraceptive Use and U.S. Selected Practice Recommendations for Contraceptive Use January 2023 meeting; Rachel Martin, employed under CommunicateHealth, contractor for U.S. Medical Eligibility Criteria for Contraceptive Use and U.S. Selected Practice Recommendations for Contraceptive Use January 2023 meeting; Lydia Pecker, consulted for Novo Nordisk and Global Blood Therapeutics, receives research support from Alexion, National Institutes of Health National Heart, Lung, and Blood Institute, Mellon Foundation, American Society of Hematology, and Doris Duke Foundation; Michael Streiff, consultant for CSL Behring data safety monitoring board member, Janssen consultant on management of cancer-associated thromboembolism, and Pfizer consultant on anticoagulation for venous thromboembolism; Katharine White, receives research support through institution from Bayer, Merck, and Evofem; Tracey Wilkinson, receives project funding from Bayer, Cooper Surgical, and Organon, and nonpaid consultant for HRA Pharma.
CDC Subject Matter Experts and Attendees, January 25–27, 2023, Atlanta, Georgia
Karon Abe, Wanda Barfield, Brook Belay, Emily Cartwright, Elizabeth Clark, Shanna Cox, Suzanne Folger, Sarah Foster, Sophia Garbarino, Karen Hacker, Lisa Hollier, Craig Hooper, Bajha Jordan, Michele Mandel, Meda Pavkov, Stephanie Ramer, Brenda Reed, Jessica Rodenhizer, Lisa Romero, Laura Schieve, Andrea Stewart, Heather Tevendale, Angela Thompson-Paul, Lee Warner, Steffanie Wright, CDC, Atlanta, Georgia.
External Reviewers
Genevieve M. Hofmann, University of Colorado, Aurora, Colorado; Raegan McDonald-Mosley, Power to Decide, Washington, DC; Bethany Samuelson Bannow, Oregon Health & Science University, Portland, Oregon; Nichole Tyson, Stanford University, Palo Alto, California.
Appendix A. Summary of Changes from U.S. Medical Eligibility Criteria for Contraceptive Use, 2016
The classification additions, deletions, and modifications from the 2016 U.S. Medical Eligibility Criteria for Contraceptive Use (U.S. MEC) are summarized in this appendix (Box A1) (Tables A1, A2, and A3). For conditions for which classifications changed for one or more contraceptive methods or for which the condition description underwent a substantive modification, the changes or modifications are noted (Tables A1, A2, and A3). Conditions that do not appear in this table remain unchanged from the 2016 U.S. MEC.
BOX A1. Categories for classifying intrauterine devices and hormonal contraceptives.
U.S. MEC 1 = A condition for which there is no restriction for the use of the contraceptive method
U.S. MEC 2 = A condition for which the advantages of using the method generally outweigh the theoretical or proven risks
U.S. MEC 3 = A condition for which the theoretical or proven risks usually outweigh the advantages of using the method
U.S. MEC 4 = A condition that represents an unacceptable health risk if the contraceptive method is used
Abbreviation: U.S. MEC = U.S. Medical Eligibility Criteria for Contraceptive Use.
TABLE A1. Summary of changes in classifications for hormonal contraceptive methods and intrauterine devices from U.S. Medical Eligibility Criteria for Contraceptive Use, 2016.
Condition | Cu-IUD |
LNG-IUD |
Implant | DMPA |
POP | CHC | Clarification | |||||
---|---|---|---|---|---|---|---|---|---|---|---|---|
Breastfeeding
| ||||||||||||
a. <21 days
postpartum |
— |
— |
2 |
2 |
2 |
4 |
Breastfeeding provides important
health benefits for breastfeeding parent and infant. The U.S.
Dietary Guidelines for Americans and American Academy of
Pediatrics recommend that infants be exclusively breastfed for
about the first 6 months with continued breastfeeding while
introducing appropriate complementary foods for 1 year or longer
(1)
or up to age 2 years or longer (2). |
|||||
b. 21 to
<30 days postpartum | ||||||||||||
i. With
other risk factors for VTE (e.g., age ≥35 years, previous
VTE, thrombophilia, immobility, transfusion at delivery,
peripartum cardiomyopathy, BMI ≥30 kg/m2,
postpartum hemorrhage, postcesarean delivery, preeclampsia, or
smoking) |
— |
— |
2 |
2 |
2 |
3 |
CHC: For persons with
other risk factors for VTE, these risk factors might increase
the classification to a category
4. Breastfeeding: Breastfeeding provides important health benefits for breastfeeding parent and infant. The U.S. Dietary Guidelines for Americans and American Academy of Pediatrics recommend that infants be exclusively breastfed for about the first 6 months with continued breastfeeding while introducing appropriate complementary foods for 1 year or longer (1) or up to age 2 years or longer (2). |
|||||
ii.
Without other risk factors for VTE |
— |
— |
2 |
2 |
2 |
3 |
Breastfeeding provides important
health benefits for breastfeeding parent and infant. The U.S.
Dietary Guidelines for Americans and American Academy of
Pediatrics recommend that infants be exclusively breastfed for
about the first 6 months with continued breastfeeding while
introducing appropriate complementary foods for 1 year or longer
(1)
or up to age 2 years or longer (2). |
|||||
c.
30–42 days postpartum | ||||||||||||
i. With
other risk factors for VTE (e.g., age ≥35 years, previous
VTE, thrombophilia, immobility, transfusion at delivery,
peripartum cardiomyopathy, BMI ≥30 kg/m2,
postpartum hemorrhage, postcesarean delivery, preeclampsia, or
smoking) |
— |
— |
1 |
2* |
1 |
3 |
CHC: For persons with
other risk factors for VTE, these risk factors might increase
the classification to a category
4. Breastfeeding: Breastfeeding provides important health benefits for breastfeeding parent and infant. The U.S. Dietary Guidelines for Americans and American Academy of Pediatrics recommend that infants be exclusively breastfed for about the first 6 months with continued breastfeeding while introducing appropriate complementary foods for 1 year or longer (1) or up to age 2 years or longer (2). |
|||||
ii.
Without other risk factors for VTE |
— |
— |
1 |
1 |
1 |
2 |
Breastfeeding provides important
health benefits for breastfeeding parent and infant. The U.S.
Dietary Guidelines for Americans and American Academy of
Pediatrics recommend that infants be exclusively breastfed for
about the first 6 months with continued breastfeeding while
introducing appropriate complementary foods for 1 year or longer
(1)
or up to age 2 years or longer (2). |
|||||
d. >42 days
postpartum |
— |
— |
1 |
1 |
1 |
2 |
Breastfeeding provides important
health benefits for breastfeeding parent and infant. The U.S.
Dietary Guidelines for Americans and American Academy of
Pediatrics recommend that infants be exclusively breastfed for
about the first 6 months with continued breastfeeding while
introducing appropriate complementary foods for 1 year or longer
(1)
or up to age 2 years or longer (2). |
|||||
Postpartum (nonbreastfeeding) | ||||||||||||
a. <21 days
postpartum |
— |
— |
1 |
2* |
1 |
4 |
— |
|||||
b.
21–42 days postpartum | ||||||||||||
i. With
other risk factors for VTE (e.g., age ≥35 years, previous
VTE, thrombophilia, immobility, transfusion at delivery,
peripartum cardiomyopathy, BMI ≥30 kg/m2,
postpartum hemorrhage, postcesarean delivery, preeclampsia, or
smoking) |
— |
— |
1 |
2* |
1 |
3 |
CHC: For persons with
other risk factors for VTE, these risk factors might increase
the classification to a category 4. |
|||||
ii.
Without other risk factors for VTE |
— |
— |
1 |
1 |
1 |
2 |
— |
|||||
c. >42 days
postpartum |
— |
— |
1 |
1 |
1 |
1 |
— |
|||||
Postpartum (including
cesarean
delivery, breastfeeding,
or
nonbreastfeeding) | ||||||||||||
a. <10 minutes after
delivery of the placenta |
2* |
2* |
— |
— |
— |
— |
IUD: Postpartum placement
of IUDs is safe and does not appear to increase health risks
associated with IUD use such as infection. Higher rates of
expulsion during the postpartum period should be considered as
they relate to effectiveness, along with patient access to
interval placement (i.e., not related to pregnancy) when
expulsion rates are lower. Breastfeeding: Breastfeeding provides important health benefits for breastfeeding parent and infant. The U.S. Dietary Guidelines for Americans and American Academy of Pediatrics recommend that infants be exclusively breastfed for about the first 6 months with continued breastfeeding while introducing appropriate complementary foods for 1 year or longer (1) or up to age 2 years or longer (2). |
|||||
b. 10 minutes after
delivery of the placenta to <4 weeks |
2 |
2 |
— |
— |
— |
— |
IUD: Postpartum placement
of IUDs is safe and does not appear to increase health risks
associated with IUD use such as infection. Higher rates of
expulsion during the postpartum period should be considered as
they relate to effectiveness, along with patient access to
interval placement (i.e., not related to pregnancy) when
expulsion rates are lower. Breastfeeding: Breastfeeding provides important health benefits for breastfeeding parent and infant. The U.S. Dietary Guidelines for Americans and American Academy of Pediatrics recommend that infants be exclusively breastfed for about the first 6 months with continued breastfeeding while introducing appropriate complementary foods for 1 year or longer (1) or up to age 2 years or longer (2). |
|||||
c. ≥4
weeks |
1 |
1 |
— |
— |
— |
— |
IUD: Postpartum placement
of IUDs is safe and does not appear to increase health risks
associated with IUD use such as infection. Higher rates of
expulsion during the postpartum period should be considered as
they relate to effectiveness, along with patient access to
interval placement (i.e., not related to pregnancy) when
expulsion rates are lower. Breastfeeding: Breastfeeding provides important health benefits for breastfeeding parent and infant. The U.S. Dietary Guidelines for Americans and American Academy of Pediatrics recommend that infants be exclusively breastfed for about the first 6 months with continued breastfeeding while introducing appropriate complementary foods for 1 year or longer (1) or up to age 2 years or longer (2). |
|||||
d. Postpartum
sepsis |
4 |
4 |
— |
— |
— |
— |
— |
|||||
Postabortion (spontaneous
or
induced) | ||||||||||||
a. First
trimester abortion | ||||||||||||
i.
Procedural (surgical)* |
1 |
1 |
1 |
1 |
1 |
1 |
IUD: IUDs may
be placed immediately after abortion
completion. POC: POCs may be started immediately after abortion completion or at time of medication abortion initiation. DMPA: After a first trimester medication abortion that did not include mifepristone, there is no restriction for the use of DMPA (category 1). After a first trimester medication abortion that included mifepristone, there is no restriction for use of DMPA after abortion completion (category 1) and benefits generally outweigh risks with DMPA use immediately at time of medication abortion initiation (category 2). Concurrent administration of DMPA with mifepristone might slightly decrease medication abortion effectiveness and increase risk for ongoing pregnancy. Risk for ongoing pregnancy with concurrent administration of DMPA with mifepristone should be considered along with personal preference and access to follow-up abortion and contraceptive care.* CHC: CHCs may be started immediately after abortion completion or at time of medication abortion initiation. |
|||||
ii.
Medication* |
1 |
1 |
1 |
1/2* |
1 |
1 |
||||||
iii.
Spontaneous abortion with no intervention* |
1 |
1 |
1 |
1 |
1 |
1 |
||||||
b. Second
trimester
abortion | ||||||||||||
i.
Procedural (surgical)* |
2 |
2 |
1 |
1 |
1 |
1 |
IUD: IUDs may
be placed immediately after abortion
completion. POC: POCs may be started immediately after abortion completion or at time of medication abortion initiation. CHC: CHCs may be started immediately after abortion completion or at time of medication abortion initiation. |
|||||
ii.
Medication* |
2 |
2 |
1 |
1 |
1 |
1 |
||||||
iii.
Spontaneous abortion with no intervention* |
2 |
2 |
1 |
1 |
1 |
1 |
||||||
c. Immediate postseptic
abortion |
4 |
4 |
1 |
1 |
1 |
1 |
POC: POCs may be started
immediately after abortion completion or at time of medication
abortion initiation. CHC: CHCs may be started immediately after abortion completion or at time of medication abortion initiation. |
|||||
Obesity
| ||||||||||||
a. BMI ≥30
kg/m2 |
1 |
1 |
1 |
1 |
1 |
2 |
CHC: Risk for thrombosis
increases with multiple risk factors, such as obesity, older age
(e.g., ≥40 years), diabetes, smoking, family history of
thrombosis, and dyslipidemia. When a person has multiple risk
factors, any of which alone would increase risk for thrombosis,
use of CHCs might increase thrombosis risk to an unacceptable
level. However, a simple addition of categories for multiple
risk factors is not intended; for example, a combination of two
category 2 risk factors might not necessarily warrant a higher
category.* |
|||||
b. Menarche to <18
years and BMI ≥30 kg/m2 |
1 |
1 |
1 |
2 |
1 |
2 |
CHC: Risk for thrombosis
increases with multiple risk factors, such as obesity, older age
(e.g., ≥40 years), diabetes, smoking, family history of
thrombosis, and dyslipidemia. When a person has multiple risk
factors, any of which alone would increase risk for thrombosis,
use of CHCs might increase thrombosis risk to an unacceptable
level. However, a simple addition of categories for multiple
risk factors is not intended; for example, a combination of two
category 2 risk factors might not necessarily warrant a higher
category.* |
|||||
Surgery
| ||||||||||||
a. Minor surgery without
immobilization |
1 |
1 |
1 |
1 |
1 |
1 |
— |
|||||
b. Major
surgery | ||||||||||||
i. Without
prolonged immobilization |
1 |
1 |
1 |
1 |
1 |
2 |
— |
|||||
ii. With
prolonged immobilization |
1 |
1* |
1* |
2 |
1* |
4 |
— |
|||||
Deep
venous thrombosis/
Pulmonary
embolism This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | ||||||||||||
a. Current or history of
DVT/PE, receiving anticoagulant therapy (therapeutic dose)
(e.g., acute DVT/PE or long-term therapeutic dose)* |
2 |
2 |
2 |
2 |
2 |
3* |
Cu-IUD: Persons using
anticoagulant therapy are at risk for gynecologic complications
of therapy, such as heavy or prolonged bleeding. Cu-IUDs might
worsen bleeding.* LNG-IUD: Persons using anticoagulant therapy are at risk for gynecologic complications of therapy, such as heavy or prolonged bleeding. LNG-IUDs can be of benefit in preventing or treating this complication. When a contraceptive method is used as a therapy, rather than solely to prevent pregnancy, the risk/benefit ratio might differ and should be considered on a case-by-case basis.* POC: Persons using anticoagulant therapy are at risk for gynecologic complications of therapy, such as heavy or prolonged bleeding and hemorrhagic ovarian cysts. POCs can be of benefit in preventing or treating these complications; benefits might vary by POC dose and formulation. When a contraceptive method is used as a therapy, rather than solely to prevent pregnancy, the risk/benefit ratio might differ and should be considered on a case-by-case basis.* CHC: Persons using anticoagulant therapy are at risk for gynecologic complications of therapy, such as heavy or prolonged bleeding and hemorrhagic ovarian cysts. CHCs can be of benefit in preventing or treating these complications. When a contraceptive method is used as a therapy, rather than solely to prevent pregnancy, the risk/benefit ratio might differ and should be considered on a case-by-case basis.* CHC: When a patient discontinues therapeutic dose of anticoagulant therapy, careful consideration should be given to transitioning from CHCs to a progestin-only or nonhormonal method, if acceptable to the patient.* |
|||||
b. History of
DVT/PE,
receiving anticoagulant
therapy
(prophylactic dose)* |
Cu-IUD:
Persons using anticoagulant therapy are at risk for gynecologic
complications of therapy, such as heavy or prolonged bleeding.
Cu-IUDs might worsen bleeding.* LNG-IUD: Persons using anticoagulant therapy are at risk for gynecologic complications of therapy, such as heavy or prolonged bleeding. LNG-IUDs can be of benefit in preventing or treating this complication. When a contraceptive method is used as a therapy, rather than solely to prevent pregnancy, the risk/benefit ratio might differ and should be considered on a case-by-case basis.* POC: Persons using anticoagulant therapy are at risk for gynecologic complications of therapy, such as heavy or prolonged bleeding and hemorrhagic ovarian cysts. POCs can be of benefit in preventing or treating these complications; benefits might vary by POC dose and formulation. When a contraceptive method is used as a therapy, rather than solely to prevent pregnancy, the risk/benefit ratio might differ and should be considered on a case-by-case basis.* CHC: Persons using anticoagulant therapy are at risk for gynecologic complications of therapy, such as heavy or prolonged bleeding and hemorrhagic ovarian cysts. CHCs can be of benefit in preventing or treating these complications. When a contraceptive method is used as a therapy, rather than solely to prevent pregnancy, the risk/benefit ratio might differ and should be considered on a case-by-case basis.* |
|||||||||||
i. Higher
risk for recurrent DVT/PE (one or more risk factors)* |
2 |
2 |
2 |
3* |
2 |
4 |
||||||
• Thrombophilia (e.g.,
factor V Leiden mutation; prothrombin gene mutation; protein S,
protein C, and antithrombin deficiencies; or antiphospholipid
syndrome)* • Active cancer (metastatic, receiving therapy, or within 6 months after clinical remission), excluding nonmelanoma skin cancer* • History of recurrent DVT/PE* | ||||||||||||
ii. Lower
risk for recurrent DVT/PE (no risk factors)* |
2 |
2 |
2 |
2 |
2 |
3 |
||||||
c. History of DVT/PE,
not
receiving anticoagulant therapy* | ||||||||||||
i. Higher
risk for recurrent DVT/PE (one or more risk factors)* |
1 |
2 |
2 |
3* |
2 |
4 |
||||||
• History of
estrogen-associated
DVT/PE • Pregnancy-associated DVT/PE* • Idiopathic DVT/PE* • Thrombophilia (e.g., factor V Leiden mutation; prothrombin gene mutation; protein S, protein C, or antithrombin deficiencies; or antiphospholipid syndrome)* • Active cancer (metastatic, receiving therapy, or within 6 months after clinical remission), excluding nonmelanoma skin cancer* • History of recurrent DVT/PE* | ||||||||||||
ii. Lower
risk for recurrent DVT/PE (no risk factors)* |
1 |
2 |
2 |
2 |
2 |
3 |
||||||
d. Family history
(first-degree relatives) |
1 |
1 |
1 |
1 |
1 |
2 |
||||||
Thrombophilia
(e.g., factor V Leiden mutation; prothrombin gene mutation;
protein S, protein C, and antithrombin deficiencies; or
antiphospholipid syndrome) This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
1 |
2 |
2 |
3* |
2 |
4 |
Routine screening in the general
population before contraceptive initiation is not
recommended. If a person has current or history of DVT/PE, see recommendations for DVT/PE.* Classification of antiphospholipid syndrome includes presence of a clinical feature (e.g., thrombosis or obstetric morbidity) and persistently abnormal antiphospholipid antibody test on two or more occasions at least 12 weeks apart (3).* |
|||||
Superficial venous disorders
| ||||||||||||
a. Varicose
veins |
1 |
1 |
1 |
1 |
1 |
1 |
— |
|||||
b. Superficial venous
thrombosis (acute or history) |
1 |
1 |
1 |
2* |
1 |
3 |
CHC: Superficial venous
thrombosis might be associated with an increased risk for VTE.
If a person has risk factors for concurrent DVT (e.g.,
thrombophilia or cancer) or has current or history of DVT, see
recommendations for DVT/PE. Superficial venous thrombosis
associated with a peripheral intravenous catheter is less likely
to be associated with additional thrombosis and use of CHCs may
be considered. |
|||||
Valvular heart disease Complicated valvular heart disease is a condition associated with increased risk for adverse health events as a result of pregnancy (Box 3). | ||||||||||||
a. Uncomplicated |
1 |
1 |
1 |
1 |
1 |
2 |
—
|
|||||
b. Complicated (pulmonary
hypertension, risk for atrial fibrillation, or history of
subacute bacterial endocarditis) |
1 |
1 |
1 |
2* |
1 |
4 |
||||||
Peripartum cardiomyopathy This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | ||||||||||||
a. Normal or
mildly impaired
cardiac function (New York
Heart
Association Functional
Class I or II: no limitation
of
activities or slight, mild limitation
of
activity) (4) | ||||||||||||
i. <6
months |
2 |
2 |
1 |
2* |
1 |
4 |
— |
|||||
ii.
≥6 months |
2 |
2 |
1 |
2* |
1 |
3 |
||||||
b. Moderately or severely
impaired cardiac function (New York Heart Association Functional
Class III or IV: marked limitation of activity or should be at
complete rest) (4) |
2 |
2 |
2 |
3* |
2 |
4 |
||||||
Chronic kidney
disease* This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
Initiation |
Continuation |
Initiation |
Continuation |
— |
|||||||
a. Current nephrotic
syndrome* |
1* |
1* |
2* |
2* |
2* |
3* |
2* DRSP POP with known hyperkalemia: 4* |
4* |
DRSP POP: Persons with
known hyperkalemia should not use DRSP POPs because of the risk
for worsening hyperkalemia (category 4). For persons with CKD
without known hyperkalemia (category 2), consider checking serum
potassium level during first cycle of DRSP POPs.* |
|||
b. Hemodialysis* |
1* |
1* |
2* |
2* |
2* |
3* |
2* DRSP POP with known hyperkalemia: 4* |
4* |
DRSP POP: Persons with
known hyperkalemia should not use DRSP POPs because of the risk
for worsening hyperkalemia (category 4). For persons with CKD
without known hyperkalemia (category 2), consider checking serum
potassium level during first cycle of DRSP POPs.* |
|||
c. Peritoneal
dialysis* |
2* |
1* |
2* |
2* |
2* |
3* |
2* DRSP POP with known hyperkalemia: 4* |
4* |
DRSP POP: Persons with
known hyperkalemia should not use DRSP POPs because of the risk
for worsening hyperkalemia (category 4). For persons with CKD
without known hyperkalemia (category 2), consider checking serum
potassium level during first cycle of DRSP POPs.* |
|||
Systemic
lupus erythematosus This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
Initiation |
Continuation |
— |
|||||||||
a. Positive (or unknown)
antiphospholipid antibodies |
1 |
1 |
2* |
2* |
3 |
3 |
2* |
4 |
Persons with SLE are at increased risk
for ischemic heart disease, stroke, and VTE. Categories assigned
to such conditions in U.S. MEC should be the same for persons
with SLE who have these conditions. For all subconditions of
SLE, classifications are based on the assumption that no other
risk factors for cardiovascular disease are present; these
classifications must be modified in the presence of such risk
factors. |
|||
b. Severe
thrombocytopenia |
3 |
2 |
2 |
2 |
3 |
2 |
2 |
2 |
Persons with SLE are at increased risk
for ischemic heart disease, stroke, and VTE. Categories assigned
to such conditions in U.S. MEC should be the same for persons
with SLE who have these conditions. For all subconditions of
SLE, classifications are based on the assumption that no other
risk factors for cardiovascular disease are present; these
classifications must be modified in the presence of such risk
factors. Severe thrombocytopenia increases the risk for bleeding. The category should be assessed according to the severity of thrombocytopenia and its clinical manifestations. In persons with very severe thrombocytopenia who are at risk for spontaneous bleeding, consultation with a specialist and certain pretreatments might be warranted. |
|||
c. Immunosuppressive
therapy |
2 |
1 |
2 |
2 |
2 |
2 |
2 |
2 |
Persons with SLE are at increased risk
for ischemic heart disease, stroke, and VTE. Categories assigned
to such conditions in U.S. MEC should be the same for persons
with SLE who have these conditions. For all subconditions of
SLE, classifications are based on the assumption that no other
risk factors for cardiovascular disease are present; these
classifications must be modified in the presence of such risk
factors. |
|||
d. None of the
above |
1 |
1 |
2 |
2 |
2 |
2 |
2 |
2 |
Persons with SLE are at increased risk
for ischemic heart disease, stroke, and VTE. Categories assigned
to such conditions in U.S. MEC should be the same for persons
with SLE who have these conditions. For all subconditions of
SLE, classifications are based on the assumption that no other
risk factors for cardiovascular disease are present; these
classifications must be modified in the presence of such risk
factors. |
|||
High
risk for HIV infection
|
Initiation |
Continuation |
Initiation |
Continuation |
1 |
1 |
1 |
1 |
IUD: Many
persons at high risk for HIV infection are also at risk for
other STIs (see recommendations for Sexually transmitted
infections in U.S. MEC and recommendations on STI screening
before IUD placement in U.S. SPR [https://www.cdc.gov/contraception/hcp/usspr])
(5).* |
|||
1* |
1* |
1* |
1* |
|||||||||
Cirrhosis Decompensated cirrhosis is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | ||||||||||||
a. Compensated (normal
liver function) |
1 |
1 |
1 |
1 |
1 |
1 |
— |
|||||
b. Decompensated (impaired
liver function) |
1 |
2* |
2* |
3 |
2* |
4 |
||||||
Liver
tumors Hepatocelluar adenoma and malignant liver tumors are associated with increased risk for adverse health events as a result of pregnancy (Box 3). | ||||||||||||
a.
Benign | ||||||||||||
i.
Focal nodular hyperplasia |
1 |
2 |
2 |
2 |
2 |
2 |
||||||
ii.
Hepatoceullular adenoma |
1 |
2* |
2* |
3 |
2* |
4 |
||||||
b. Malignant
(hepatocellular carcinoma) |
1 |
3 |
3 |
3 |
3 |
4 |
||||||
Sickle cell
disease This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
2 |
1 |
1 |
2/3* |
1 |
4* |
DMPA: The category should
be assessed according to the severity of the condition and risk
for thrombosis.* |
|||||
Solid organ
transplantation This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
Initiation |
Continuation |
Initiation |
Continuation |
— |
|||||||
a. No graft
failure |
1* |
1* |
1* |
1* |
2 |
2/3* |
2 |
2 |
DMPA: DMPA use among
persons receiving long-term immunosuppressive therapy with a
history of, or risk factors for, nontraumatic fractures is
classified as category 3. Otherwise, DMPA use for persons with
solid organ transplantation is classified as category
2.* CHC: Persons with transplant due to Budd-Chiari syndrome should not use CHCs because of the increased risk for thrombosis.* |
|||
b. Graft failure |
2* |
1* |
2* |
1* |
2 |
2/3* |
2 |
4 |
DMPA: DMPA use among
persons receiving long-term immunosuppressive therapy with a
history of, or risk factors for, nontraumatic fractures is
classified as category 3. Otherwise, DMPA use for persons with
solid organ transplantation is classified as category
2.* |
|||
Antiretrovirals used for
prevention (PrEP) or
treatment
of HIV
infection*,†
| ||||||||||||
See the
following guidelines for the most up-to-date recommendations on
drug-drug interactions between hormonal contraception and
antiretrovirals: 1) Recommendations for the Use of
Antiretroviral Drugs During Pregnancy and Interventions to
Reduce Perinatal HIV Transmission in the United States
(https://clinicalinfo.hiv.gov/en/guidelines/perinatal/prepregnancy-counseling-childbearing-age-overview?view=full#table-3)
(6)
and 2) Guidelines for the Use of Antiretroviral Agents in Adults
and Adolescents With HIV (https://clinicalinfo.hiv.gov/en/guidelines/hiv-clinical-guidelines-adult-and-adolescent-arv/drug-interactions-overview?view=full)
(7). |
Abbreviations: ARV = antiretroviral; BMI = body mass index; CHC = combined hormonal contraceptive; CKD = chronic kidney disease; Cu-IUD = copper intrauterine device; DMPA = depot medroxyprogesterone acetate; DRSP = drospirenone; DVT = deep venous thrombosis; IUD = intrauterine device; LNG-IUD = levonorgestrel intrauterine device; PE = pulmonary embolism; POC = progestin-only contraceptive; POP = progestin-only pill; PrEP = pre-exposure prophylaxis; SLE = systemic lupus erythematous; STI = sexually transmitted infection; U.S. MEC = U.S. Medical Eligibility Criteria for Contraceptive Use; U.S. SPR = U.S. Selected Practice Recommendations for Contraceptive Use; VTE = venous thromboembolism.
* Indicates a condition for which the classification changed for one or more contraceptive methods or for which the condition description underwent a substantive modification.
† U.S. MEC recommendations for concurrent use of hormonal contraceptives or IUDs and ARVs for treatment of HIV infection also apply to use of ARVs for PrEP.
TABLE A2. Summary of changes for barrier methods from U.S. Medical Eligibility Criteria for Contraceptive Use, 2016.
Condition | Condom | Spermicide/Vaginal pH modulator*,† | Diaphragm/Cap (with spermicide) | Clarification |
---|---|---|---|---|
Chronic
kidney disease* This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | ||||
a. Current nephrotic
syndrome* |
1* |
1* |
1* |
— |
b. Hemodialysis* |
1* |
1* |
1* |
— |
c. Peritoneal
dialysis* |
1* |
1* |
1* |
— |
Cervical cancer
(awaiting treatment)
|
1 |
Vaginal pH modulator:
1* Spermicide: 2 |
1 |
The cap should not be used. Diaphragm
use has no restrictions. |
High risk for HIV
infection
|
1 |
Vaginal pH modulator:
1* Spermicide: 4 |
4 |
— |
HIV
infection
For persons with HIV infection who are
not clinically well or not receiving ARV therapy, this condition
is associated with increased risk for adverse health events as a
result of pregnancy (Box
3). |
1 |
Vaginal pH modulator:
1* Spermicide: 3 |
3 |
|
Antiretrovirals used for prevention (PrEP) or treatment of HIV infection*,§ | 1 | 1/3/4* | 3/4 | No drug interaction between ARV therapy and barrier method use is known. HIV infection is classified as category 1 for vaginal pH modulator and category 3 for spermicide and diaphragm or cap (see recommendations for HIV infection). High risk for HIV infection is classified as category 1 for vaginal pH modulator and category 4 for spermicide and diaphragm or cap (see recommendations for High risk for HIV infection).* |
Abbreviations: ARV = antiretroviral; PrEP = pre-exposure prophylaxis.
* Indicates a condition for which the classification changed for one or more contraceptive methods or for which the condition description underwent a substantive modification.
† The contraceptive method “Spermicide” has been changed to “Spermicide/Vaginal pH modulator.” Recommendations for “Spermicide/Vaginal pH modulator” are the same as those previously for “Spermicide,” with exceptions noted.
§ U.S. Medical Eligibility Criteria for Contraceptive Use recommendations for concurrent use of barrier methods and ARVs for treatment of HIV infection also apply to use of ARVs for PrEP.
TABLE A3. Summary of changes for emergency contraception from U.S. Medical Eligibility Criteria for Contraceptive Use, 2016.
Condition | Category |
Clarification | |||
---|---|---|---|---|---|
Cu-IUD | UPA | LNG | COC | ||
Solid
organ transplantation
This condition is
associated with
increased risk for adverse
health
events as a result of pregnancy
(Box 3). | |||||
a. No graft
failure |
1* |
1 |
1 |
1 |
— |
b. Graft failure | 2* | 1 | 1 | 1 | — |
Abbreviations: COC = combined oral contraceptive; Cu-IUD = copper intrauterine device; LNG = levonorgestrel; UPA = ulipristal acetate.
* Indicates a condition for which the classification changed for one or more contraceptive methods or for which the condition description underwent a substantive modification.
References
- 1.US Department of Agriculture; US Department of Health and Human Services. Dietary guidelines for Americans, 2020–2025. 9th ed. Washington, DC: US Department of Agriculture and US Department of Health and Human Services; 2020. https://www.dietaryguidelines.gov/sites/default/files/2021-03/Dietary_Guidelines_for_Americans-2020-2025.pdf
- 2.Meek JY, Noble L; Section on Breastfeeding. Policy statement: breastfeeding and the use of human milk. Pediatrics 2022;150:e2022057988. 10.1542/peds.2022-057988 [DOI] [PubMed] [Google Scholar]
- 3.Barbhaiya M, Zuily S, Naden R, et al. ; ACR/EULAR APS Classification Criteria Collaborators. The 2023 ACR/EULAR Antiphospholipid Syndrome Classification Criteria. Arthritis Rheumatol 2023;75:1687–702. 10.1002/art.42624 [DOI] [PubMed] [Google Scholar]
- 4.The Criteria Committee of the New York Heart Association. Nomenclature and criteria for diagnosis of diseases of the heart and great vessels. 9th ed. Boston, MA: Little, Brown and Co; 1994. [Google Scholar]
- 5.Curtis KM, Nguyen AT, Tepper NK, et al. U.S. selected practice recommendations for contraceptive use, 2024. MMWR Recomm Rep 2024;73(No. RR-3):1–77. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 6.Panel on Treatment of HIV During Pregnancy and Prevention of Perinatal Transmission. Recommendations for the use of antiretroviral drugs during pregnancy and interventions to reduce perinatal HIV transmission in the United States. Washington, DC: US Department of Health and Human Services; 2023. https://clinicalinfo.hiv.gov/en/guidelines/perinatal/recommendations-arv-drugs-pregnancy-overview [Google Scholar]
- 7.Panel on Antiretroviral Guidelines for Adults and Adolescents. Guidelines for the use of antiretroviral agents in adults and adolescents with HIV. Washington, DC: US Department of Health and Human Services; 2023. https://clinicalinfo.hiv.gov/sites/default/files/guidelines/documents/adult-adolescent-arv/guidelines-adult-adolescent-arv.pdf [Google Scholar]
Appendix B. Classifications for Intrauterine Devices
Classifications for intrauterine devices (IUDs) are for the copper (380 mm2) and levonorgestrel (13.5 mg, 19.5 mg, or 52 mg) IUDs (Box B1) (Table B1). IUDs do not protect against sexually transmitted infections (STIs), including HIV infection, and patients using IUDs should be counseled that consistent and correct use of external (male) latex condoms reduces the risk for STIs, including HIV infection (1). Use of internal (female) condoms can provide protection from transmission of STIs, although data are limited (1). Patients also should be counseled that pre-exposure prophylaxis, when taken as prescribed, is highly effective for preventing HIV infection (2).
BOX B1. Categories for classifying intrauterine devices.
U.S. MEC 1 = A condition for which there is no restriction for the use of the contraceptive method
U.S. MEC 2 = A condition for which the advantages of using the method generally outweigh the theoretical or proven risks
U.S. MEC 3 = A condition for which the theoretical or proven risks usually outweigh the advantages of using the method
U.S. MEC 4 = A condition that represents an unacceptable health risk if the contraceptive method is used
Abbreviation: U.S. MEC = U.S. Medical Eligibility Criteria for Contraceptive Use.
TABLE B1. Classifications for intrauterine devices, including the copper intrauterine device and levonorgestrel intrauterine device.
Condition | Category |
Clarification/Evidence/Comment | |||
---|---|---|---|---|---|
Cu-IUD |
LNG-IUD |
||||
Personal
Characteristics and Reproductive History
| |||||
Pregnancy
|
4 |
4 |
Clarification: The IUD is
not indicated during pregnancy and should not be used because of
the risk for serious pelvic infection and septic spontaneous
abortion. |
||
Age
| |||||
a. Menarche to <20
years |
2 |
2 |
Comment: Concern exists
both about the risk for expulsion from nulliparity and for STIs
from sexual behavior in younger age groups (see U.S. SPR for
recommendations on STI screening before IUD placement (https://www.cdc.gov/contraception/hcp/usspr)
(3). |
||
b. ≥20
years |
1 |
1 |
— |
||
Parity
| |||||
a. Nulliparous |
2 |
2 |
Evidence: Data conflict
about whether IUD use is associated with infertility among
nulliparous women, although well-conducted studies suggest no
increased risk (4–12). |
||
b. Parous |
1 |
1 |
— |
||
Postpartum (including
cesarean
delivery,
breastfeeding,
or
nonbreastfeeding) | |||||
a. <10 minutes after
delivery of the placenta |
2 |
2 |
Clarification: Postpartum
placement of IUDs is safe and does not appear to increase health
risks associated with IUD use such as infection. Higher rates of
expulsion during the postpartum period should be considered as
they relate to effectiveness, along with patient access to
interval placement (i.e., not related to pregnancy) when
expulsion rates are lower. Clarification (breastfeeding): Breastfeeding provides important health benefits for breastfeeding parent and infant. The U.S. Dietary Guidelines for Americans and American Academy of Pediatrics recommend that infants be exclusively breastfed for about the first 6 months with continued breastfeeding while introducing appropriate complementary foods for 1 year or longer (13) or up to age 2 years or longer (14). Evidence: Studies suggest that immediate postplacental (<10 minutes) and early postpartum (10 minutes up until 72 hours) placement of Cu-IUDs and LNG-IUDs is associated with increased risk for expulsion compared with interval placement (i.e., not related to pregnancy). A meta-analysis found an increased risk for expulsion with immediate postplacental placement (8.6%; range = 0%–31.9%) and early postpartum placement (25.1%; range = 3.5%–46.7%) compared with interval placement (1.6%; range = 0%–4.8%) (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). Although immediate postplacental placement at the time of cesarean delivery might have increased risk for expulsion compared with interval placement, risk appears lower than that for placement at the time of vaginal delivery. Evidence for infection, perforation, and removals for pain or bleeding are limited; however, these events are rare (15–67). Evidence (breastfeeding): Two RCTs found conflicting results on breastfeeding outcomes when LNG-IUDs were initiated immediately postpartum compared with 6–8 weeks postpartum. Initiation of LNG-IUDs immediately postpartum had no other harmful effect on infant health, growth, or development (19,68). Breastfeeding women using IUDs do not have an increased risk for certain IUD-related adverse events including expulsion, infection, pain, or bleeding compared with nonbreastfeeding women. The risk for perforation is increased independently among breastfeeding women and among women ≤36 weeks postpartum, compared with nonpostpartum women; however, the absolute risk for perforation remains low (15–67,69). Comment: Risk factors for breastfeeding difficulties include previous breastfeeding difficulties, certain medical conditions, certain perinatal complications, and preterm birth. For all breastfeeding persons, with or without risk factors for breastfeeding difficulties, discussions about contraception should include information about risks, benefits, and alternatives. |
||
b. 10 minutes after
delivery of the placenta to <4 weeks |
2 |
2 |
Clarification: Postpartum
placement of IUDs is safe and does not appear to increase health
risks associated with IUD use such as infection. Higher rates of
expulsion during the postpartum period should be considered as
they relate to effectiveness, along with patient access to
interval placement (i.e., not related to pregnancy) when
expulsion rates are lower. Clarification (breastfeeding): Breastfeeding provides important health benefits for breastfeeding parent and infant. The U.S. Dietary Guidelines for Americans and American Academy of Pediatrics recommend that infants be exclusively breastfed for about the first 6 months with continued breastfeeding while introducing appropriate complementary foods for 1 year or longer (13) or up to age 2 years or longer (14). Evidence: Studies suggest that immediate postplacental (<10 minutes) and early postpartum (10 minutes up until 72 hours) placement of Cu-IUDs and LNG-IUDs is associated with increased risk for expulsion compared with interval placement (i.e., not related to pregnancy). A meta-analysis found an increased risk for expulsion with immediate postplacental placement (8.6%; range = 0%–31.9%) and early postpartum placement (25.1%; range = 3.5%–46.7%) compared with interval placement (1.6%; range = 0%–4.8%) (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). Although immediate postplacental placement at the time of cesarean delivery might have increased risk for expulsion compared with interval placement, risk appears lower than that for placement at the time of vaginal delivery. Evidence for infection, perforation, and removals for pain or bleeding are limited; however, these events are rare (15–67). Evidence (breastfeeding): Two RCTs found conflicting results on breastfeeding outcomes when LNG-IUDs were initiated immediately postpartum compared with 6–8 weeks postpartum. Initiation of LNG-IUDs immediately postpartum had no other harmful effect on infant health, growth, or development (19,68). Breastfeeding women using IUDs do not have an increased risk for certain IUD-related adverse events including expulsion, infection, pain, or bleeding compared with nonbreastfeeding women. The risk for perforation is increased independently among breastfeeding women and among women ≤36 weeks postpartum, compared with nonpostpartum women; however, the absolute risk for perforation remains low (15–67,69). Comment: Risk factors for breastfeeding difficulties include previous breastfeeding difficulties, certain medical conditions, certain perinatal complications, and preterm birth. For all breastfeeding persons, with or without risk factors for breastfeeding difficulties, discussions about contraception should include information about risks, benefits, and alternatives. |
||
c. ≥4
weeks |
1 |
1 |
Clarification: Postpartum
placement of IUDs is safe and does not appear to increase health
risks associated with IUD use such as infection. Higher rates of
expulsion during the postpartum period should be considered as
they relate to effectiveness, along with patient access to
interval placement (i.e., not related to pregnancy) when
expulsion rates are lower. Clarification (breastfeeding): Breastfeeding provides important health benefits for breastfeeding parent and infant. The U.S. Dietary Guidelines for Americans and American Academy of Pediatrics recommend that infants be exclusively breastfed for about the first 6 months with continued breastfeeding while introducing appropriate complementary foods for 1 year or longer (13) or up to age 2 years or longer (14). Evidence (breastfeeding): Initiation of LNG-IUDs at 4 weeks postpartum or later demonstrated no detrimental effect on breastfeeding outcomes and no harmful effect on infant health, growth, or development (19,68). Breastfeeding women using IUDs do not have an increased risk for certain IUD-related adverse events including expulsion, infection, pain, or bleeding compared with nonbreastfeeding women. The risk for perforation is increased independently among breastfeeding women and among women ≤36 weeks postpartum, compared with nonpostpartum women; however, the absolute risk for perforation remains low (15–67,69). Comment: Risk factors for breastfeeding difficulties include previous breastfeeding difficulties, certain medical conditions, certain perinatal complications, and preterm birth. For all breastfeeding persons, with or without risk factors for breastfeeding difficulties, discussions about contraception should include information about risks, benefits, and alternatives. |
||
d. Postpartum
sepsis |
4 |
4 |
Comment: Theoretical
concern exists that postpartum placement of an IUD in a person
with recent chorioamnionitis or current endometritis might be
associated with increased complications. |
||
Postabortion
(spontaneous or
induced) | |||||
a. First
trimester abortion |
Clarification: IUDs may be placed immediately
after abortion completion. Evidence: Risk for complications from immediate versus delayed placement of an IUD after abortion did not differ. Expulsion was greater when an IUD was placed after a second trimester procedural abortion than when placed after a first trimester procedural abortion. Safety or expulsion for postabortion placement of an LNG-IUD did not differ from that of a Cu-IUD (70). |
||||
i.
Procedural (surgical) |
1 |
1 |
|||
ii.
Medication |
1 |
1 |
|||
iii.
Spontaneous abortion with no intervention |
1 |
1 |
|||
b. Second
trimester abortion | |||||
i.
Procedural (surgical) |
2 |
2 |
|||
ii.
Medication |
2 |
2 |
|||
iii.
Spontaneous abortion with no intervention |
2 |
2 |
|||
c. Immediate postseptic
abortion |
4 |
4 |
Comment: Placement of an
IUD might substantially worsen the condition. |
||
Past ectopic
pregnancy
|
1 |
1 |
Comment: The absolute
risk for ectopic pregnancy is extremely low because of the high
effectiveness of IUDs. However, when a person becomes pregnant
during IUD use, the relative likelihood of ectopic pregnancy
increases substantially. |
||
History of pelvic
surgery (see recommendations for Postpartum [including cesarean delivery]) |
1 |
1 |
— |
||
Smoking
| |||||
a. Age <35
years |
1 |
1 |
— |
||
b. Age
≥35 years | |||||
i. <15
cigarettes per day |
1 |
1 |
— |
||
ii.
≥15 cigarettes per day |
1 |
1 |
— |
||
Obesity
| |||||
a. BMI ≥30
kg/m2 |
1 |
1 |
— |
||
b. Menarche to <18
years and BMI ≥30 kg/m2 |
1 |
1 |
— |
||
History
of bariatric surgery This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | |||||
a. Restrictive procedures:
decrease storage capacity of the stomach (vertical banded
gastroplasty, laparoscopic adjustable gastric band, or
laparoscopic sleeve gastrectomy) |
1 |
1 |
— |
||
b. Malabsorptive
procedures: decrease absorption of nutrients and calories by
shortening the functional length of the small intestine
(Roux-en-Y gastric bypass or biliopancreatic
diversion) |
1 |
1 |
— |
||
Surgery
| |||||
a. Minor surgery without
immobilization |
1 |
1 |
— |
||
b. Major
surgery | |||||
i. Without
prolonged immobilization |
1 |
1 |
— |
||
ii. With
prolonged immobilization |
1 |
1 |
Evidence: No direct
evidence was identified on risk for thrombosis with POC use
among those undergoing major surgery (Supplementary Appendix,
https://stacks.cdc.gov/view/cdc/156516). |
||
Cardiovascular Disease
| |||||
Multiple risk
factors for atherosclerotic cardiovascular disease
(e.g., older age, smoking, diabetes, hypertension, low HDL, high
LDL, or high triglyceride levels) |
1 |
2 |
— |
||
Hypertension Systolic blood pressure ≥160 mm Hg or diastolic blood pressure ≥100 mm Hg are associated with increased risk for adverse health events as a result of pregnancy (Box 3). | |||||
a. Adequately controlled
hypertension |
1 |
1 |
Clarification: For all
categories of hypertension, classifications are based on the
assumption that no other risk factors for cardiovascular disease
exist. When multiple risk factors do exist, risk for
cardiovascular disease might increase substantially. A single
reading of blood pressure level is not sufficient to classify a
person as hypertensive. |
||
b. Elevated
blood pressure levels
(properly taken
measurements) |
Clarification: For all categories of
hypertension, classifications are based on the assumption that
no other risk factors for cardiovascular disease exist. When
multiple risk factors do exist, risk for cardiovascular disease
might increase substantially. A single reading of blood pressure
level is not sufficient to classify a person as
hypertensive. Comment: Theoretical concern exists about the effect of LNG on lipids. Use of Cu-IUDs has no restrictions. |
||||
i.
Systolic 140–159 mm Hg or diastolic 90–99 mm
Hg |
1 |
1 |
|||
ii.
Systolic ≥160 mm Hg or diastolic ≥100 mm
Hg |
1 |
2 |
|||
c. Vascular
disease |
1 |
2 |
Clarification: For all
categories of hypertension, classifications are based on the
assumption that no other risk factors for cardiovascular disease
exist. When multiple risk factors do exist, risk for
cardiovascular disease might increase substantially. A single
reading of blood pressure level is not sufficient to classify a
person as hypertensive. Comment: Theoretical concern exists about the effect of LNG on lipids. Use of Cu-IUDs has no restrictions. |
||
History of high
blood pressure during pregnancy (when current blood
pressure is measurable and normal) |
1 |
1 |
— |
||
Deep
venous thrombosis/
Pulmonary
embolism This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | |||||
a. Current or history of
DVT/PE, receiving anticoagulant therapy (therapeutic dose)
(e.g., acute DVT/PE or long-term therapeutic dose) |
2 |
2 |
Clarification (Cu-IUD):
Persons using anticoagulant therapy are at risk for gynecologic
complications of therapy, such as heavy or prolonged bleeding.
Cu-IUDs might worsen bleeding. Clarification (LNG-IUD): Persons using anticoagulant therapy are at risk for gynecologic complications of therapy, such as heavy or prolonged bleeding. LNG-IUDs can be of benefit in preventing or treating this complication. When a contraceptive method is used as a therapy, rather than solely to prevent pregnancy, the risk/benefit ratio might differ and should be considered on a case-by-case basis. Evidence: Limited evidence was identified on use of POCs or Cu-IUDs among women with acute DVT/PE receiving anticoagulant therapy (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). In one study among women with a history of acute VTE currently receiving therapeutic anticoagulant therapy (i.e., rivaroxaban or enoxaparin/vitamin K antagonist [warfarin or acenocoumarol]), the incidence of recurrent VTE was similar among estrogen users (CHC or estrogen-only pills), POC users, and women not on hormonal therapy (71). Limited evidence suggests that placement of a Cu-IUD or LNG-IUD does not increase risk for bleeding complications in women receiving anticoagulant therapy (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). |
||
b. History of
DVT/PE, receiving
anticoagulant
therapy
(prophylactic dose) |
Clarification
(Cu-IUD): Persons using anticoagulant therapy are at
risk for gynecologic complications of therapy, such as heavy or
prolonged bleeding. Cu-IUDs might worsen
bleeding. Clarification (LNG-IUD): Persons using anticoagulant therapy are at risk for gynecologic complications of therapy, such as heavy or prolonged bleeding. LNG-IUDs can be of benefit in preventing or treating this complication. When a contraceptive method is used as a therapy, rather than solely to prevent pregnancy, the risk/benefit ratio might differ and should be considered on a case-by-case basis. Evidence: Limited evidence suggests that placement of the LNG-IUD does not increase risk for bleeding complications in women receiving anticoagulant therapy (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). |
||||
i. Higher
risk for recurrent DVT/PE (one or more risk factors) |
2 |
2 |
|||
• Thrombophilia (e.g.,
factor V Leiden mutation; prothrombin gene mutation; protein S,
protein C, and antithrombin deficiencies; or antiphospholipid
syndrome) • Active cancer (metastatic, receiving therapy, or within 6 months after clinical remission), excluding nonmelanoma skin cancer • History of recurrent DVT/PE | |||||
ii. Lower
risk for recurrent DVT/PE (no risk factors) |
2 |
2 |
|||
c. History of
DVT/PE, not
receiving anticoagulant therapy | |||||
i. Higher
risk for recurrent DVT/PE (one or more risk factors) |
1 |
2 |
— |
||
• History of
estrogen-associated
DVT/PE • Pregnancy-associated DVT/PE • Idiopathic DVT/PE • Thrombophilia (e.g., factor V Leiden mutation; prothrombin gene mutation; protein S, protein C, and antithrombin deficiencies; or antiphospholipid syndrome) • Active cancer (metastatic, receiving therapy, or within 6 months after clinical remission), excluding nonmelanoma skin cancer • History of recurrent DVT/PE | |||||
ii. Lower
risk for recurrent DVT/PE (no risk factors) |
1 |
2 |
— |
||
d. Family history
(first-degree relatives) |
1 |
1 |
— |
||
Thrombophilia
(e.g., factor V Leiden mutation; prothrombin gene mutation;
protein S, protein C, and antithrombin deficiencies; or
antiphospholipid syndrome)
This condition is associated
with increased risk for adverse health events as a result of
pregnancy (Box
3). |
1 |
2 |
Clarification: Routine
screening in the general population before contraceptive
initiation is not
recommended. Clarification: If a person has current or history of DVT/PE, see recommendations for DVT/PE. Clarification: Classification of antiphospholipid syndrome includes presence of a clinical feature (e.g., thrombosis or obstetric morbidity) and persistently abnormal antiphospholipid antibody test on two or more occasions at least 12 weeks apart (72). Evidence: Limited evidence was identified on LNG-IUD use among persons with thrombophilia. Among women with factor V Leiden mutation, one study found that women using LNG-IUD had similar risk for venous thrombosis as those not using hormonal contraception (73). No evidence was identified on POC use among persons with prothrombin gene mutation, protein S deficiency, protein C deficiency, antithrombin deficiency, or antiphospholipid syndrome (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). |
||
Superficial venous disorders
| |||||
a. Varicose
veins |
1 |
1 |
— |
||
b. Superficial venous
thrombosis (acute or history) |
1 |
1 |
— |
||
Current
and history of ischemic heart disease This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
1 |
Initiation |
Continuation |
Comment:
Theoretical concern exists about the effect of LNG on lipids.
Use of Cu-IUDs has no restrictions. |
|
2 |
3 |
||||
Stroke
(history of cerebrovascular accident)
This condition is
associated with increased risk for adverse health events as a
result of pregnancy (Box
3). |
1 |
2 |
Comment: Theoretical
concern exists about the effect of LNG on lipids. Use of Cu-IUDs
has no restrictions. |
||
Valvular
heart disease Complicated valvular heart disease is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
Comment:
According to the American Heart Association, administration of
prophylactic antibiotics solely to prevent endocarditis is not
recommended for patients who undergo genitourinary tract
procedures, including placement or removal of IUDs (74). |
||||
a. Uncomplicated |
1 |
1 |
|||
b. Complicated (pulmonary
hypertension, risk for atrial fibrillation, or history of
subacute bacterial endocarditis) |
1 |
1 |
|||
Peripartum cardiomyopathy This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
Evidence: No
direct evidence exists on the safety of IUDs among women with
peripartum cardiomyopathy. Limited indirect evidence from
noncomparative studies did not demonstrate any cases of
arrhythmia or infective endocarditis in women with cardiac
disease who used IUDs (75). Comment: IUD placement might induce cardiac arrhythmias in healthy persons; persons with peripartum cardiomyopathy have a high incidence of cardiac arrhythmias. |
||||
a. Normal or
mildly impaired
cardiac function (New York
Heart
Association Functional Class I or II:
no
limitation of activities or slight,
mild limitation of
activity) (76) | |||||
i. <6
months |
2 |
2 |
|||
ii.
≥6 months |
2 |
2 |
|||
b. Moderately or severely
impaired cardiac function (New York Heart Association Functional
Class III or IV: marked limitation of activity or should be at
complete rest) (76) |
2 |
2 |
|||
Renal
Disease
| |||||
Chronic kidney
disease This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
Initiation |
Continuation |
Initiation |
Continuation |
|
a. Current nephrotic
syndrome |
1 |
1 |
2 |
2 |
Comment: A person might
have CKD without current nephrotic syndrome, but might have
other conditions often associated with CKD (e.g., diabetes,
hypertension, SLE). See recommendations for other conditions if
they apply. |
b. Hemodialysis |
1 |
1 |
2 |
2 |
Evidence: No comparative
studies were identified on the safety of IUD use among persons
with CKD on hemodialysis (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). One
case report of LNG-IUD use in a person with CKD on hemodialysis
reported improved abnormal uterine bleeding and anemia (77). Comment: A person might have CKD without hemodialysis, but might have other conditions often associated with CKD (e.g., diabetes, hypertension, and SLE). See recommendations for other conditions if they apply. |
c. Peritoneal
dialysis |
2 |
1 |
2 |
2 |
Evidence: No comparative
studies were identified on IUD use among persons with CKD on
peritoneal dialysis (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). Four
case reports of IUD use among women with CKD on peritoneal
dialysis identified one case of peritoneal allergic reaction
(78), three cases of peritonitis (78–80) and
one case of TOA (78). Comment: A person might have CKD without peritoneal dialysis, but might have other conditions often associated with CKD (e.g., diabetes, hypertension, and SLE). See recommendations for other conditions if they apply. |
Rheumatic Diseases
| |||||
Systemic lupus
erythematosus This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
Initiation |
Continuation |
— |
||
a. Positive (or unknown)
antiphospholipid antibodies |
1 |
1 |
2 |
Clarification: Persons
with SLE are at increased risk for ischemic heart disease,
stroke, and VTE. Categories assigned to such conditions in U.S.
MEC should be the same for persons with SLE who have these
conditions. For all subconditions of SLE, classifications are
based on the assumption that no other risk factors for
cardiovascular disease are present; these classifications must
be modified in the presence of such risk factors (81–99). Evidence: No direct evidence was identified on POC use among persons with SLE with antiphospholipid antibodies (100) (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). |
|
b. Severe
thrombocytopenia |
3 |
2 |
2 |
Clarification: Persons
with SLE are at increased risk for ischemic heart disease,
stroke, and VTE. Categories assigned to such conditions in U.S.
MEC should be the same for persons with SLE who have these
conditions. For all subconditions of SLE, classifications are
based on the assumption that no other risk factors for
cardiovascular disease are present; these classifications must
be modified in the presence of such risk factors (81–99). Clarification: Severe thrombocytopenia increases the risk for bleeding. The category should be assessed according to the severity of thrombocytopenia and its clinical manifestations. In persons with very severe thrombocytopenia who are at risk for spontaneous bleeding, consultation with a specialist and certain pretreatments might be warranted. Evidence: The LNG-IUD might be a useful treatment for menorrhagia in women with severe thrombocytopenia (94). |
|
c. Immunosuppressive
therapy |
2 |
1 |
2 |
Clarification: Persons
with SLE are at increased risk for ischemic heart disease,
stroke, and VTE. Categories assigned to such conditions in U.S.
MEC should be the same for persons with SLE who have these
conditions. For all subconditions of SLE, classifications are
based on the assumption that no other risk factors for
cardiovascular disease are present; these classifications must
be modified in the presence of such risk factors (81–99). |
|
d. None of the
above |
1 |
1 |
2 |
Clarification: Persons
with SLE are at increased risk for ischemic heart disease,
stroke, and VTE. Categories assigned to such conditions in U.S.
MEC should be the same for persons with SLE who have these
conditions. For all subconditions of SLE, classifications are
based on the assumption that no other risk factors for
cardiovascular disease are present; these classifications must
be modified in the presence of such risk factors (81–99). |
|
Rheumatoid
arthritis
|
Initiation |
Continuation |
Initiation |
Continuation |
— |
a. Not receiving
immunosuppressive therapy |
1 |
1 |
1 |
1 |
— |
b. Receiving
immunosuppressive therapy |
2 |
1 |
2 |
1 |
— |
Neurologic Conditions
| |||||
Headaches
| |||||
a. Nonmigraine (mild or
severe) |
1 |
1 |
— |
||
b.
Migraine | |||||
i. Without
aura (includes menstrual migraine) |
1 |
1 |
Evidence: No
studies directly examined the risk for stroke among women with
migraine using LNG-IUDs (101). Limited evidence
demonstrated that women using LNG-IUDs do not have an increased
risk for ischemic stroke compared with women not using hormonal
contraceptives (102). Comment: Menstrual migraine is a subtype of migraine without aura. For more information see the International Headache Society’s International Classification of Headache Disorders, 3rd ed. (https://ichd-3.org) (103). |
||
ii. With
aura |
1 |
1 |
|||
Epilepsy This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
1 |
1 |
— |
||
Multiple
sclerosis
| |||||
a. Without prolonged
immobility |
1 |
1 |
— |
||
b. With prolonged
immobility |
1 |
1 |
— |
||
Depressive Disorders
| |||||
Depressive
disorders
|
1 |
1 |
Clarification: If a
person is receiving psychotropic medications or St.
John’s wort, see recommendations for Drug
Interactions. Evidence: The frequency of psychiatric hospitalizations for women with bipolar disorder or depression did not significantly differ among women using DMPA, LNG-IUD, Cu-IUD, or sterilization (104). |
||
Reproductive Tract Infections and
Disorders
| |||||
Vaginal
bleeding patterns
|
Initiation |
Continuation |
— |
||
a. Irregular pattern
without heavy bleeding |
1 |
1 |
1 |
||
b. Heavy or prolonged
bleeding (includes regular and irregular patterns) |
2 |
1 |
2 |
Clarification: Unusually
heavy bleeding should raise suspicion of a serious underlying
condition. Evidence: Evidence from studies examining the treatment effects of the LNG-IUD among women with heavy or prolonged bleeding reported no increase in adverse effects and found the LNG-IUD to be beneficial in treating menorrhagia (105–112). |
|
Unexplained vaginal bleeding (suspicious for
serious condition) before evaluation |
Initiation |
Continuation |
Initiation |
Continuation |
Clarification: If pregnancy or an underlying
pathological condition (e.g., pelvic malignancy) is suspected,
it must be evaluated and the category adjusted after evaluation.
The IUD does not need to be removed before evaluation. |
4 |
2 |
4 |
2 |
||
Endometriosis
|
2 |
1 |
Evidence: LNG-IUD use
among women with endometriosis decreased dysmenorrhea, pelvic
pain, and dyspareunia (113–117). |
||
Benign ovarian
tumors (including cysts) |
1 |
1 |
— |
||
Severe
dysmenorrhea
|
2 |
1 |
Comment: Dysmenorrhea
might intensify with Cu-IUD use. LNG-IUD use has been associated
with reduction of dysmenorrhea. |
||
Gestational trophoblastic disease This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | |||||
a. Suspected
gestational trophoblastic
disease (immediate
postevacuation) |
Clarification: For all subconditions of
gestational trophoblastic disease, classifications are based on
the assumption that persons are under close medical supervision
because of the need for monitoring of β-hCG levels for
appropriate disease surveillance. Evidence: Limited evidence suggests that women using an IUD after uterine evacuation for a molar pregnancy are not at greater risk for postmolar trophoblastic disease than are women using other methods of contraception (118). Comment: The risk for expulsion immediately postevacuation for gestational trophoblastic disease is unknown. Expulsion is greater after IUD placement immediately postevacuation for a spontaneous or induced abortion in the second trimester compared with IUD placement after a first trimester abortion. |
||||
i. Uterine
size first trimester |
1 |
1 |
|||
ii.
Uterine size second trimester |
2 |
2 |
|||
b. Confirmed gestational
trophoblastic disease (after initial evacuation and during
monitoring) |
Initiation |
Continuation |
Initiation |
Continuation |
— |
i.
Undetectable or nonpregnant β-hCG levels |
1 |
1 |
1 |
1 |
Clarification: For all
subconditions of gestational trophoblastic disease,
classifications are based on the assumption that persons are
under close medical supervision because of the need for
monitoring of β-hCG levels for appropriate disease
surveillance. Evidence: Limited evidence suggests that women using an IUD after uterine evacuation for a molar pregnancy are not at greater risk for postmolar trophoblastic disease than are women using other methods of contraception (118). Comment: Once β-hCG levels have decreased to nonpregnant levels, the risk for disease progression is likely to be very low. |
ii.
Decreasing β-hCG levels |
2 |
1 |
2 |
1 |
Clarification: For all
subconditions of gestational trophoblastic disease,
classifications are based on the assumption that persons are
under close medical supervision because of the need for
monitoring of β-hCG levels for appropriate disease
surveillance. Clarification: For persons at higher risk for disease progression, the benefits of effective contraception must be weighed against the potential need for early IUD removal. Evidence: Limited evidence suggests that women using an IUD after uterine evacuation for a molar pregnancy are not at greater risk for postmolar trophoblastic disease than are women using other methods of contraception (118). |
iii.
Persistently elevated β-hCG levels or malignant disease,
with no evidence or suspicion of intrauterine disease |
2 |
1 |
2 |
1 |
Clarification: For all
subconditions of gestational trophoblastic disease,
classifications are based on the assumption that persons are
under close medical supervision because of the need for
monitoring of β-hCG levels for appropriate disease
surveillance. Evidence: Limited evidence suggests that women using an IUD after uterine evacuation for a molar pregnancy are not at greater risk for postmolar trophoblastic disease than are women using other methods of contraception (118). |
iv.
Persistently elevated β-hCG levels or malignant disease,
with evidence or suspicion of intrauterine disease |
4 |
2 |
4 |
2 |
Clarification: For all
subconditions of gestational trophoblastic disease,
classifications are based on the assumption that persons are
under close medical supervision because of the need for
monitoring of β-hCG levels for appropriate disease
surveillance. Evidence: Limited evidence suggests that women using an IUD after uterine evacuation for a molar pregnancy are not at greater risk for postmolar trophoblastic disease than are women using other methods of contraception (118). Comment: For persons with suspected or confirmed intrauterine disease, an IUD should not be placed because of theoretical risk for perforation, infection, and hemorrhage. For persons who already have an IUD in place, individual circumstance along with the benefits of effective contraception must be weighed against theoretical risks of either removal or continuation of the IUD. |
Cervical
ectropion
|
1 |
1 |
— |
||
Cervical
intraepithelial neoplasia
|
1 |
2 |
Comment: Theoretical
concern exists that LNG-IUDs might enhance progression of
cervical intraepithelial neoplasia. |
||
Cervical
cancer (awaiting treatment) |
Initiation |
Continuation |
Initiation |
Continuation |
Comment:
Concern exists about the increased risk for infection and
bleeding at placement. The IUD most likely will need to be
removed at the time of treatment but until then, the person is
at risk for pregnancy. |
4 |
2 |
4 |
2 |
||
Breast
disease Breast cancer is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | |||||
a. Undiagnosed
mass |
1 |
2 |
Clarification (LNG-IUD):
Evaluation of mass should be pursued as early as
possible. |
||
b. Benign breast
disease |
1 |
1 |
— |
||
c. Family history of
cancer |
1 |
1 |
— |
||
d. Breast cancer |
|
|
Comment:
Breast cancer is a hormonally sensitive tumor. Concerns about
progression of the disease might be less with LNG-IUDs than with
COCs or higher-dose POCs. |
||
i.
Current |
1 |
4 |
|||
ii. Past
and no evidence of current disease for 5 years |
1 |
3 |
|||
Endometrial
hyperplasia
|
1 |
1 |
Evidence: Among women
with endometrial hyperplasia, no adverse health events occurred
with LNG-IUD use; most women experienced disease regression
(119). |
||
Endometrial cancer This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
Initiation |
Continuation |
Initiation |
Continuation |
Comment:
Concern exists about the increased risk for infection,
perforation, and bleeding at placement. The IUD most likely will
need to be removed at the time of treatment, but until then, the
person is at risk for pregnancy. |
4 |
2 |
4 |
2 |
||
Ovarian
cancer This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
1 |
1 |
Comment: Persons with
ovarian cancer who undergo fertility-sparing treatment and need
contraception can use an IUD. |
||
Uterine
fibroids
|
2 |
2 |
Evidence: Among women
with uterine fibroids using an LNG-IUD, most experienced
improvements in serum levels of hemoglobin, hematocrit, and
ferritin and in menstrual blood loss (120). Rates of LNG-IUD
expulsion were higher in women with uterine fibroids (11%) than
in women without fibroids (0%–3%); these findings were
either not statistically significant or significance testing was
not conducted (120). Rates of expulsion found
in noncomparative studies ranged from 0%–20% (120). Comment: Persons with heavy or prolonged bleeding should be assigned the category for that condition. |
||
Anatomical abnormalities
| |||||
a. Distorted uterine
cavity (any congenital or acquired uterine abnormality
distorting the uterine cavity in a manner that is incompatible
with IUD placement) |
4 |
4 |
Comment: An anatomical
abnormality that distorts the uterine cavity might preclude
proper IUD placement. |
||
b. Other abnormalities
(including cervical stenosis or cervical lacerations) not
distorting the uterine cavity or interfering with IUD
placement |
2 |
2 |
— |
||
Pelvic inflammatory
disease
|
Initiation |
Continuation |
Initiation |
Continuation |
Clarification
(continuation): Treat the PID using appropriate
antibiotics. The IUD usually does not need to be removed if the
person wants to continue using it. Continued use of an IUD
depends on the person’s informed choice and current risk
factors for STIs and PID. Evidence: Among IUD users treated for PID, clinical course did not differ regardless of whether the IUD was removed or left in place (121). |
a. Current PID |
4 |
2 |
4 |
2 |
|
b. Past
PID |
Comment: IUDs
do not protect against STIs, including HIV infection, or PID. In
persons at low risk for STIs, IUD placement poses little risk
for PID. |
||||
i. With
subsequent pregnancy |
1 |
1 |
1 |
1 |
|
ii.
Without subsequent pregnancy |
2 |
2 |
2 |
2 |
|
Sexually transmitted
infections
|
Initiation |
Continuation |
Initiation |
Continuation |
|
a. Current purulent
cervicitis or chlamydial infection or gonococcal
infection |
4 |
2 |
4 |
2 |
Clarification
(continuation): Treat the STI using appropriate
antibiotics. The IUD usually does not need to be removed if the
person wants to continue using it. Continued use of an IUD
depends on the person’s informed choice and current risk
factors for STIs and PID. Evidence: Among women who had an IUD placed, the absolute risk for subsequent PID was low among women with STI at the time of placement but greater than among women with no STI at the time of IUD placement (122–128). |
b. Vaginitis (including
Trichomonas vaginalis and bacterial
vaginosis) |
2 |
2 |
2 |
2 |
— |
c. Other factors related
to STIs |
2 |
2 |
2 |
2 |
Clarification
(initiation): Most persons do not require additional
STI screening at the time of IUD placement. If a person with
risk factors for STIs has not been screened for gonorrhea and
chlamydia according to CDC STI treatment guidelines (1),
screening may be performed at the time of IUD placement and
placement should not be delayed. Evidence: Women who undergo same-day STI screening and IUD placement have low incidence rates of PID. Algorithms for predicting PID among women with risk factors for STIs have poor predictive value. Risk for PID among women with risk factors for STIs is low (129). |
HIV
| |||||
High
risk for HIV infection
|
Initiation |
Continuation |
Initiation |
Continuation |
Clarification: Many persons at high risk for
HIV infection are also at risk for other STIs (see
recommendations for Sexually transmitted Infections in U.S. MEC
and recommendations on STI screening before IUD placement in
U.S. SPR (https://www.cdc.gov/contraception/hcp/usspr)
(3). Evidence: High-quality evidence from one RCT, along with low-quality evidence from two observational studies, suggested no increased risk for HIV acquisition with Cu-IUD use. No studies were identified for LNG-IUDs (130–132). |
1 |
1 |
1 |
1 |
||
HIV
infection For persons with HIV infection who are not clinically well or not receiving ARV therapy, this condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
Evidence:
Among IUD users, limited evidence demonstrates a low risk for
PID among HIV-infected women using IUDs and no higher risk for
pelvic infectious complications in HIV-infected than in
HIV-noninfected women or among women with varying degrees of HIV
severity. IUD use did not adversely affect progression of HIV
infection during 6–45 months of follow-up or when
compared with hormonal contraceptive use among HIV-infected
women. Furthermore, IUD use among HIV-infected women was not
associated with increased risk for transmission to sex partners
or with increased genital viral shedding (133). |
||||
a. Clinically well
receiving ARV therapy |
1 |
1 |
1 |
1 |
|
b. Not clinically well or
not receiving ARV therapy |
2 |
1 |
2 |
1 |
|
Other
Infections
| |||||
Schistosomiasis Schistosomiasis with fibrosis of the liver is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | |||||
A. Uncomplicated |
1 |
1 |
— |
||
b. Fibrosis of the liver
(if severe, see recommendations for Cirrhosis) |
1 |
1 |
— |
||
Tuberculosis
This condition is associated
with
increased risk for adverse health
events as a
result of pregnancy
(Box 3). |
Initiation |
Continuation |
Initiation |
Continuation |
|
a. Nonpelvic |
1 |
1 |
1 |
1 |
— |
b. Pelvic |
4 |
3 |
4 |
3 |
Comment: Placement of an
IUD might substantially worsen the condition. |
Malaria
|
1 |
1 |
— |
||
Endocrine Conditions
| |||||
Diabetes Insulin-dependent diabetes diabetes with nephropathy, retinopathy, or neuropathy; diabetes with other vascular disease; or diabetes of >20 years’ duration are associated with increased risk for adverse health events as a result of pregnancy (Box 3). | |||||
a. History of gestational
disease |
1 |
1 |
— |
||
b. Nonvascular
disease |
|
|
Evidence:
Limited evidence on the use of the LNG-IUD among women with
insulin-dependent or non–insulin-dependent diabetes
suggests that these methods have little effect on short-term or
long-term diabetes control (e.g., glycosylated hemoglobin
levels), hemostatic markers, or lipid profile (134,135). |
||
i.
Non-insulin dependent |
1 |
2 |
|||
ii.
Insulin dependent |
1 |
2 |
|||
c. Nephropathy,
retinopathy, or neuropathy |
1 |
2 |
— |
||
d. Other vascular disease
or diabetes of >20 years’ duration |
1 |
2 |
— |
||
Thyroid
disorders
| |||||
a. Simple goiter |
1 |
1 |
— |
||
b. Hyperthyroid |
1 |
1 |
— |
||
c. Hypothyroid |
1 |
1 |
— |
||
Gastrointestinal Conditions
| |||||
Inflammatory bowel
disease (ulcerative colitis or Crohn’s
disease) |
1 |
1 |
Evidence: Although two
case reports described three women with IBD who experienced
exacerbation of disease 5 days–25 months after LNG-IUD
placement (136), no comparative studies have
examined the safety of IUD use among women with IBD (136). |
||
Gallbladder disease
| |||||
a. Asymptomatic |
1 |
2 |
— |
||
b.
Symptomatic | |||||
i.
Current |
1 |
2 |
— |
||
ii.
Treated by cholecystectomy |
1 |
2 |
— |
||
iii.
Medically treated |
1 |
2 |
— |
||
History of cholestasis
| |||||
a. Pregnancy
related |
1 |
1 |
— |
||
b. Past COC
related |
1 |
2 |
Comment: Concern exists
that history of COC related cholestasis might predict subsequent
cholestasis with LNG use. Whether risk exists with use of
LNG-IUD is unclear. |
||
Viral
hepatitis
| |||||
a. Acute or
flare |
1 |
1 |
Evidence: No direct
evidence was identified on IUD use among persons with viral
hepatitis (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). |
||
b. Chronic |
1 |
1 |
Evidence: No direct
evidence was identified on IUD use among persons with viral
hepatitis (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). |
||
Cirrhosis Decompensated cirrhosis is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | |||||
a. Compensated (normal
liver function) |
1 |
1 |
Evidence: No direct
evidence was identified on IUD use among persons with cirrhosis
(Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). |
||
b. Decompensated (impaired
liver function) |
1 |
2 |
Evidence: No direct
evidence was identified on IUD use among persons with cirrhosis
(Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). Comment: Hepatic metabolism of exogenous hormones might be impaired in persons with liver dysfunction, which could lead to increased progestin levels in circulation and progestin-related side effects and adverse events, which might vary by dose and formulation. Any progestin-related hepatotoxicity might be less tolerated in persons with existing liver dysfunction. |
||
Liver
tumors Hepatocellular adenoma and malignant liver tumors are associated with increased risk for adverse health events as a result of pregnancy (Box 3). | |||||
a.
Benign | |||||
i. Focal
nodular hyperplasia |
1 |
2 |
Evidence: Limited
evidence suggests that progestin use does not influence either
progression or regression of focal nodular hyperplasia
(Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). |
||
ii.
Hepatocellular adenoma |
1 |
2 |
Evidence: Limited
evidence suggests that hepatocellular adenomas generally regress
or remain stable during progestin use (Supplementary Appendix,
https://stacks.cdc.gov/view/cdc/156516). |
||
b. Malignant
(hepatocellular carcinoma) |
1 |
3 |
Evidence: No direct
evidence was identified on IUD use among persons with
hepatocellular carcinoma (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). |
||
Respiratory Conditions
| |||||
Cystic
fibrosis This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
1 |
1 |
Clarification: Persons
with cystic fibrosis are at increased risk for diabetes, liver
disease, gallbladder disease, and VTE (particularly related to
use of central venous catheters) and are frequently prescribed
antibiotics. Categories assigned to such conditions in U.S. MEC
should be the same for persons with cystic fibrosis who have
these conditions. For cystic fibrosis, classifications are based
on the assumption that no other conditions are present; these
classifications must be modified in the presence of such
conditions. |
||
Hematologic Conditions
| |||||
Thalassemia
|
2 |
1 |
Comment: Concern exists
about an increased risk for blood loss with Cu-IUDs. |
||
Sickle cell
disease This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
2 |
1 |
Comment: Concern exists
about an increased risk for blood loss with Cu-IUDs. |
||
Iron deficiency
anemia
|
2 |
1 |
Comment: Concern exists
about an increased risk for blood loss with Cu-IUDs. |
||
Solid
Organ Transplantation
| |||||
Solid organ
transplantation This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
Initiation |
Continuation |
Initiation |
Continuation |
Evidence:
Limited evidence suggests that LNG-IUD use among solid organ
transplantation recipients does not increase risk for pelvic
infections or decrease contraceptive effectiveness over time or
compared with persons without solid organ transplantation No
evidence was identified for Cu-IUD (Supplementary Appendix,
https://stacks.cdc.gov/view/cdc/156516). |
a. No graft
failure |
1 |
1 |
1 |
1 |
|
b. Graft failure |
2 |
1 |
2 |
1 |
|
Drug
Interactions
| |||||
Antiretrovirals used
for prevention (PrEP) or treatment of HIV
|
Initiation |
Continuation |
Initiation |
Continuation |
Clarification: No known interaction exists
between ARV therapy and IUD use. However, for persons with HIV
infection, IUD placement is classified as category 2 if the
person is not clinically well or not receiving ARV therapy.
Otherwise, both placement and continuation are classified as
category 1 (see recommendations for HIV infection). For persons
at high risk for HIV infection, IUDs are category 1 for
initiation and continuation (see recommendations for High risk
for HIV infection). |
a. Nucleoside
reverse
transcriptase inhibitors
(NRTIs) | |||||
i.
Abacavir (ABC) |
1/2 |
1 |
1/2 |
1 |
|
ii.
Tenofovir (TDF) |
1/2 |
1 |
1/2 |
1 |
|
iii.
Zidovudine (AZT) |
1/2 |
1 |
1/2 |
1 |
|
iv.
Lamivudine (3TC) |
1/2 |
1 |
1/2 |
1 |
|
v.
Didanosine (DDI) |
1/2 |
1 |
1/2 |
1 |
|
vi.
Emtricitabine (FTC) |
1/2 |
1 |
1/2 |
1 |
|
vii.
Stavudine (D4T) |
1/2 |
1 |
1/2 |
1 |
|
b.
Nonnucleoside reverse
transcriptase inhibitors
(NNRTIs) | |||||
i.
Efavirenz (EFV) |
1/2 |
1 |
1/2 |
1 |
|
ii.
Etravirine (ETR) |
1/2 |
1 |
1/2 |
1 |
|
iii.
Nevirapine (NVP) |
1/2 |
1 |
1/2 |
1 |
|
iv.
Rilpivirine (RPV) |
1/2 |
1 |
1/2 |
1 |
|
c.
Ritonavir-boosted protease
inhibitors | |||||
i.
Ritonavir-boosted atazanavir (ATV/r) |
1/2 |
1 |
1/2 |
1 |
|
ii.
Ritonavir-boosted darunavir (DRV/r) |
1/2 |
1 |
1/2 |
1 |
|
iii.
Ritonavir-boosted fosamprenavir (FPV/r) |
1/2 |
1 |
1/2 |
1 |
|
iv.
Ritonavir-boosted lopinavir (LPV/r) |
1/2 |
1 |
1/2 |
1 |
|
v.
Ritonavir-boosted saquinavir (SQV/r) |
1/2 |
1 |
1/2 |
1 |
|
vi.
Ritonavir-boosted tipranavir (TPV/r) |
1/2 |
1 |
1/2 |
1 |
|
d. Protease
inhibitors without
ritonavir | |||||
i.
Atazanavir (ATV) |
1/2 |
1 |
1/2 |
1 |
|
ii.
Fosamprenavir (FPV) |
1/2 |
1 |
1/2 |
1 |
|
iii.
Indinavir (IDV) |
1/2 |
1 |
1/2 |
1 |
|
iv.
Nelfinavir (NFV) |
1/2 |
1 |
1/2 |
1 |
|
e. CCR5
co-receptor antagonists | |||||
i.
Maraviroc (MVC) |
1/2 |
1 |
1/2 |
1 |
|
f. HIV
integrase strand transfer
inhibitors | |||||
i.
Raltegravir (RAL) |
1/2 |
1 |
1/2 |
1 |
|
ii.
Dolutegravir (DTG) |
1/2 |
1 |
1/2 |
1 |
|
iii.
Elvitegravir (EVG) |
1/2 |
1 |
1/2 |
1 |
|
g. Fusion
inhibitors | |||||
i.
Enfuvirtide |
1/2 |
1 |
1/2 |
1 |
|
Anticonvulsant therapy
| |||||
a. Certain anticonvulsants
(phenytoin, carbamazepine, barbiturates, primidone, topiramate,
and oxcarbazepine) |
1 |
1 |
Evidence: Limited
evidence suggests use of certain anticonvulsants does not
interfere with the contraceptive effectiveness of the LNG-IUD
(137,138). |
||
b. Lamotrigine |
1 |
1 |
Evidence: No drug
interactions have been reported among women with epilepsy who
are receiving lamotrigine and using the LNG-IUD (138,139). |
||
Antimicrobial therapy
| |||||
a. Broad-spectrum
antibiotics |
1 |
1 |
— |
||
b. Antifungals |
1 |
1 |
— |
||
c.
Antiparasitics |
1 |
1 |
— |
||
d. Rifampin or rifabutin
therapy |
1 |
1 |
Evidence: One
cross-sectional survey found that rifabutin had no impact on the
effectiveness of the LNG-IUD (137). |
||
Psychotropic medications
| |||||
a. Selective serotonin
reuptake inhibitors (SSRIs) |
1 |
1 |
Comment: For many common
psychotropic agents, limited or no theoretical concern exists
for clinically significant drug interactions when
co-administered with hormonal contraceptives. However, either no
or very limited data exist examining potential interactions for
these classes of medications. |
||
St. John’s wort | 1 |
1 |
— |
Abbreviations: ARV = antiretroviral; BMI = body mass index; CHC = combined hormonal contraceptive; CKD = chronic kidney disease; COC = combined oral contraceptive; Cu-IUD = copper intrauterine device; DMPA = depot medroxyprogesterone acetate; DVT = deep venous thrombosis; hCG = human chorionic gonadotropin; HDL = high-density lipoprotein; IBD = inflammatory bowel disease; IUD = intrauterine device; LDL = low-density lipoprotein; LNG = levonorgestrel; LNG-IUD = levonorgestrel intrauterine device; NA = not applicable; PE = pulmonary embolism; PID = pelvic inflammatory disease; POC = progestin-only contraceptive; PrEP = pre-exposure prophylaxis; RCT = randomized clinical trial; SLE = systemic lupus erythematous; STI = sexually transmitted infection; TOA = tubo-ovarian abscess; U.S. MEC = U.S. Medical Eligibility Criteria for Contraceptive Use; U.S. SPR = U.S. Selected Practice Recommendations for Contraceptive Use; VTE = venous thromboembolism.
References
- 1.Workowski KA, Bachmann LH, Chan PA, et al. Sexually transmitted infections treatment guidelines, 2021. MMWR Recomm Rep 2021;70(No. RR-4):1–187. 10.15585/mmwr.rr7004a1 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2.CDC. US Public Health Service preexposure prophylaxis for the prevention of HIV infection in the United States—2021 update: a clinical practice guideline. Atlanta, GA: US Department of Health and Human Services, CDC; 2021. https://www.cdc.gov/hiv/pdf/risk/prep/cdc-hiv-prep-guidelines-2021.pdf
- 3.Curtis KM, Nguyen AT, Tepper NK, et al. U.S. selected practice recommendations for contraceptive use, 2024. MMWR Recomm Rep 2024;73(No. RR-3):1–77. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4.Cramer DW, Schiff I, Schoenbaum SC, et al. Tubal infertility and the intrauterine device. N Engl J Med 1985;312:941–7. 10.1056/NEJM198504113121502 [DOI] [PubMed] [Google Scholar]
- 5.Daling JR, Weiss NS, Metch BJ, et al. Primary tubal infertility in relation to the use of an intrauterine device. N Engl J Med 1985;312:937–41. 10.1056/NEJM198504113121501 [DOI] [PubMed] [Google Scholar]
- 6.Daling JR, Weiss NS, Voigt LF, McKnight B, Moore DE. The intrauterine device and primary tubal infertility. N Engl J Med 1992;326:203–4. 10.1056/NEJM199201163260314 [DOI] [PubMed] [Google Scholar]
- 7.Delbarge W, Bátár I, Bafort M, et al. Return to fertility in nulliparous and parous women after removal of the GyneFix intrauterine contraceptive system. Eur J Contracept Reprod Health Care 2002;7:24–30. 10.1080/ejc.7.1.24.30 [DOI] [PubMed] [Google Scholar]
- 8.Doll H, Vessey M, Painter R. Return of fertility in nulliparous women after discontinuation of the intrauterine device: comparison with women discontinuing other methods of contraception. BJOG 2001;108:304–14. 10.1111/j.1471-0528.2001.00075.x [DOI] [PubMed] [Google Scholar]
- 9.Hubacher D, Lara-Ricalde R, Taylor DJ, Guerra-Infante F, Guzmán-Rodríguez R. Use of copper intrauterine devices and the risk of tubal infertility among nulligravid women. N Engl J Med 2001;345:561–7. 10.1056/NEJMoa010438 [DOI] [PubMed] [Google Scholar]
- 10.Skjeldestad FE, Bratt H. Return of fertility after use of IUDs (Nova-T, MLCu250 and MLCu375). Adv Contracept 1987;3:139–45. 10.1007/BF01890702 [DOI] [PubMed] [Google Scholar]
- 11.Urbach DR, Marrett LD, Kung R, Cohen MM. Association of perforation of the appendix with female tubal infertility. Am J Epidemiol 2001;153:566–71. 10.1093/aje/153.6.566 [DOI] [PubMed] [Google Scholar]
- 12.Wilson JC. A prospective New Zealand study of fertility after removal of copper intrauterine contraceptive devices for conception and because of complications: a four-year study. Am J Obstet Gynecol 1989;160:391–6. 10.1016/0002-9378(89)90455-9 [DOI] [PubMed] [Google Scholar]
- 13.US Department of Agriculture; US Department of Health and Human Services. Dietary guidelines for Americans, 2020–2025. 9th ed. Washington, DC: US Department of Agriculture and US Department of Health and Human Services; 2020. https://www.dietaryguidelines.gov/sites/default/files/2021-03/Dietary_Guidelines_for_Americans-2020-2025.pdf
- 14.Meek JY, Noble L; Section on Breastfeeding. Policy statement: breastfeeding and the use of human milk. Pediatrics 2022;150:e2022057988. 10.1542/peds.2022-057988 [DOI] [PubMed] [Google Scholar]
- 15.Annus J, Brat T, Diethelm MP, et al. ; World Health Organization Special. Comparative multicentre trial of three IUDs inserted immediately following delivery of the placenta. Contraception 1980;22:9–18. 10.1016/0010-7824(80)90112-2 [DOI] [PubMed] [Google Scholar]
- 16.Apelo RA, Waszak CS. Postpartum IUD insertions in Manila, Philippines. Adv Contracept 1985;1:319–28. 10.1007/BF01849307 [DOI] [PubMed] [Google Scholar]
- 17.Baldwin MK, Edelman AB, Lim JY, Nichols MD, Bednarek PH, Jensen JT. Intrauterine device placement at 3 versus 6 weeks postpartum: a randomized trial. Contraception 2016;93:356–63. 10.1016/j.contraception.2015.12.006 [DOI] [PubMed] [Google Scholar]
- 18.Bonilla Rosales F, Aguilar Zamudio ME, Cázares Montero ML, Hernández Ortiz ME, Luna Ruiz MA. [Factors for expulsion of intrauterine device Tcu380A applied immediately postpartum and after a delayed period]. Rev Med Inst Mex Seguro Soc 2005;43:5–10. [PubMed] [Google Scholar]
- 19.Braniff K, Gomez E, Muller R. A randomised clinical trial to assess satisfaction with the levonorgestrel-releasing intrauterine system inserted at caesarean section compared to postpartum placement. Aust N Z J Obstet Gynaecol 2015;55:279–83. 10.1111/ajo.12335 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 20.Bryant AG, Kamanga G, Stuart GS, Haddad LB, Meguid T, Mhango C. Immediate postpartum versus 6-week postpartum intrauterine device insertion: a feasibility study of a randomized controlled trial. Afr J Reprod Health 2013;17:72–9. [PubMed] [Google Scholar]
- 21.Caliskan E, Oztürk N, Dilbaz BO, Dilbaz S. Analysis of risk factors associated with uterine perforation by intrauterine devices. Eur J Contracept Reprod Health Care 2003;8:150–5. 10.1080/ejc.8.3.150.155 [DOI] [PubMed] [Google Scholar]
- 22.Celen S, Möröy P, Sucak A, Aktulay A, Danişman N. Clinical outcomes of early postplacental insertion of intrauterine contraceptive devices. Contraception 2004;69:279–82. 10.1016/j.contraception.2003.12.004 [DOI] [PubMed] [Google Scholar]
- 23.Çelen Ş, Sucak A, Yıldız Y, Danışman N. Immediate postplacental insertion of an intrauterine contraceptive device during cesarean section. Contraception 2011;84:240–3. 10.1016/j.contraception.2011.01.006 [DOI] [PubMed] [Google Scholar]
- 24.Chen BA, Reeves MF, Hayes JL, Hohmann HL, Perriera LK, Creinin MD. Postplacental or delayed insertion of the levonorgestrel intrauterine device after vaginal delivery: a randomized controlled trial. Obstet Gynecol 2010;116:1079–87. 10.1097/AOG.0b013e3181f73fac [DOI] [PMC free article] [PubMed] [Google Scholar]
- 25.Chen JH, Wu SC, Shao WQ, et al. The comparative trial of TCu 380A IUD and progesterone-releasing vaginal ring used by lactating women. Contraception 1998;57:371–9. 10.1016/S0010-7824(98)00043-2 [DOI] [PubMed] [Google Scholar]
- 26.Cohen R, Sheeder J, Arango N, Teal SB, Tocce K. Twelve-month contraceptive continuation and repeat pregnancy among young mothers choosing postdelivery contraceptive implants or postplacental intrauterine devices. Contraception 2016;93:178–83. 10.1016/j.contraception.2015.10.001 [DOI] [PubMed] [Google Scholar]
- 27.Dahlke JD, Terpstra ER, Ramseyer AM, Busch JM, Rieg T, Magann EF. Postpartum insertion of levonorgestrel—intrauterine system at three time periods: a prospective randomized pilot study. Contraception 2011;84:244–8. 10.1016/j.contraception.2011.01.007 [DOI] [PubMed] [Google Scholar]
- 28.Dias T, Abeykoon S, Kumarasiri S, Gunawardena C, Padeniya T, D’Antonio F. Use of ultrasound in predicting success of intrauterine contraceptive device insertion immediately after delivery. Ultrasound Obstet Gynecol 2015;46:104–8. 10.1002/uog.14733 [DOI] [PubMed] [Google Scholar]
- 29.El-Shafei MMMA, Hassan EO, El-Boghdad L, El-Lakkany N. Postpartum and postabortion intrauterine device insertion unmet needs of safe reproductive health: three years experience of Mansoura University Hospital. J Egypt 2000;26:253–62. [Google Scholar]
- 30.Elsedeek MS. Puerperal and menstrual bleeding patterns with different types of contraceptive device fitted during elective cesarean delivery. Int J Gynaecol Obstet 2012;116:31–4. 10.1016/j.ijgo.2011.07.036 [DOI] [PubMed] [Google Scholar]
- 31.Elsedeek MS. Five-year follow-up of two types of contraceptive device fitted during elective cesarean delivery. Int J Gynaecol Obstet 2015;130:179–82. 10.1016/j.ijgo.2015.02.031 [DOI] [PubMed] [Google Scholar]
- 32.Eroğlu K, Akkuzu G, Vural G, et al. Comparison of efficacy and complications of IUD insertion in immediate postplacental/early postpartum period with interval period: 1 year follow-up. Contraception 2006;74:376–81. 10.1016/j.contraception.2006.07.003 [DOI] [PubMed] [Google Scholar]
- 33.Gueye M, Gaye YF, Diouf AA, et al. [Trancesarean intra-uterine device. Pilot study performed at Dakar teaching hospital]. J Gynecol Obstet Biol Reprod (Paris) 2013;42:585–90. 10.1016/j.jgyn.2013.06.003 [DOI] [PubMed] [Google Scholar]
- 34.Gupta S, Malik S, Sinha R, Shyamsunder S, Mittal MK. Association of the position of the Copper T 380A as determined by the ultrasonography following its insertion in the immediate postpartum period with the subsequent complications: an observational study. J Obstet Gynaecol India 2014;64:349–53. 10.1007/s13224-014-0532-5 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 35.Hagbard L, Ingemanson CA, Sorbe B. Early postpartum insertion of copper IUD. Contraception 1978;17:355–63. 10.1016/0010-7824(78)90081-1 [DOI] [PubMed] [Google Scholar]
- 36.Hayes JL, Cwiak C, Goedken P, Zieman M. A pilot clinical trial of ultrasound-guided postplacental insertion of a levonorgestrel intrauterine device. Contraception 2007;76:292–6. 10.1016/j.contraception.2007.06.003 [DOI] [PubMed] [Google Scholar]
- 37.Jatlaoui TC, Marcus M, Jamieson DJ, Goedken P, Cwiak C. Postplacental intrauterine device insertion at a teaching hospital. Contraception 2014;89:528–33. 10.1016/j.contraception.2013.10.008 [DOI] [PubMed] [Google Scholar]
- 38.Jatlaoui TC, Whiteman MK, Jeng G, et al. Intrauterine device expulsion after postpartum placement: a systematic review and meta-analysis. Obstet Gynecol 2018;132:895–905. 10.1097/AOG.0000000000002822 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 39.Kumar S, Sethi R, Balasubramaniam S, et al. Women’s experience with postpartum intrauterine contraceptive device use in India. Reprod Health 2014;11:32. 10.1186/1742-4755-11-32 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 40.Laes E, Lehtovirta P, Weintraub D, Pyörälä T, Luukkainen T. Early puerperal insertions of copper-T-200. Contraception 1975;11:289–95. 10.1016/0010-7824(75)90037-2 [DOI] [PubMed] [Google Scholar]
- 41.Lara Ricalde R, Menocal Tobías G, Ramos Pérez C, Velázquez Ramírez N. [Random comparative study between intrauterine device Multiload Cu375 and TCu 380a inserted in the postpartum period]. Ginecol Obstet Mex 2006;74:306–11. [PubMed] [Google Scholar]
- 42.Lavin P, Bravo C, Waszak C. Comparison of T Cu 200 and Progestasert IUDs. Contracept Deliv Syst 1983;4:143–7. [PubMed] [Google Scholar]
- 43.Lavin P, Waszak C, Bravo C. Preliminary report on a postpartum CuT 200 study, Santiago, Chile. Int J Gynaecol Obstet 1983;21:71–5. 10.1016/0020-7292(83)90073-5 [DOI] [PubMed] [Google Scholar]
- 44.Lester F, Kakaire O, Byamugisha J, et al. Intracesarean insertion of the Copper T380A versus 6 weeks postcesarean: a randomized clinical trial. Contraception 2015;91:198–203. 10.1016/j.contraception.2014.12.002 [DOI] [PubMed] [Google Scholar]
- 45.Letti Müller AL, Lopes Ramos JG, Martins-Costa SH, et al. Transvaginal ultrasonographic assessment of the expulsion rate of intrauterine devices inserted in the immediate postpartum period: a pilot study. Contraception 2005;72:192–5. 10.1016/j.contraception.2005.03.014 [DOI] [PubMed] [Google Scholar]
- 46.Levi E, Cantillo E, Ades V, Banks E, Murthy A. Immediate postplacental IUD insertion at cesarean delivery: a prospective cohort study. Contraception 2012;86:102–5. 10.1016/j.contraception.2011.11.019 [DOI] [PubMed] [Google Scholar]
- 47.Levi EE, Stuart GS, Zerden ML, Garrett JM, Bryant AG. Intrauterine device placement during cesarean delivery and continued use 6 months postpartum. Obstet Gynecol 2015;126:5–11. 10.1097/AOG.0000000000000882 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 48.Mishra S. Evaluation of safety, efficacy, and expulsion of post-placental and intra-cesarean insertion of intrauterine contraceptive devices (PPIUCD). J Obstet Gynaecol India 2014;64:337–43. 10.1007/s13224-014-0550-3 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 49.Morrison C, Waszak C, Katz K, Diabaté F, Mate EM. Clinical outcomes of two early postpartum IUD insertion programs in Africa. Contraception 1996;53:17–21. 10.1016/0010-7824(95)00254-5 [DOI] [PubMed] [Google Scholar]
- 50.Nelson AL, Chen S, Eden R. Intraoperative placement of the Copper T-380 intrauterine devices in women undergoing elective cesarean delivery: a pilot study. Contraception 2009;80:81–3. 10.1016/j.contraception.2009.01.014 [DOI] [PubMed] [Google Scholar]
- 51.Newton J, Harper M, Chan KK. Immediate post-placental insertion of intrauterine contraceptive devices. Lancet 1977;2:272–4. 10.1016/S0140-6736(77)90955-2 [DOI] [PubMed] [Google Scholar]
- 52.Prema K, Gayathri TL, Philips FS. Comparative study of early postpartum, postabortal and interval insertion of Cu T 200 mm2 device. J Obstet Gynaecol India 1978;28:946–8. [PubMed] [Google Scholar]
- 53.Puzey M. Mirena at caesarean section. Eur J Contracept Reprod Health Care 2005;10:164–7. 10.1080/13625180500233851 [DOI] [PubMed] [Google Scholar]
- 54.Ragab A, Hamed HO, Alsammani MA, et al. Expulsion of Nova-T380, Multiload 375, and Copper-T380A contraceptive devices inserted during cesarean delivery. Int J Gynaecol Obstet 2015;130:174–8. 10.1016/j.ijgo.2015.03.025 [DOI] [PubMed] [Google Scholar]
- 55.Shukla M, Qureshi S; Chandrawati. Post-placental intrauterine device insertion—a five year experience at a tertiary care centre in north India. Indian J Med Res 2012;136:432–5. [PMC free article] [PubMed] [Google Scholar]
- 56.Singal S, Bharti R, Dewan R, et al. Clinical outcome of postplacental Copper T 380A insertion in women delivering by caesarean section. J Clin Diagn Res 2014;8:OC01–04. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 57.Stuart GS, Bryant AG, O’Neill E, Doherty IA. Feasibility of postpartum placement of the levonorgestrel intrauterine system more than 6 h after vaginal birth. Contraception 2012;85:359–62. 10.1016/j.contraception.2011.08.005 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 58.Stuart GS, Lesko CR, Stuebe AM, Bryant AG, Levi EE, Danvers AI. A randomized trial of levonorgestrel intrauterine system insertion 6 to 48 h compared to 6 weeks after vaginal delivery; lessons learned. Contraception 2015;91:284–8. 10.1016/j.contraception.2014.12.009 [DOI] [PubMed] [Google Scholar]
- 59.Thiery M, Van Kets H, Van der Pas H. Immediate post-placental IUD insertion: the expulsion problem. Contraception 1985;31:331–49. 10.1016/0010-7824(85)90002-2 [DOI] [PubMed] [Google Scholar]
- 60.Van Der Pas MT, Delbeke L, Van Dets H. Comparative performance of two copper-wired IUDs (ML Cu 250 and T Cu 200: immediate postpartum and interval insertion. Contracept Deliv Syst 1980;1:27–35. [PubMed] [Google Scholar]
- 61.Welkovic S, Costa LO, Faúndes A, de Alencar Ximenes R, Costa CF. Post-partum bleeding and infection after post-placental IUD insertion. Contraception 2001;63:155–8. 10.1016/S0010-7824(01)00180-9 [DOI] [PubMed] [Google Scholar]
- 62.Whitaker AK, Endres LK, Mistretta SQ, Gilliam ML. Postplacental insertion of the levonorgestrel intrauterine device after cesarean delivery vs. delayed insertion: a randomized controlled trial. Contraception 2014;89:534–9. 10.1016/j.contraception.2013.12.007 [DOI] [PubMed] [Google Scholar]
- 63.Woo CJ, Alamgir H, Potter JE. Women’s experiences after Planned Parenthood’s exclusion from a family planning program in Texas. Contraception 2016;93:298–302. 10.1016/j.contraception.2015.12.004 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 64.Wu SC; Research Group on Failure Causes and Prevention Measures of Intrauterine Device. [Efficacy of intrauterine device TCu380A when inserted in four different periods]. Zhonghua Fu Chan Ke Za Zhi 2009;44:431–5. [PubMed] [Google Scholar]
- 65.Xu J, Yang X, Gu X, et al. Comparison between two techniques used in immediate postplacental insertion of TCu 380A intrauterine device: 36-month follow-up. Reprod Contracept 1999;10:156–62. [PubMed] [Google Scholar]
- 66.Xu J, Zhuang L, Yu G. [Comparison of two techniques used in immediate postplacental insertion of TCu 380A intrauterine device: 12 month follow-up of 910 cases]. Zhonghua Fu Chan Ke Za Zhi 1997;32:354–7. [PubMed] [Google Scholar]
- 67.Xu JX, Rivera R, Dunson TR, et al. A comparative study of two techniques used in immediate postplacental insertion (IPPI) of the Copper T-380A IUD in Shanghai, People’s Republic of China. Contraception 1996;54:33–8. 10.1016/0010-7824(96)00117-5 [DOI] [PubMed] [Google Scholar]
- 68.Phillips SJ, Tepper NK, Kapp N, Nanda K, Temmerman M, Curtis KM. Progestogen-only contraceptive use among breastfeeding women: a systematic review. Contraception 2016;94:226–52. 10.1016/j.contraception.2015.09.010 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 69.Berry-Bibee EN, Tepper NK, Jatlaoui TC, Whiteman MK, Jamieson DJ, Curtis KM. The safety of intrauterine devices in breastfeeding women: a systematic review. Contraception 2016;94:725–38. 10.1016/j.contraception.2016.07.006 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 70.Steenland MW, Tepper NK, Curtis KM, Kapp N. Intrauterine contraceptive insertion postabortion: a systematic review. Contraception 2011;84:447–64. 10.1016/j.contraception.2011.03.007 [DOI] [PubMed] [Google Scholar]
- 71.Martinelli I, Lensing AW, Middeldorp S, et al. Recurrent venous thromboembolism and abnormal uterine bleeding with anticoagulant and hormone therapy use. Blood 2016;127:1417–25. 10.1182/blood-2015-08-665927 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 72.Barbhaiya M, Zuily S, Naden R, et al. ; ACR/EULAR APS Classification Criteria Collaborators. The 2023 ACR/EULAR Antiphospholipid Syndrome Classification Criteria. Arthritis Rheumatol 2023;75:1687–702. 10.1002/art.42624 [DOI] [PubMed] [Google Scholar]
- 73.Bergendal A, Persson I, Odeberg J, et al. Association of venous thromboembolism with hormonal contraception and thrombophilic genotypes. Obstet Gynecol 2014;124:600–9. 10.1097/AOG.0000000000000411 [DOI] [PubMed] [Google Scholar]
- 74.Wilson W, Taubert KA, Gewitz M, et al. ; American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee; American Heart Association Council on Cardiovascular Disease in the Young; American Heart Association Council on Clinical Cardiology; American Heart Association Council on Cardiovascular Surgery and Anesthesia; Quality of Care and Outcomes Research Interdisciplinary Working Group. Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group. Circulation 2007;116:1736–54. 10.1161/CIRCULATIONAHA.106.183095 [DOI] [PubMed] [Google Scholar]
- 75.Tepper NK, Paulen ME, Marchbanks PA, Curtis KM. Safety of contraceptive use among women with peripartum cardiomyopathy: a systematic review. Contraception 2010;82:95–101. 10.1016/j.contraception.2010.02.004 [DOI] [PubMed] [Google Scholar]
- 76.The Criteria Committee of the New York Heart Association. Nomenclature and criteria for diagnosis of diseases of the heart and great vessels. 9th ed. Boston, MA: Little, Brown and Co; 1994. [Google Scholar]
- 77.Fedele L, Gammaro L, Bianchi S. Levonorgestrel-releasing intrauterine device for the treatment of menometrorrhagia in a woman on hemodialysis. N Engl J Med 1999;341:541. 10.1056/NEJM199908123410718 [DOI] [PubMed] [Google Scholar]
- 78.Chen Y, Li Z, Mo L, et al. Eosinophilia in peritoneal effluent due to a levonorgestrel-releasing intrauterine system in a woman on peritoneal dialysis. Perit Dial Int 2017;37:349–50. 10.3747/pdi.2016.00154 [DOI] [PubMed] [Google Scholar]
- 79.Korzets A, Chagnac A, Ori Y, Zevin D, Levi J. Pneumococcal peritonitis complicating CAPD—was the indwelling intrauterine device to blame? Clin Nephrol 1991;35:24–5. [PubMed] [Google Scholar]
- 80.Plaza MM. Intrauterine device-related peritonitis in a patient on CAPD. Perit Dial Int 2002;22:538–9. 10.1177/089686080202200420 [DOI] [PubMed] [Google Scholar]
- 81.Bernatsky S, Clarke A, Ramsey-Goldman R, et al. Hormonal exposures and breast cancer in a sample of women with systemic lupus erythematosus. Rheumatology (Oxford) 2004;43:1178–81. 10.1093/rheumatology/keh282 [DOI] [PubMed] [Google Scholar]
- 82.Bernatsky S, Ramsey-Goldman R, Gordon C, et al. Factors associated with abnormal Pap results in systemic lupus erythematosus. Rheumatology (Oxford) 2004;43:1386–9. 10.1093/rheumatology/keh331 [DOI] [PubMed] [Google Scholar]
- 83.Chopra N, Koren S, Greer WL, et al. Factor V Leiden, prothrombin gene mutation, and thrombosis risk in patients with antiphospholipid antibodies. J Rheumatol 2002;29:1683–8. [PubMed] [Google Scholar]
- 84.Esdaile JM, Abrahamowicz M, Grodzicky T, et al. Traditional Framingham risk factors fail to fully account for accelerated atherosclerosis in systemic lupus erythematosus. Arthritis Rheum 2001;44:2331–7. [DOI] [PubMed] [Google Scholar]
- 85.Julkunen HA, Kaaja R, Friman C. Contraceptive practice in women with systemic lupus erythematosus. Br J Rheumatol 1993;32:227–30. 10.1093/rheumatology/32.3.227 [DOI] [PubMed] [Google Scholar]
- 86.Manzi S, Meilahn EN, Rairie JE, et al. Age-specific incidence rates of myocardial infarction and angina in women with systemic lupus erythematosus: comparison with the Framingham Study. Am J Epidemiol 1997;145:408–15. 10.1093/oxfordjournals.aje.a009122 [DOI] [PubMed] [Google Scholar]
- 87.McAlindon T, Giannotta L, Taub N, D’Cruz D, Hughes G. Environmental factors predicting nephritis in systemic lupus erythematosus. Ann Rheum Dis 1993;52:720–4. 10.1136/ard.52.10.720 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 88.McDonald J, Stewart J, Urowitz MB, Gladman DD. Peripheral vascular disease in patients with systemic lupus erythematosus. Ann Rheum Dis 1992;51:56–60. 10.1136/ard.51.1.56 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 89.Mintz G, Gutiérrez G, Delezé M, Rodríguez E. Contraception with progestagens in systemic lupus erythematosus. Contraception 1984;30:29–38. 10.1016/0010-7824(84)90076-3 [DOI] [PubMed] [Google Scholar]
- 90.Petri M. Musculoskeletal complications of systemic lupus erythematosus in the Hopkins Lupus Cohort: an update. Arthritis Care Res 1995;8:137–45. 10.1002/art.1790080305 [DOI] [PubMed] [Google Scholar]
- 91.Petri M. Lupus in Baltimore: evidence-based ‘clinical pearls’ from the Hopkins Lupus Cohort. Lupus 2005;14:970–3. 10.1191/0961203305lu2230xx [DOI] [PubMed] [Google Scholar]
- 92.Sánchez-Guerrero J, Uribe AG, Jiménez-Santana L, et al. A trial of contraceptive methods in women with systemic lupus erythematosus. N Engl J Med 2005;353:2539–49. 10.1056/NEJMoa050817 [DOI] [PubMed] [Google Scholar]
- 93.Sarabi ZS, Chang E, Bobba R, et al. Incidence rates of arterial and venous thrombosis after diagnosis of systemic lupus erythematosus. Arthritis Rheum 2005;53:609–12. 10.1002/art.21314 [DOI] [PubMed] [Google Scholar]
- 94.Schaedel ZE, Dolan G, Powell MC. The use of the levonorgestrel-releasing intrauterine system in the management of menorrhagia in women with hemostatic disorders. Am J Obstet Gynecol 2005;193:1361–3. 10.1016/j.ajog.2005.05.002 [DOI] [PubMed] [Google Scholar]
- 95.Somers E, Magder LS, Petri M. Antiphospholipid antibodies and incidence of venous thrombosis in a cohort of patients with systemic lupus erythematosus. J Rheumatol 2002;29:2531–6. [PubMed] [Google Scholar]
- 96.Urowitz MB, Bookman AA, Koehler BE, Gordon DA, Smythe HA, Ogryzlo MA. The bimodal mortality pattern of systemic lupus erythematosus. Am J Med 1976;60:221–5. 10.1016/0002-9343(76)90431-9 [DOI] [PubMed] [Google Scholar]
- 97.Julkunen HA. Oral contraceptives in systemic lupus erythematosus: side-effects and influence on the activity of SLE. Scand J Rheumatol 1991;20:427–33. 10.3109/03009749109096822 [DOI] [PubMed] [Google Scholar]
- 98.Jungers P, Dougados M, Pélissier C, et al. Influence of oral contraceptive therapy on the activity of systemic lupus erythematosus. Arthritis Rheum 1982;25:618–23. 10.1002/art.1780250603 [DOI] [PubMed] [Google Scholar]
- 99.Petri M, Kim MY, Kalunian KC, et al. ; OC-SELENA Trial. Combined oral contraceptives in women with systemic lupus erythematosus. N Engl J Med 2005;353:2550–8. 10.1056/NEJMoa051135 [DOI] [PubMed] [Google Scholar]
- 100.Culwell KR, Curtis KM, Del Carmen Cravioto M. Safety of contraceptive method use among women with systemic lupus erythematosus: a systematic review. Obstet Gynecol 2009;114:341–53. 10.1097/AOG.0b013e3181ae9c64 [DOI] [PubMed] [Google Scholar]
- 101.Tepper NK, Whiteman MK, Zapata LB, Marchbanks PA, Curtis KM. Safety of hormonal contraceptives among women with migraine: asystematic review. Contraception 2016;94:630–40. 10.1016/j.contraception.2016.04.016 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 102.Tepper NK, Whiteman MK, Marchbanks PA, James AH, Curtis KM. Progestin-only contraception and thromboembolism: asystematic review. Contraception 2016;94:678–700. 10.1016/j.contraception.2016.04.014 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 103.Headache Classification Committee of the International Headache Society (IHS) The International Classification of Headache Disorders. 3rd ed. Cephalalgia 2018;38:1–211. https://www.ichd-3.org/wp-content/uploads/2018/01/The-International-Classification-of-Headache-Disorders-3rd-Edition-2018.pdf [DOI] [PubMed] [Google Scholar]
- 104.Pagano HP, Zapata LB, Berry-Bibee EN, Nanda K, Curtis KM. Safety of hormonal contraception and intrauterine devices among women with depressive and bipolar disorders: a systematic review. Contraception 2016;94:641–9. 10.1016/j.contraception.2016.06.012 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 105.Barrington JW, Arunkalaivanan AS, Abdel-Fattah M. Comparison between the levonorgestrel intrauterine system (LNG-IUS) and thermal balloon ablation in the treatment of menorrhagia. Eur J Obstet Gynecol Reprod Biol 2003;108:72–4. 10.1016/S0301-2115(02)00408-6 [DOI] [PubMed] [Google Scholar]
- 106.Gupta B, Mittal S, Misra R, Deka D, Dadhwal V. Levonorgestrel-releasing intrauterine system vs. transcervical endometrial resection for dysfunctional uterine bleeding. Int J Gynaecol Obstet 2006;95:261–6. 10.1016/j.ijgo.2006.07.004 [DOI] [PubMed] [Google Scholar]
- 107.Hurskainen R, Teperi J, Rissanen P, et al. Quality of life and cost-effectiveness of levonorgestrel-releasing intrauterine system versus hysterectomy for treatment of menorrhagia: a randomised trial. [see comment]. Lancet 2001;357:273–7. 10.1016/S0140-6736(00)03615-1 [DOI] [PubMed] [Google Scholar]
- 108.Istre O, Trolle B. Treatment of menorrhagia with the levonorgestrel intrauterine system versus endometrial resection. Fertil Steril 2001;76:304–9. 10.1016/S0015-0282(01)01909-4 [DOI] [PubMed] [Google Scholar]
- 109.Koh SC, Singh K. The effect of levonorgestrel-releasing intrauterine system use on menstrual blood loss and the hemostatic, fibrinolytic/inhibitor systems in women with menorrhagia. J Thromb Haemost 2007;5:133–8. 10.1111/j.1538-7836.2006.02243.x [DOI] [PubMed] [Google Scholar]
- 110.Lethaby AE, Cooke I, Rees M. Progesterone/progestogen releasing intrauterine systems versus either placebo or any other medication for heavy menstrual bleeding. Cochrane Database Syst Rev 2000;(2):CD002126. [DOI] [PubMed] [Google Scholar]
- 111.Magalhães J, Aldrighi JM, de Lima GR. Uterine volume and menstrual patterns in users of the levonorgestrel-releasing intrauterine system with idiopathic menorrhagia or menorrhagia due to leiomyomas. Contraception 2007;75:193–8. 10.1016/j.contraception.2006.11.004 [DOI] [PubMed] [Google Scholar]
- 112.Stewart A, Cummins C, Gold L, Jordan R, Phillips W. The effectiveness of the levonorgestrel-releasing intrauterine system in menorrhagia: a systematic review. BJOG 2001;108:74–86. 10.1111/j.1471-0528.2001.00020.x [DOI] [PubMed] [Google Scholar]
- 113.Fedele L, Bianchi S, Zanconato G, Portuese A, Raffaelli R. Use of a levonorgestrel-releasing intrauterine device in the treatment of rectovaginal endometriosis. Fertil Steril 2001;75:485–8. 10.1016/S0015-0282(00)01759-3 [DOI] [PubMed] [Google Scholar]
- 114.Lockhat FBE, Emembolu J, Konje JC. The effect of a levonorgestrel intrauterine system (LNG-IUS) on symptomatic endometriosis. Fertil Steril 2002;77(Suppl 1):S24. 10.1016/S0015-0282(01)03086-2 [DOI] [Google Scholar]
- 115.Petta CA, Ferriani RA, Abrao MS, et al. Randomized clinical trial of a levonorgestrel-releasing intrauterine system and a depot GnRH analogue for the treatment of chronic pelvic pain in women with endometriosis. Hum Reprod 2005;20:1993–8. 10.1093/humrep/deh869 [DOI] [PubMed] [Google Scholar]
- 116.Vercellini P, Aimi G, Panazza S, De Giorgi O, Pesole A, Crosignani PG. A levonorgestrel-releasing intrauterine system for the treatment of dysmenorrhea associated with endometriosis: a pilot study. Fertil Steril 1999;72:505–8. 10.1016/S0015-0282(99)00291-5 [DOI] [PubMed] [Google Scholar]
- 117.Vercellini P, Frontino G, De Giorgi O, Aimi G, Zaina B, Crosignani PG. Comparison of a levonorgestrel-releasing intrauterine device versus expectant management after conservative surgery for symptomatic endometriosis: a pilot study. Fertil Steril 2003;80:305–9. 10.1016/S0015-0282(03)00608-3 [DOI] [PubMed] [Google Scholar]
- 118.Gaffield ME, Kapp N, Curtis KM. Combined oral contraceptive and intrauterine device use among women with gestational trophoblastic disease. Contraception 2009;80:363–71. 10.1016/j.contraception.2009.03.022 [DOI] [PubMed] [Google Scholar]
- 119.Whiteman MK, Zapata LB, Tepper NK, Marchbanks PA, Curtis KM. Use of contraceptive methods among women with endometrial hyperplasia: a systematic review. Contraception 2010;82:56–63. 10.1016/j.contraception.2010.02.005 [DOI] [PubMed] [Google Scholar]
- 120.Zapata LB, Whiteman MK, Tepper NK, Jamieson DJ, Marchbanks PA, Curtis KM. Intrauterine device use among women with uterine fibroids: a systematic review. Contraception 2010;82:41–55. 10.1016/j.contraception.2010.02.011 [DOI] [PubMed] [Google Scholar]
- 121.Tepper NK, Steenland MW, Gaffield ME, Marchbanks PA, Curtis KM. Retention of intrauterine devices in women who acquire pelvic inflammatory disease: a systematic review. Contraception 2013;87:655–60. 10.1016/j.contraception.2012.08.011 [DOI] [PubMed] [Google Scholar]
- 122.Faúndes A, Telles E, Cristofoletti ML, Faúndes D, Castro S, Hardy E. The risk of inadvertent intrauterine device insertion in women carriers of endocervical Chlamydia trachomatis. Contraception 1998;58:105–9. 10.1016/S0010-7824(98)00064-X [DOI] [PubMed] [Google Scholar]
- 123.Ferraz do Lago R, Simões JA, Bahamondes L, Camargo RP, Perrotti M, Monteiro I. Follow-up of users of intrauterine device with and without bacterial vaginosis and other cervicovaginal infections. Contraception 2003;68:105–9. 10.1016/S0010-7824(03)00109-4 [DOI] [PubMed] [Google Scholar]
- 124.Morrison CS, Sekadde-Kigondu C, Miller WC, Weiner DH, Sinei SK. Use of sexually transmitted disease risk assessment algorithms for selection of intrauterine device candidates. Contraception 1999;59:97–106. 10.1016/S0010-7824(99)00006-2 [DOI] [PubMed] [Google Scholar]
- 125.Pap-Akeson M, Solheim F, Thorbert G, Akerlund M. Genital tract infections associated with the intrauterine contraceptive device can be reduced by inserting the threads into the uterine cavity. Br J Obstet Gynaecol 1992;99:676–9. 10.1111/j.1471-0528.1992.tb13854.x [DOI] [PubMed] [Google Scholar]
- 126.Sinei SK, Schulz KFLP, Lamptey PR, et al. Preventing IUCD-related pelvic infection: the efficacy of prophylactic doxycycline at insertion. Br J Obstet Gynaecol 1990;97:412–9. 10.1111/j.1471-0528.1990.tb01828.x [DOI] [PubMed] [Google Scholar]
- 127.Skjeldestad FE, Halvorsen LE, Kahn H, Nordbø SA, Saake K. IUD users in Norway are at low risk for genital C. trachomatis infection. Contraception 1996;54:209–12. 10.1016/S0010-7824(96)00190-4 [DOI] [PubMed] [Google Scholar]
- 128.Walsh TL, Bernstein GS, Grimes DA, Frezieres R, Bernstein L, Coulson AH; IUD Study Group. Effect of prophylactic antibiotics on morbidity associated with IUD insertion: results of a pilot randomized controlled trial. Contraception 1994;50:319–27. 10.1016/0010-7824(94)90019-1 [DOI] [PubMed] [Google Scholar]
- 129.Jatlaoui TC, Simmons KB, Curtis KM. The safety of intrauterine contraception initiation among women with current asymptomatic cervical infections or at increased risk of sexually transmitted infections. Contraception 2016;94:701–12. 10.1016/j.contraception.2016.05.013 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 130.Curtis KM, Hannaford PC, Rodriguez MI, Chipato T, Steyn PS, Kiarie JN. Hormonal contraception and HIV acquisition among women: an updated systematic review. BMJ Sex Reprod Health 2020;46:8–16. 10.1136/bmjsrh-2019-200509 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 131.Hannaford PC, Ti A, Chipato T, Curtis KM. Copper intrauterine device use and HIV acquisition in women: a systematic review. BMJ Sex Reprod Health 2020;46:17–25. 10.1136/bmjsrh-2019-200512 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 132.Tepper NK, Curtis KM, Cox S, Whiteman MK. Update to U.S. medical eligibility criteria for contraceptive use, 2016: updated recommendations for the use of contraception among women at high risk for HIV infection. MMWR Morb Mortal Wkly Rep 2020;69:405–10. 10.15585/mmwr.mm6914a3 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 133.Tepper NK, Curtis KM, Nanda K, Jamieson DJ. Safety of intrauterine devices among women with HIV: a systematic review. Contraception 2016;94:713–24. 10.1016/j.contraception.2016.06.011 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 134.Grigoryan OR, Grodnitskaya EE, Andreeva EN, Shestakova MV, Melnichenko GA, Dedov II. Contraception in perimenopausal women with diabetes mellitus. Gynecol Endocrinol 2006;22:198–206. 10.1080/09513590600624317 [DOI] [PubMed] [Google Scholar]
- 135.Rogovskaya S, Rivera R, Grimes DA, et al. Effect of a levonorgestrel intrauterine system on women with type 1 diabetes: a randomized trial. Obstet Gynecol 2005;105:811–5. 10.1097/01.AOG.0000156301.11939.56 [DOI] [PubMed] [Google Scholar]
- 136.Zapata LB, Paulen ME, Cansino C, Marchbanks PA, Curtis KM. Contraceptive use among women with inflammatory bowel disease: a systematic review. Contraception 2010;82:72–85. 10.1016/j.contraception.2010.02.012 [DOI] [PubMed] [Google Scholar]
- 137.Bounds W, Guillebaud J. Observational series on women using the contraceptive Mirena concurrently with anti-epileptic and other enzyme-inducing drugs. J Fam Plann Reprod Health Care 2002;28:78–80. 10.1783/147118902101195992 [DOI] [PubMed] [Google Scholar]
- 138.Gaffield ME, Culwell KR, Lee CR. The use of hormonal contraception among women taking anticonvulsant therapy. Contraception 2011;83:16–29. 10.1016/j.contraception.2010.06.013 [DOI] [PubMed] [Google Scholar]
- 139.Reimers A, Helde G, Brodtkorb E. Ethinyl estradiol, not progestogens, reduces lamotrigine serum concentrations. Epilepsia 2005;46:1414–7. 10.1111/j.1528-1167.2005.10105.x [DOI] [PubMed] [Google Scholar]
Appendix C. Classifications for Progestin-Only Contraceptives
Classifications for progestin-only contraceptives (POCs) include those for progestin-only implants (68 mg etonogestrel), progestin-only injectables (depot medroxyprogesterone acetate [DMPA], 150 mg intramuscular [DMPA-IM] or 104 mg subcutaneous [DMPA-SC]), and progestin-only pills (POPs) (containing norethindrone, norgestrel, or drospirenone [DRSP]) (Box C1) (Table C1). DMPA-SC can be administered by a health care provider or through self-administration. Recommendations in this report and U.S. Selected Practice Recommendations for Contraceptive Use, 2024 (1) for provider-administered DMPA (IM or SC) also apply to self-administered DMPA-SC. POCs do not protect against sexually transmitted infections (STIs), including HIV infection, and patients using POCs should be counseled that consistent and correct use of external (male) latex condoms reduces the risk for STIs, including HIV infection (2). Use of internal (female) condoms can provide protection from transmission of STIs, although data are limited (2). Patients also should be counseled that pre-exposure prophylaxis, when taken as prescribed, is highly effective for preventing HIV infection (3).
BOX C1. Categories for classifying progestin-only contraceptives.
U.S. MEC 1 = A condition for which there is no restriction for the use of the contraceptive method
U.S. MEC 2 = A condition for which the advantages of using the method generally outweigh the theoretical or proven risks
U.S. MEC 3 = A condition for which the theoretical or proven risks usually outweigh the advantages of using the method
U.S. MEC 4 = A condition that represents an unacceptable health risk if the contraceptive method is used
Abbreviation: U.S. MEC = U.S. Medical Eligibility Criteria for Contraceptive Use.
TABLE C1. Classifications for progestin-only contraceptives, including implants, depot medroxyprogesterone acetate, and progestin-only pills.
Condition | Category |
Clarification/Evidence/Comment | |||||
---|---|---|---|---|---|---|---|
Implant |
DMPA |
POP |
|||||
Personal
Characteristics and Reproductive History
| |||||||
Pregnancy
|
NA |
NA |
NA |
Clarification: Use of
POCs is not required. No known harm to the patient, the course
of pregnancy, or the fetus occurs if POCs are inadvertently used
during pregnancy. However, the relation between DMPA use during
pregnancy and its effects on the fetus remains
unclear. |
|||
Age
|
Evidence:
Most studies have found that women lose BMD during DMPA use but
recover BMD after discontinuation (4). Limited evidence
demonstrates a weak association with fracture. However, one
large study suggests that women who choose DMPA might be at
higher risk for fracture before initiation (5). It is
unclear whether adult women with long durations of DMPA use can
regain BMD to baseline levels before entering menopause and
whether adolescents can reach peak bone mass after
discontinuation of DMPA. The relation between these changes in
BMD during the reproductive years and future fracture risk is
unknown. Studies generally find no effect of POCs other than
DMPA on BMD (4–52). |
||||||
a. Menarche to <18
years |
1 |
2 |
1 |
||||
b. 18–45
years |
1 |
1 |
1 |
||||
c. >45 years |
1 |
2 |
1 |
||||
Parity
| |||||||
a. Nulliparous |
1 |
1 |
1 |
— |
|||
b. Parous |
1 |
1 |
1 |
— |
|||
Breastfeeding
| |||||||
a. <21 days
postpartum |
2 |
2 |
2 |
Clarification
(breastfeeding): Breastfeeding provides important
health benefits for breastfeeding parent and infant. The U.S.
Dietary Guidelines for Americans and American Academy of
Pediatrics recommend that infants be exclusively breastfed for
about the first 6 months with continued breastfeeding while
introducing appropriate complementary foods for 1 year or longer
(53)
or up to age 2 years or longer (54). Evidence (breastfeeding): Two small, RCTs found no adverse impact on breastfeeding with initiation of etonogestrel implants within 48 hours postpartum. Other studies found that initiation of POPs, injectables, and implants at ≤6 weeks postpartum compared with nonhormonal use had no detrimental effect on breastfeeding outcomes or infant health, growth, and development in the first year postpartum. In general, these studies are of poor quality, lack standard definitions of breastfeeding or outcome measures, and have not included premature or ill infants (55,56). Evidence: Limited evidence suggests that DMPA use might further elevate risk for VTE among postpartum women compared with non-use (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). Comment: Risk factors for breastfeeding difficulties include previous breastfeeding difficulties, certain medical conditions, certain perinatal complications, and preterm birth. For all breastfeeding persons, with or without breastfeeding difficulties, discussions about contraception should include information about risks, benefits, and alternatives. |
|||
b. 21 to
<30 days postpartum |
Clarification
(breastfeeding): Breastfeeding provides important
health benefits for breastfeeding parent and infant. The U.S.
Dietary Guidelines for Americans and American Academy of
Pediatrics recommend that infants be exclusively breastfed for
about the first 6 months with continued breastfeeding while
introducing appropriate complementary foods for 1 year or longer
(53)
or up to age 2 years or longer (54). Evidence (breastfeeding): Two small, RCTs found no adverse impact on breastfeeding with initiation of etonogestrel implants within 48 hours postpartum. Other studies found that initiation of POPs, injectables, and implants at ≤6 weeks postpartum compared with nonhormonal use had no detrimental effect on breastfeeding outcomes or infant health, growth, and development in the first year postpartum. In general, these studies are of poor quality, lack standard definitions of breastfeeding or outcome measures, and have not included premature or ill infants (55,56). Evidence: Limited evidence suggests that DMPA use might further elevate risk for VTE among postpartum women compared with nonuse (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). Comment: Risk factors for breastfeeding difficulties include previous breastfeeding difficulties, certain medical conditions, certain perinatal complications, and preterm birth. For all breastfeeding persons, with or without difficulties, discussions about contraception should include information about risks, benefits, and alternatives. |
||||||
i. With
other risk factors for VTE (e.g., age ≥35 years, previous
VTE, thrombophilia, immobility, transfusion at delivery,
peripartum cardiomyopathy, BMI ≥30 kg/m2,
postpartum hemorrhage, postcesarean delivery, preeclampsia, or
smoking) |
2 |
2 |
2 |
||||
ii.
Without other risk factors for VTE |
2 |
2 |
2 |
||||
c.
30–42 days postpartum |
Clarification
(breastfeeding): Breastfeeding provides important
health benefits for breastfeeding parent and infant. The U.S.
Dietary Guidelines for Americans and American Academy of
Pediatrics recommend that infants be exclusively breastfed for
about the first 6 months with continued breastfeeding while
introducing appropriate complementary foods for 1 year or longer
(53)
or up to age 2 years or longer (54). Evidence (breastfeeding): Two small, RCTs found no adverse impact on breastfeeding with initiation of etonogestrel implants within 48 hours postpartum. Other studies found that initiation of POPs, injectables, and implants at ≤6 weeks postpartum compared with nonhormonal use had no detrimental effect on breastfeeding outcomes or infant health, growth, and development in the first year postpartum. In general, these studies are of poor quality, lack standard definitions of breastfeeding or outcome measures, and have not included premature or ill infants (55,56). Evidence: Limited evidence suggests that DMPA use might further elevate risk for VTE among postpartum women compared with nonuse (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). Comment: Risk factors for breastfeeding difficulties include previous breastfeeding difficulties, certain medical conditions, certain perinatal complications, and preterm birth. For all breastfeeding persons, with or without breastfeeding difficulties, discussions about contraception should include information about risks, benefits, and alternatives. |
||||||
i. With
other risk factors for VTE (e.g., age ≥35 years, previous
VTE, thrombophilia, immobility, transfusion at delivery,
peripartum cardiomyopathy, BMI ≥30 kg/m2,
postpartum hemorrhage, postcesarean delivery, preeclampsia, or
smoking) |
1 |
2 |
1 |
||||
ii.
Without other risk factors for VTE |
1 |
1 |
1 |
||||
d. >42 days
postpartum |
1 |
1 |
1 |
Clarification
(breastfeeding): Breastfeeding provides important
health benefits for breastfeeding parent and infant. The U.S.
Dietary Guidelines for Americans and American Academy of
Pediatrics recommend that infants be exclusively breastfed for
about the first 6 months with continued breastfeeding while
introducing appropriate complementary foods for 1 year or longer
(53)
or up to age 2 years or longer (54). Evidence: Overall, studies found that initiation of POPs, injectables, and implants at >6 weeks postpartum compared with nonhormonal use had no detrimental effect on breastfeeding outcomes or infant health, growth, and development in the first year postpartum. In general, these studies are of poor quality, lack standard definitions of breastfeeding or outcome measures, and have not included premature or ill infants (56). Comment: Risk factors for breastfeeding difficulties include previous breastfeeding difficulties, certain medical conditions, certain perinatal complications, and preterm birth. For all breastfeeding persons, with or without breastfeeding difficulties, discussions about contraception should include information about risks, benefits, and alternatives. |
|||
Postpartum
(nonbreastfeeding) | |||||||
a. <21 days
postpartum |
1 |
2 |
1 |
Evidence: Limited
evidence suggests that DMPA use might further elevate risk for
VTE among postpartum women compared with nonuse (Supplementary
Appendix, https://stacks.cdc.gov/view/cdc/156516). |
|||
b.
21–42 days postpartum | |||||||
i. With
other risk factors for VTE (e.g., age ≥35 years, previous
VTE, thrombophilia, immobility, transfusion at delivery,
peripartum cardiomyopathy, BMI ≥30 kg/m2,
postpartum hemorrhage, postcesarean delivery, preeclampsia, or
smoking) |
1 |
2 |
1 |
Evidence: Limited
evidence suggests that DMPA use might further elevate risk for
VTE among postpartum women compared with nonuse (Supplementary
Appendix, https://stacks.cdc.gov/view/cdc/156516). |
|||
ii.
Without other risk factors for VTE |
1 |
1 |
1 |
— |
|||
c. >42 days
postpartum |
1 |
1 |
1 |
— |
|||
Postabortion
(spontaneous
or
induced) | |||||||
a. First
trimester abortion |
Clarification: POCs may be started immediately
after abortion completion or at time of medication abortion
initiation. Clarification (DMPA): After a first trimester medication abortion that did not include mifepristone, there is no restriction for the use of DMPA (category 1). After a first trimester medication abortion that included mifepristone, there is no restriction for use of DMPA after abortion completion (category 1) and benefits generally outweigh risks with DMPA use immediately at time of medication abortion initiation (category 2). Concurrent administration of DMPA with mifepristone might slightly decrease medication abortion effectiveness and increase risk for ongoing pregnancy. Risk for ongoing pregnancy with concurrent administration of DMPA with mifepristone should be considered along with personal preference and access to follow-up abortion and contraceptive care. Evidence: Limited evidence suggests decreased first trimester medication abortion effectiveness with concurrent administration of DMPA with mifepristone (immediate) versus DMPA administration after abortion completion (delayed). In one study, the risk for ongoing pregnancy, while overall low, was higher with immediate (3.6%) versus delayed (0.9%) DMPA administration (difference 2.7%; 90% CI = 0.4–5.6%) (57). This difference was not seen with other progestin-only methods (58). Evidence suggests that there is no increased risk for adverse events when POCs are initiated after first trimester procedural or medication abortion (immediately or delayed) (58) (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). |
||||||
i.
Procedural (surgical) |
1 |
1 |
1 |
||||
ii.
Medication |
1 |
1/2 |
1 |
||||
iii.
Spontaneous abortion with no intervention |
1 |
1 |
1 |
||||
b. Second
trimester abortion |
Clarification: POCs may be started immediately
after abortion completion or at time of medication abortion
initiation. |
||||||
i.
Procedural (surgical) |
1 |
1 |
1 |
||||
ii.
Medication |
1 |
1 |
1 |
||||
iii.
Spontaneous abortion with no intervention |
1 |
1 |
1 |
||||
c. Immediate postseptic
abortion |
1 |
1 |
1 |
Clarification: POCs may
be started immediately after abortion completion or at time of
medication abortion initiation. |
|||
Past ectopic
pregnancy
|
1 |
1 |
2 |
Comment: POP users have a
higher absolute rate of ectopic pregnancy than do users of other
POCs but still lower than those using no method. |
|||
History of pelvic
surgery
|
1 |
1 |
1 |
— |
|||
Smoking
| |||||||
a. Age <35
years |
1 |
1 |
1 |
— |
|||
b. Age
≥35 years | |||||||
i. <15
cigarettes per day |
1 |
1 |
1 |
— |
|||
ii.
≥15 cigarettes per day |
1 |
1 |
1 |
— |
|||
Obesity
| |||||||
a. BMI ≥30
kg/m2 |
1 |
1 |
1 |
— |
|||
b. Menarche to <18
years and BMI ≥30 kg/m2 |
1 |
2 |
1 |
Evidence: Among adult
women, generally no association has been found between baseline
weight and weight gain among DMPA users compared with nonusers.
Evidence is mixed for adolescent DMPA users, with certain
studies observing greater weight gain among users with obesity
compared with those without obesity but other studies
demonstrating no association; methodologic differences across
studies might account for the differences in findings. Data on
other POC methods and other adverse outcomes including weight
gain are limited (59–76). |
|||
History
of bariatric
surgery This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | |||||||
a. Restrictive procedures:
decrease storage capacity of the stomach (vertical banded
gastroplasty, laparoscopic adjustable gastric band, or
laparoscopic sleeve gastrectomy) |
1 |
1 |
1 |
Evidence: Limited
evidence demonstrated no substantial decrease in effectiveness
of oral contraceptives among women who underwent laparoscopic
placement of an adjustable gastric band (77). |
|||
b. Malabsorptive
procedures: decrease absorption of nutrients and calories by
shortening the functional length of the small intestine
(Roux-en-Y gastric bypass or biliopancreatic
diversion) |
1 |
1 |
3 |
Evidence: Limited
evidence demonstrated no substantial decrease in effectiveness
of oral contraceptives among women who underwent a
biliopancreatic diversion; however, evidence from
pharmacokinetic studies suggested conflicting results regarding
oral contraceptive effectiveness among women who underwent a
jejunoileal bypass (77). Comment: Bariatric surgical procedures involving a malabsorptive component have the potential to decrease oral contraceptive effectiveness, perhaps further decreased by postoperative complications such as long-term diarrhea, vomiting, or both. |
|||
Surgery
| |||||||
a. Minor surgery without
immobilization |
1 |
1 |
1 |
— |
|||
b. Major
surgery | |||||||
i. Without
prolonged immobilization |
1 |
1 |
1 |
— |
|||
ii. With
prolonged immobilization |
1 |
2 |
1 |
Evidence: No direct
evidence was identified on risk for thrombosis with POC use
among those undergoing major surgery. Use of DMPA, which has
been associated with a higher risk for venous thrombosis
compared with nonuse (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516), might
further elevate risk for thrombosis among persons with prolonged
immobilization after major surgery. |
|||
Cardiovascular Disease
| |||||||
Multiple risk
factors for atherosclerotic cardiovascular disease
(e.g., older age, smoking, diabetes, hypertension, low HDL, high
LDL, or high triglyceride levels) |
2 |
3 |
2 |
Clarification: When
multiple major risk factors exist, risk for cardiovascular
disease might increase substantially. Certain POCs might
increase the risk for thrombosis, although this increase is
substantially less than with COCs. The effects of DMPA might
persist for some time after
discontinuation. Clarification: The recommendations apply to known pre-existing medical conditions or characteristics. Few if any screening tests are needed before initiation of contraception. See U.S. SPR (https://www.cdc.gov/contraception/hcp/usspr) (1). |
|||
Hypertension Systolic blood pressure ≥160 mm Hg or diastolic blood pressure ≥100 mm Hg are associated with increased risk for adverse health events as a result of pregnancy (Box 3). | |||||||
a. Adequately controlled
hypertension |
1 |
2 |
1 |
Clarification: For all
categories of hypertension, classifications are based on the
assumption that no other risk factors exist for cardiovascular
disease. When multiple risk factors do exist, risk for
cardiovascular disease might increase substantially. A single
reading of blood pressure level is not sufficient to classify a
person as hypertensive. Clarification: Persons adequately treated for hypertension are at lower risk for acute myocardial infarction and stroke than are untreated persons. Although no data exist, POC users with adequately controlled and monitored hypertension should be at lower risk for acute myocardial infarction and stroke than are untreated hypertensive POC users. |
|||
b. Elevated
blood pressure
levels (properly
taken
measurements) |
Clarification: For all categories of
hypertension, classifications are based on the assumption that
no other risk factors exist for cardiovascular disease. When
multiple risk factors do exist, risk for cardiovascular disease
might increase substantially. A single reading of blood pressure
level is not sufficient to classify a person as
hypertensive. Evidence: Limited evidence suggests that among women with hypertension, those who used POPs or progestin-only injectables had a small increased risk for cardiovascular events compared with women who did not use these methods (78). |
||||||
i.
Systolic 140–159 mm Hg or diastolic 90–99 mm
Hg |
1 |
2 |
1 |
||||
ii.
Systolic ≥160 mm Hg or diastolic ≥100 mm
Hg |
2 |
3 |
2 |
||||
c. Vascular
disease |
2 |
3 |
2 |
Clarification: For all
categories of hypertension, classifications are based on the
assumption that no other risk factors exist for cardiovascular
disease. When multiple risk factors do exist, risk for
cardiovascular disease might increase substantially. A single
reading of blood pressure level is not sufficient to classify a
person as hypertensive. Comment: Concern exists about hypoestrogenic effects and reduced HDL levels, particularly among users of DMPA. However, little concern exists about these effects with regard to POPs. The effects of DMPA might persist for some time after discontinuation. |
|||
History of high
blood pressure during pregnancy (when current blood
pressure is measurable and normal) |
1 |
1 |
1 |
— |
|||
Deep
venous thrombosis/
Pulmonary
embolism This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | |||||||
a. Current or history of
DVT/PE, receiving anticoagulant therapy (therapeutic dose)
(e.g., acute DVT/PE or long-term therapeutic dose) |
2 |
2 |
2 |
Clarification: Persons
using anticoagulant therapy are at risk for gynecologic
complications of therapy, such as heavy or prolonged bleeding
and hemorrhagic ovarian cysts. POCs can be of benefit in
preventing or treating these complications; benefits might vary
by POC dose and formulation. When a contraceptive method is used
as a therapy, rather than solely to prevent pregnancy, the
risk/benefit ratio might differ and should be considered on a
case-by-case basis. Evidence: Limited evidence was identified on use of POCs among women with acute DVT/PE receiving anticoagulant therapy (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516 In one study among women with a history of acute VTE currently receiving therapeutic anticoagulant therapy (i.e., rivaroxaban or enoxaparin/vitamin K antagonist [warfarin or acenocoumarol]), the incidence of recurrent VTE was similar among estrogen users (CHC or estrogen-only pills), POC users, and women not on hormonal therapy (79). Limited evidence suggests that intramuscular injections of DMPA in women receiving chronic anticoagulation therapy do not pose a significant risk for hematoma at the injection site or increase the risk for heavy or irregular vaginal bleeding (80). |
|||
b. History of
DVT/PE,
receiving anticoagulant
therapy
(prophylactic dose) |
Clarification: Persons using anticoagulant
therapy are at risk for gynecologic complications of therapy,
such as heavy or prolonged bleeding and hemorrhagic ovarian
cysts. POCs can be of benefit in preventing or treating these
complications; benefits might vary by POC dose and formulation.
When a contraceptive method is used as a therapy, rather than
solely to prevent pregnancy, the risk/benefit ratio might differ
and should be considered on a case-by-case
basis. Evidence: Limited evidence was identified on use of POCs among women with acute DVT/PE receiving anticoagulant therapy (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). Use of DMPA, which has been associated with a higher risk for venous thrombosis compared with nonuse (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516), might further elevate risk for thrombosis among persons with a history of DVT/PE and at higher risk for recurrent DVT/PE. Limited evidence suggests that intramuscular injections of DMPA in women receiving chronic anticoagulation therapy do not pose a significant risk for hematoma at the injection site or increase the risk for heavy or irregular vaginal bleeding (80). |
||||||
i. Higher
risk for recurrent DVT/PE (one or more risk factors) |
2 |
3 |
2 |
||||
•
Thrombophilia (e.g., factor V Leiden mutation; prothrombin gene
mutation; protein S, protein C, and antithrombin deficiencies;
or antiphospholipid
syndrome) • Active cancer (metastatic, receiving therapy, or within 6 months after clinical remission), excluding nonmelanoma skin cancer • History of recurrent DVT/PE | |||||||
ii. Lower
risk for recurrent DVT/PE (no risk factors) |
2 |
2 |
2 |
||||
c. History of
DVT/PE, not
receiving
anticoagulant
therapy | |||||||
i. Higher
risk for recurrent DVT/PE (one or more risk factors) |
2 |
3 |
2 |
Evidence: Use
of DMPA, which has been associated with a higher risk for venous
thrombosis compared with nonuse (Supplementary Appendix,
https://stacks.cdc.gov/view/cdc/156516), might
further elevate risk for thrombosis among persons with a history
of DVT/PE and at higher risk for recurrent DVT/PE. |
|||
• History of
estrogen-associated
DVT/PE • Pregnancy-associated DVT/PE • Idiopathic DVT/PE • Thrombophilia (e.g., factor V Leiden mutation; prothrombin gene mutation; protein S, protein C, and antithrombin deficiencies; or antiphospholipid syndrome) • Active cancer (metastatic, receiving therapy, or within 6 months after clinical remission), excluding nonmelanoma skin cancer • History of recurrent DVT/PE | |||||||
ii. Lower
risk for recurrent DVT/PE (no risk factors) |
2 |
2 |
2 |
— |
|||
d. Family
history
(first-degree relatives) |
1 |
1 |
1 |
— |
|||
Thrombophilia
(e.g., factor V Leiden mutation; prothrombin gene mutation;
protein S, protein C, and antithrombin deficiencies; or
antiphospholipid syndrome)
This condition is associated
with increased risk for adverse health events as a result of
pregnancy (Box
3). |
2 |
3 |
2 |
Clarification: Routine
screening in the general population before contraceptive
initiation is not
recommended. Clarification: If a person has current or history of DVT/PE, see recommendations for DVT/PE. Clarification: Classification of antiphospholipid syndrome includes presence of a clinical feature (e.g., thrombosis or obstetric morbidity) and persistently abnormal antiphospholipid antibody test on two or more occasions at least 12 weeks apart (81). Evidence: Among women with factor V Leiden mutation, one study found that women using POCs had an increased risk for venous thrombosis compared with non-users without the mutation, with the highest relative risk for DMPA users (82). Women with prothrombin gene mutation using POCs did not have an increased risk for venous thrombosis compared with nonusers without the mutation (82). No evidence was identified on POC use among persons with protein S deficiency, protein C deficiency, antithrombin deficiency, or antiphospholipid syndrome (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). |
|||
Superficial venous
disorders
| |||||||
a. Varicose
veins |
1 |
1 |
1 |
— |
|||
b. Superficial venous
thrombosis (acute or history) |
1 |
2 |
1 |
Evidence: No direct
evidence was identified on risk for thrombosis with POC use
among persons with superficial venous thrombosis (Supplementary
Appendix, https://stacks.cdc.gov/view/cdc/156516). Persons
with superficial venous thrombosis are at higher risk for venous
thrombosis than the general population (83). Use of DMPA, which
has been associated with a higher risk for venous thrombosis
compared with non-use (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516), might
further elevate risk for thrombosis among persons with acute or
history of superficial venous thrombosis. |
|||
Current
and history of ischemic heart disease This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
Initiation |
Continuation |
Initiation |
Continuation |
Comment:
Concern exists about hypoestrogenic effects and reduced HDL
levels, particularly among users of DMPA. However, little
concern exists about these effects with regard to POPs. The
effects of DMPA might persist for some time after
discontinuation. |
||
2 |
3 |
3 |
2 |
3 |
|||
Stroke (history of cerebrovascular
accident) This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
Initiation |
Continuation |
Initiation |
Continuation |
Comment:
Concern exists about hypoestrogenic effects and reduced HDL
levels, particularly among users of DMPA. However, little
concern exists about these effects with regard to POPs. The
effects of DMPA might persist for some time after
discontinuation. |
||
2 |
3 |
3 |
2 |
3 |
|||
Valvular
heart disease Complicated valvular heart disease is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | |||||||
a. Uncomplicated |
1 |
1 |
1 |
— |
|||
b. Complicated (pulmonary
hypertension, risk for atrial fibrillation, or history of
subacute bacterial endocarditis) |
1 |
2 |
1 |
Evidence: No direct
evidence was identified on risk for thrombosis with POC use
among persons with valvular heart disease (Supplementary
Appendix, https://stacks.cdc.gov/view/cdc/156516). Use of
DMPA, which has been associated with a higher risk for venous
thrombosis compared with nonuse (Supplementary Appendix,
https://stacks.cdc.gov/view/cdc/156516), might
further elevate risk for thrombosis among persons with
complicated valvular heart disease. |
|||
Peripartum
cardiomyopathy This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
Evidence: No
direct evidence was identified on the safety of POC use among
persons with peripartum cardiomyopathy (Supplementary Appendix,
https://stacks.cdc.gov/view/cdc/156516). Limited
indirect evidence from noncomparative studies of women with
cardiac disease demonstrated few cases of hypertension,
thromboembolism, and heart failure in women with cardiac disease
using POPs and DMPA (84). Use of DMPA, which has
been associated with a higher risk for venous thrombosis
compared with nonuse (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516), might
further elevate risk for thrombosis among persons with
peripartum cardiomyopathy. Comment: Progestin-only implants might induce cardiac arrhythmias in healthy persons; persons with peripartum cardiomyopathy have a high incidence of cardiac arrhythmias. |
||||||
a. Normal or
mildly
impaired cardiac function
(New York
Heart
Association Functional
Class I or II: no
limitation
of activities or slight,
mild
limitation of activity) (85) | |||||||
i. <6
months |
1 |
2 |
1 |
||||
ii.
≥6 months |
1 |
2 |
1 |
||||
b. Moderately or severely
impaired cardiac function (New York Heart Association Functional
Class III or IV: marked limitation of activity or should be at
complete rest) (85) |
2 |
3 |
2 |
||||
Renal
Disease
| |||||||
Chronic
kidney disease This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | |||||||
a. Current nephrotic
syndrome |
2 |
3 |
2 DRSP POP with known hyperkalemia: 4 |
Clarification (DRSP POP):
Persons with known hyperkalemia should not use DRSP POPs because
of the risk for worsening hyperkalemia (category 4). For persons
with CKD without known hyperkalemia (category 2), consider
checking serum potassium level during first cycle of DRSP
POPs. Evidence: No direct evidence was identified on POC use among persons with CKD with current nephrotic syndrome (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). Persons with severe CKD or nephrotic syndrome are at higher risk for thrombosis than the general population (86–90). Use of DMPA, which has been associated with increased risk for thrombosis compared with nonuse (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516), might further elevate risk for thrombosis among those with CKD with current nephrotic syndrome. Persons with severe CKD have a higher prevalence of fracture than the general population (91–93). Use of DMPA, which has been associated with small changes in bone mineral density (4) might further elevate risk for fracture among persons with CKD with current nephrotic syndrome. Comment: A person might have CKD without current nephrotic syndrome, but might have other conditions often associated with CKD (e.g., diabetes, hypertension, SLE). See recommendations for other conditions if they apply. |
|||
b. Hemodialysis |
2 |
3 |
2 DRSP POP with known hyperkalemia: 4 |
Clarification (DRSP POP):
Persons with known hyperkalemia should not use DRSP POPs because
of the risk for worsening hyperkalemia (category 4). For persons
with CKD without known hyperkalemia (category 2), consider
checking serum potassium level during first cycle of DRSP
POPs. Evidence: No direct evidence was identified on POC use among persons with CKD on hemodialysis (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). Persons with CKD on dialysis are at higher risk for thrombosis than the general population (94-96). Use of DMPA, which has been associated with increased risk for thrombosis compared with nonuse (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516), might further elevate risk for thrombosis among those with CKD on dialysis. Persons with CKD on dialysis have a higher prevalence of fracture than the general population (97–99). Use of DMPA, which has been associated with small changes in bone mineral density (4), might further elevate risk for fracture among persons with CKD on dialysis. Comment: A person might have CKD without hemodialysis, but might have other conditions often associated with CKD (e.g., diabetes, hypertension, SLE). See recommendations for other conditions if they apply. |
|||
c. Peritoneal
dialysis |
2 |
3 |
2 DRSP POP with known hyperkalemia: 4 |
Clarification (DRSP POP):
Persons with known hyperkalemia should not use DRSP POPs because
of the risk for worsening hyperkalemia (category 4). For persons
with CKD without known hyperkalemia (category 2), consider
checking serum potassium level during first cycle of DRSP
POPs. Evidence: No direct evidence was identified on POC use among persons with CKD on peritoneal dialysis (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). Persons with CKD on dialysis are at higher risk for thrombosis than the general population (94–96). Use of DMPA, which has been associated with increased risk for thrombosis compared with nonuse (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516), might further elevate risk for thrombosis among those with CKD on dialysis. Persons with CKD on dialysis have a higher prevalence of fracture than the general population (97–99). Use of DMPA, which has been associated with small changes in bone mineral density (4), might further elevate risk for fracture among persons with CKD on dialysis. Comment: A person might have CKD without peritoneal dialysis but might have other conditions often associated with CKD (e.g., diabetes, hypertension, and SLE). See recommendations for other conditions if they apply. |
|||
Rheumatic Diseases
| |||||||
Systemic
lupus
erythematosus This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
Initiation |
Continuation |
— |
||||
a. Positive (or unknown)
antiphospholipid antibodies |
2 |
3 |
3 |
2 |
Clarification: Persons
with SLE are at increased risk for ischemic heart disease,
stroke, and VTE. Categories assigned to such conditions in U.S.
MEC should be the same for persons with SLE who have these
conditions. For all subconditions of SLE, classifications are
based on the assumption that no other risk factors for
cardiovascular disease are present; these classifications
must be modified in the presence of such risk factors (100–118). Evidence: No direct evidence was identified on POC use among persons with SLE with antiphospholipid antibodies (119) (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). Persons with SLE with antiphospholipid antibodies are at higher risk for thrombosis than the general population (120,121). Use of DMPA, which has been associated with a higher risk for venous thrombosis compared with nonuse (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516), might further elevate risk for thrombosis among persons with SLE with antiphospholipid antibodies. |
||
b. Severe
thrombocytopenia |
2 |
3 |
2 |
2 |
Clarification: Persons
with SLE are at increased risk for ischemic heart disease,
stroke, and VTE. Categories assigned to such conditions in U.S.
MEC should be the same for persons with SLE who have these
conditions. For all subconditions of SLE, classifications are
based on the assumption that no other risk factors for
cardiovascular disease are present; these classifications must
be modified in the presence of such risk factors (100–118). Comment: Severe thrombocytopenia increases the risk for bleeding. POCs might be useful in treating heavy or prolonged bleeding in persons with severe thrombocytopenia. However, given the increased or erratic bleeding that might be seen on initiation of DMPA and its irreversibility for 11–13 weeks after administration, initiation of this method in persons with severe thrombocytopenia should be done with caution. |
||
c. Immunosuppressive
therapy |
2 |
2 |
2 |
2 |
Clarification: Persons
with SLE are at increased risk for ischemic heart disease,
stroke, and VTE. Categories assigned to such conditions in U.S.
MEC should be the same for persons with SLE who have these
conditions. For all subconditions of SLE, classifications are
based on the assumption that no other risk factors for
cardiovascular disease are present; these classifications must
be modified in the presence of such risk factors (100–118). |
||
d. None of the
above |
2 |
2 |
2 |
2 |
Clarification: Persons
with SLE are at increased risk for ischemic heart disease,
stroke, and VTE. Categories assigned to such conditions in U.S.
MEC should be the same for persons with SLE who have these
conditions. For all subconditions of SLE, classifications are
based on the assumption that no other risk factors for
cardiovascular disease are present; these classifications must
be modified in the presence of such risk factors (100–118). |
||
Rheumatoid arthritis
| |||||||
a. Not receiving
immunosuppressive therapy |
1 |
2 |
1 |
Evidence: Limited
evidence demonstrates no consistent pattern of improvement or
worsening of rheumatoid arthritis with use of oral
contraceptives, progesterone, or estrogen (122). |
|||
b. Receiving
immunosuppressive therapy |
1 |
2/3 |
1 |
Clarification (DMPA):
DMPA use among persons receiving long-term corticosteroid
therapy with a history of, or with risk factors for,
nontraumatic fractures is classified as category 3. Otherwise,
DMPA use for persons with rheumatoid arthritis is classified as
category 2. Evidence: Limited evidence demonstrates no consistent pattern of improvement or worsening of rheumatoid arthritis with use of oral contraceptives, progesterone, or estrogen (122). |
|||
Neurologic Conditions
| |||||||
Headaches
| |||||||
a. Nonmigraine (mild or
severe) |
1 |
1 |
1 |
— |
|||
b.
Migraine |
Evidence: No
studies directly examined the risk for stroke among women with
migraine using POCs (123). Limited evidence
demonstrated that women using POPs, DMPA, or implants do not
have an increased risk for ischemic stroke compared with
nonusers (124). Comment: Menstrual migraine is a subtype of migraine without aura. For more information, see the International Headache Society’s International Classification of Headache Disorders, 3rd ed. (https://ichd-3.org) (125). |
||||||
i. Without
aura (includes menstrual migraine) |
1 |
1 |
1 |
||||
ii. With
aura |
1 |
1 |
1 |
||||
Epilepsy This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
1 |
1 |
1 |
Clarification: If a
person is taking anticonvulsants, see recommendations for Drug
Interactions. Certain anticonvulsants lower POC
effectiveness. |
|||
Multiple
sclerosis
|
Evidence:
Limited evidence demonstrates that use of COCs or oral
contraceptives (type not specified) among women with multiple
sclerosis does not worsen the clinical course of disease (126). Comment: Persons with multiple sclerosis might have compromised bone health from disease-related disability, immobility, and use of corticosteroids. Use of DMPA, which has been associated with small changes in BMD, might be of concern. |
||||||
a. Without prolonged
immobility |
1 |
2 |
1 |
||||
b. With prolonged
immobility |
1 |
2 |
1 |
||||
Depressive Disorders
| |||||||
Depressive
disorders
|
1 |
1 |
1 |
Clarification: If a
person is taking psychotropic medications or St. John’s
wort, see recommendations for Drug
Interactions. Evidence: The frequency of psychiatric hospitalizations for women with bipolar disorder or depression did not significantly differ among women using DMPA, LNG-IUD, Cu-IUD, or sterilization (127). |
|||
Reproductive Tract Infections and
Disorders
| |||||||
Vaginal
bleeding patterns
| |||||||
a. Irregular pattern
without heavy bleeding |
2 |
2 |
2 |
Comment: Irregular
menstrual bleeding patterns are common among healthy persons.
POC use frequently induces an irregular bleeding pattern.
Implant use might induce irregular bleeding patterns, especially
during the first 3–6 months, although these patterns
might persist longer. |
|||
b. Heavy or prolonged
bleeding (includes regular and irregular patterns) |
2 |
2 |
2 |
Clarification: Unusually
heavy bleeding should raise the suspicion of a serious
underlying condition. |
|||
Unexplained vaginal
bleeding (suspicious for serious condition) before
evaluation |
3 |
3 |
2 |
Clarification: If
pregnancy or an underlying pathological condition (e.g., pelvic
malignancy) is suspected, it must be evaluated and the category
adjusted after evaluation. Comment: POCs might cause irregular bleeding patterns, which might mask symptoms of underlying pathologic conditions. The effects of DMPA might persist for some time after discontinuation. |
|||
Endometriosis
|
1 |
1 |
1 |
— |
|||
Benign ovarian
tumors (including cysts) |
1 |
1 |
1 |
— |
|||
Severe
dysmenorrhea
|
1 |
1 |
1 |
— |
|||
Gestational
trophoblastic
disease This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
Clarification: For all subconditions of
gestational trophoblastic disease, classifications are based on
the assumption that persons are under close medical supervision
because of the need for monitoring of β-hCG levels for
appropriate disease surveillance. |
||||||
a. Suspected
gestational
trophoblastic
disease
(immediate
postevacuation) | |||||||
i. Uterine
size first trimester |
1 |
1 |
1 |
||||
ii.
Uterine size second trimester |
1 |
1 |
1 |
||||
b. Confirmed
gestational
trophoblastic disease
(after initial
evacuation
and during monitoring) | |||||||
i.
Undetectable or nonpregnant β–hCG levels |
1 |
1 |
1 |
||||
ii.
Decreasing β–hCG levels |
1 |
1 |
1 |
||||
iii.
Persistently elevated β-hCG levels or malignant disease,
with no evidence or suspicion of intrauterine disease |
1 |
1 |
1 |
||||
iv.
Persistently elevated β-hCG levels or malignant disease,
with evidence or suspicion of intrauterine disease |
1 |
1 |
1 |
||||
Cervical
ectropion
|
1 |
1 |
1 |
— |
|||
Cervical
intraepithelial neoplasia
|
2 |
2 |
1 |
Evidence: Among women
with persistent human papillomavirus infection, long-term DMPA
use (≥5 years) might increase the risk for carcinoma in
situ and invasive carcinoma (128). |
|||
Cervical
cancer (awaiting treatment) |
2 |
2 |
1 |
Comment: Theoretical
concern exists that POC use might affect prognosis of the
existing disease. While awaiting treatment, POCs may be used. In
general, treatment of this condition can render a person
infertile. |
|||
Breast
disease Breast cancer is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | |||||||
a. Undiagnosed
mass |
2 |
2 |
2 |
Clarification: Evaluation
of mass should be pursued as early as possible. |
|||
b. Benign breast
disease |
1 |
1 |
1 |
— |
|||
c. Family history of
cancer |
1 |
1 |
1 |
— |
|||
d. Breast
cancer | |||||||
i.
Current |
4 |
4 |
4 |
Comment:
Breast cancer is a hormonally sensitive tumor, and the prognosis
for persons with current or recent breast cancer might worsen
with POC use. |
|||
ii. Past
and no evidence of current disease for 5 years |
3 |
3 |
3 |
||||
Endometrial
hyperplasia
|
1 |
1 |
1 |
— |
|||
Endometrial
cancer This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
1 |
1 |
1 |
Comment: While awaiting
treatment, POCs may be used. In general, treatment of this
condition renders a person infertile. |
|||
Ovarian
cancer This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
1 |
1 |
1 |
Comment: While awaiting
treatment, POCs may be used. In general, treatment of this
condition renders a person infertile. |
|||
Uterine
fibroids
|
1 |
1 |
1 |
Comment: POCs do not
appear to cause growth of uterine fibroids. |
|||
Pelvic
inflammatory disease
|
Comment:
Whether POCs, like COCs, reduce the risk for PID among persons
with STIs is unknown; however, they do not protect against HIV
infection or lower genital tract STIs. |
||||||
a. Current PID |
1 |
1 |
1 |
||||
b. Past
PID | |||||||
i. With
subsequent pregnancy |
1 |
1 |
1 |
||||
ii.
Without subsequent pregnancy |
1 |
1 |
1 |
||||
Sexually
transmitted
infections
| |||||||
a. Current purulent
cervicitis or chlamydial infection or gonococcal
infection |
1 |
1 |
1 |
— |
|||
b. Vaginitis (including
Trichomonas vaginalis and bacterial
vaginosis) |
1 |
1 |
1 |
— |
|||
c. Other factors related
to STIs |
1 |
1 |
1 |
— |
|||
HIV
| |||||||
High risk for HIV
infection
|
1 |
1 |
1 |
Evidence: High-quality
evidence from one RCT observed no statistically significant
differences in HIV acquisition between DMPA-IM versus Cu-IUD,
DMPA-IM versus LNG implant, and Cu-IUD versus LNG implant. Of
the low-to-moderate-quality evidence from 14 observational
studies, certain studies suggested a possible increased risk for
HIV infection with progestin-only injectable use, which was most
likely due to unmeasured confounding. Low-quality evidence from
three observational studies did not suggest an increased HIV
infection risk for implant users. No studies of sufficient
quality were identified for POPs (129–131). |
|||
HIV
infection For persons with HIV infection who are not clinically well or not receiving ARV therapy, this condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
1 |
1 |
1 |
Clarification: Drug
interactions might exist between hormonal contraceptives and ARV
drugs (see recommendations for Drug
Interactions). Evidence: Overall, evidence does not support an association between POC use and progression of HIV infection. Limited direct evidence on an association between POC use and transmission of HIV to noninfected partners, as well as studies measuring genital viral shedding as a proxy for infectivity, have had mixed results. Studies measuring whether hormonal contraceptive methods affect plasma HIV viral load generally have found no effect (132–134). |
|||
Other
Infections
| |||||||
Schistosomiasis Schistosomiasis with fibrosis of the liver is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | |||||||
a. Uncomplicated |
1 |
1 |
1 |
Evidence: Among women
with uncomplicated schistosomiasis, limited evidence
demonstrated that DMPA use had no adverse effects on liver
function (135). |
|||
b. Fibrosis of the liver
(if severe, see recommendations for Cirrhosis) |
1 |
1 |
1 |
— |
|||
Tuberculosis This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
Clarification: If a person is taking rifampin,
see recommendations for Drug Interactions. Rifampin is likely to
decrease the effectiveness of certain POCs. |
||||||
a. Nonpelvic |
1 |
1 |
1 |
||||
b. Pelvic |
1 |
1 |
1 |
||||
Malaria
|
1 |
1 |
1 |
— |
|||
Endocrine Conditions
| |||||||
Diabetes Insulin-dependent diabetes; diabetes with nephropathy, retinopathy or neuropathy; diabetes with other vascular disease; or diabetes of >20 years’ duration are associated with increased risk for adverse health events as a result of pregnancy (Box 3). | |||||||
a. History of gestational
disease |
1 |
1 |
1 |
Evidence: POCs
had no adverse effects on serum lipid levels in
women with a history of gestational diabetes in two small
studies (136,137).
Limited evidence is inconsistent about the development of
noninsulin-dependent diabetes among users of POCs with a history
of gestational diabetes (138–141). |
|||
b. Nonvascular
disease |
Evidence:
Among women with insulin-dependent or noninsulin-dependent
diabetes, limited evidence on use of POCs (POPs, DMPA, and LNG
implant) suggests that these methods have little effect on
short-term or long-term diabetes control (e.g., glycosylated
hemoglobin levels), hemostatic markers, or lipid profile (142–145). |
||||||
i.
Non-insulin dependent |
2 |
2 |
2 |
||||
ii.
Insulin dependent |
2 |
2 |
2 |
||||
c. Nephropathy,
retinopathy or neuropathy |
2 |
3 |
2 |
Comment: Concern exists
about hypoestrogenic effects and reduced HDL levels,
particularly among users of DMPA. The effects of DMPA might
persist for some time after discontinuation. Certain POCs might
increase the risk for thrombosis, although this increase is
substantially less than with COCs. |
|||
d. Other vascular disease
or diabetes of >20 years’ duration |
2 |
3 |
2 |
Comment: Concern exists
about hypoestrogenic effects and reduced HDL levels,
particularly among users of DMPA. The effects of DMPA might
persist for some time after discontinuation. Certain POCs might
increase the risk for thrombosis, although this increase is
substantially less than with COCs. |
|||
Thyroid
disorders
| |||||||
a. Simple goiter |
1 |
1 |
1 |
— |
|||
b. Hyperthyroid |
1 |
1 |
1 |
— |
|||
c. Hypothyroid |
1 |
1 |
1 |
— |
|||
Gastrointestinal Conditions
| |||||||
Inflammatory bowel
disease (ulcerative colitis or Crohn’s
disease) |
1 |
2 |
2 |
Evidence: Risk for
disease relapse among women with IBD using oral contraceptives
(most studies did not specify formulation) did not increase
significantly from that for nonusers (146). Comment: Absorption of POPs among persons with IBD might be reduced if the person has substantial malabsorption caused by severe disease or small bowel surgery. Women with IBD have a higher prevalence of osteoporosis and osteopenia than the general population. Use of DMPA, which has been associated with small changes in BMD, might be of concern. |
|||
Gallbladder disease
| |||||||
a. Asymptomatic |
2 |
2 |
2 |
— |
|||
b.
Symptomatic | |||||||
i.
Current |
2 |
2 |
2 |
— |
|||
ii.
Treated by cholecystectomy |
2 |
2 |
2 |
— |
|||
iii.
Medically treated |
2 |
2 |
2 |
— |
|||
History
of cholestasis
| |||||||
a. Pregnancy
related |
1 |
1 |
1 |
|
|||
b. Past COC
related |
2 |
2 |
2 |
Comment: Theoretical
concern exists that a history of COC-related cholestasis might
predict subsequent cholestasis with POC use. However, this has
not been documented. |
|||
Viral
hepatitis
| |||||||
a. Acute or
flare |
1 |
1 |
1 |
Evidence: No direct
evidence was identified on POC use among persons with viral
hepatitis (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). |
|||
b. Chronic |
1 |
1 |
1 |
Evidence: No evidence was
identified on POC use among persons with viral hepatitis
(Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). |
|||
Cirrhosis Decompensated cirrhosis is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | |||||||
a. Compensated (normal
liver function) |
1 |
1 |
1 |
Evidence: No direct
evidence was identified on POC use among persons with cirrhosis
(Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). |
|||
b. Decompensated (impaired
liver function) |
2 |
3 |
2 |
Evidence: No direct
evidence was identified on POC use among persons with cirrhosis.
(Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). DMPA
use has been associated with a higher risk for venous thrombosis
compared with nonuse (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). Comment: Hepatic metabolism of exogenous hormones might be impaired in persons with liver dysfunction, which could lead to increased progestin levels in circulation and progestin-related side effects and adverse events (e.g., thrombosis), which might vary by dose and formulation. Any progestin-related hepatotoxicity might be less tolerated in persons with existing liver dysfunction. |
|||
Liver
tumors Hepatocellular adenoma and malignant liver tumors are associated with increased risk for adverse health events as a result of pregnancy (Box 3). | |||||||
a.
Benign | |||||||
i. Focal
nodular hyperplasia |
2 |
2 |
2 |
Evidence: Limited
evidence suggests that progestin use does not influence either
progression or regression of focal nodular hyperplasia
(Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). |
|||
ii.
Hepatocellular adenoma |
2 |
3 |
2 |
Evidence: Limited
evidence suggests that hepatocellular adenomas generally regress
or remain stable during progestin use (Supplementary Appendix,
https://stacks.cdc.gov/view/cdc/156516). |
|||
b. Malignant
(hepatocellular carcinoma) |
3 |
3 |
3 |
Evidence: No direct
evidence was identified on POC use among persons with
hepatocellular carcinoma (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). |
|||
Respiratory Conditions
| |||||||
Cystic
fibrosis This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
1 |
2 |
1 |
Clarification: Persons
with cystic fibrosis are at increased risk for diabetes, liver
disease, gallbladder disease, and VTE (particularly related to
use of central venous catheters) and are frequently prescribed
antibiotics. Categories assigned to such conditions in U.S. MEC
should be the same for persons with cystic fibrosis who have
these conditions. For cystic fibrosis, classifications are based
on the assumption that no other conditions are present; these
classifications must be modified in the presence of such
conditions. Clarification: Certain drugs to treat cystic fibrosis (e.g., lumacaftor) might reduce effectiveness of hormonal contraceptives, including oral, injectable, transdermal, and implantable contraceptives. Evidence: Limited evidence suggests that use of COCs or oral contraceptives (type not specified) among women with cystic fibrosis is not associated with worsening of disease severity. Very limited evidence suggests that cystic fibrosis does not impair the effectiveness of hormonal contraception (147). Comment: Persons with cystic fibrosis have a higher prevalence of osteopenia, osteoporosis, and fragility fractures than the general population. Use of DMPA, which has been associated with small changes in BMD, might be of concern. |
|||
Hematologic Conditions
| |||||||
Thalassemia
|
1 |
1 |
1 |
— |
|||
Sickle cell
disease This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
1 |
2/3 |
1 |
Clarification (DMPA): The
category should be assessed according to the severity of the
condition and risk for thrombosis. Evidence: Limited evidence suggests that POC use does not increase risk for thrombosis among persons with sickle cell disease (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). Persons with sickle cell disease are at higher risk for stroke and venous thrombosis than the general population (148–151). Use of DMPA, which has been associated with a higher risk for venous thrombosis compared with nonuse (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516), might further elevate risk for thrombosis among persons with sickle cell disease. POC might be beneficial in reducing clinical symptoms (e.g., pain crises) (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). |
|||
Iron deficiency
anemia
|
1 |
1 |
1 |
Comment: Changes in the
menstrual pattern associated with POC use have little effect on
hemoglobin levels. |
|||
Solid
Organ Transplantation
| |||||||
Solid
organ
transplantation This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | |||||||
a. No graft
failure |
2 |
2/3 |
2 |
Clarification
(DMPA): DMPA use among persons receiving long-term
immunosuppressive therapy with a history of, or risk factors
for, nontraumatic fractures is classified as category 3.
Otherwise, DMPA use for persons with solid organ transplantation
is classified as category 2. Evidence: One study observed no differences in transplant-related adverse outcomes (e.g., infection, graft failure, and graft rejection) or occurrence of pregnancy between transplant recipients using the implant and those using no hormonal method (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). No direct evidence was identified on bone health or fracture with use of POCs, including DMPA, among persons with solid organ transplantation. Persons with solid organ transplantation have a higher prevalence of osteoporosis and fracture than the general population, especially in the early posttransplantation period (152). Use of DMPA, which has been associated with small changes in bone mineral density compared with nonuse (4) might further elevate risk for fracture among persons with solid organ transplantation. |
|||
b. Graft failure |
2 |
2/3 |
2 |
||||
Drug
Interactions
| |||||||
Antiretrovirals used for
prevention (PrEP)
or
treatment of HIV infection
|
Comment: These
recommendations generally are for ARV agents used alone.
However, most persons receiving ARV are using multiple drugs in
combination. In general, whether interactions between ARVs and
hormonal contraceptives differ when ARVs are given alone or in
combination is unknown. |
||||||
See the
following guidelines for the most up-to-date recommendations on
drug-drug interactions between hormonal contraception and
antiretrovirals: 1) Recommendations for the Use of
Antiretroviral Drugs During Pregnancy and Interventions to
Reduce Perinatal HIV Transmission in the United States
(https://clinicalinfo.hiv.gov/en/guidelines/perinatal/prepregnancy-counseling-childbearing-age-overview?view=full#table-3)
(153) and 2) Guidelines for the Use
of Antiretroviral Agents in Adults and Adolescents with HIV
(https://clinicalinfo.hiv.gov/en/guidelines/hiv-clinical-guidelines-adult-and-adolescent-arv/drug-interactions-overview?view=full)
(154). | |||||||
a. Nucleoside
reverse
transcriptase inhibitors
(NRTIs) | |||||||
i.
Abacavir (ABC) |
1 |
1 |
1 |
Evidence:
NRTIs do not appear to have significant risk for interactions
with hormonal contraceptive methods (155–160). |
|||
ii.
Tenofovir (TDF) |
1 |
1 |
1 |
||||
iii.
Zidovudine (AZT) |
1 |
1 |
1 |
||||
iv.
Lamivudine (3TC) |
1 |
1 |
1 |
||||
v.
Didanosine (DDI) |
1 |
1 |
1 |
||||
vi.
Emtricitabine (FTC) |
1 |
1 |
1 |
||||
vii.
Stavudine (D4T) |
1 |
1 |
1 |
||||
b.
Nonnucleoside reverse
transcriptase
inhibitors
(NNRTIs) | |||||||
i.
Efavirenz (EFV) |
2 |
1 |
2 |
Clarification: Evidence
suggests drug interactions between EFV and certain hormonal
contraceptives. These interactions might reduce the
effectiveness of the hormonal
contraceptive. Evidence: One study found that women using etonogestrel implants with EFV had a higher pregnancy rate than women not using ARVs, although confidence intervals overlapped and absolute pregnancy rates were still lower than for other hormonal methods; another study found that etonogestrel levels were decreased and 5% of women had presumptive ovulation while using etonogestrel implants with EFV (161,162). Three studies of women using LNG implants demonstrated increased pregnancy rates for women using EFV-containing ARV therapy compared with no ARV use, although absolute pregnancy rates were still lower than for other hormonal methods in one study (162–164); another study of LNG implant users found no difference in pregnancy rates with EFV compared with no EFV (165). No significant effects were found on pregnancy rates, DMPA levels, EFV levels, or HIV disease progression in women using DMPA and EFV compared with DMPA alone (162,165–169). No significant effects were found on HIV disease progression in women using LNG implants and EFV compared with no ARVs (164). No data have assessed effectiveness of contraceptive implants during later years of use when progestin concentrations are lower and risk for failure from drug interactions might be greater. |
|||
ii.
Etravirine (ETR) |
1 |
1 |
1 |
— |
|||
iii.
Nevirapine (NVP) |
1 |
1 |
1 |
Evidence: Five studies
found no significant increase in pregnancy rates among women
using implants and NVP compared with implants alone (162–165,170).
Four studies found no significant increase in pregnancy rates
among women using DMPA or other contraceptive injectables and
NVP compared with DMPA or other contraceptive injectables alone
(162,165,168,171). One
study found no ovulations or changes in DMPA concentrations
(166). No effect was found on HIV
disease progression with use of NVP and DMPA or LNG implants
(164,166,168–170,172). No
data have assessed effectiveness of contraceptive implants
during later years of use when progestin concentrations are
lower and risk for failure from drug interactions might be
greater. |
|||
iv.
Rilpivirine (RPV) |
1 |
1 |
1 |
— |
|||
c.
Ritonavir-boosted
protease inhibitors | |||||||
i.
Ritonavir-boosted atazanavir (ATV/r) |
2 |
1 |
2 |
Clarification:
Theoretically, drug interactions might occur between certain
ritonavir-boosted protease inhibitors and certain hormonal
contraceptives that might reduce the effectiveness of the
hormonal contraceptive. Any potential effect on contraceptive
effectiveness is likely to be lower with DMPA than with other
POCs because of the higher dose of
DMPA. Evidence: One pharmacokinetic study demonstrated increased progestin concentrations with use of POPs and ATV/r compared with POPs alone (173). |
|||
ii.
Ritonavir-boosted darunavir (DRV/r) |
2 |
1 |
2 |
Clarification:
Theoretically, drug interactions might occur between certain
ritonavir-boosted protease inhibitors and certain hormonal
contraceptives that might reduce the effectiveness of the
hormonal contraceptive. Any potential effect on contraceptive
effectiveness is likely to be lower with DMPA than with other
POCs because of the higher dose of DMPA. |
|||
iii.
Ritonavir-boosted fosamprenavir (FPV/r) |
2 |
1 |
2 |
Clarification:
Theoretically, drug interactions might occur between certain
ritonavir-boosted protease inhibitors and certain hormonal
contraceptives that might reduce the effectiveness of the
hormonal contraceptive. Any potential effect on contraceptive
effectiveness is likely to be lower with DMPA than with other
POCs because of the higher dose of DMPA. |
|||
iv.
Ritonavir-boosted lopinavir (LPV/r) |
1 |
1 |
1 |
Evidence: One study
demonstrated no pregnancies, no ovulations, no change in LPV/r
level, and no change in HIV disease progression in women using
DMPA (174); another study found a small
increase in pregnancy rate in women using DMPA with LPV/r
compared with no ARV therapy, however confidence intervals
overlapped (162). Two studies found no
increased risk for pregnancy in women using implants (162,163). Two
studies found contraceptive hormones increased in women using
LPV/r with DMPA or etonogestrel implants (161,174). |
|||
v.
Ritonavir-boosted saquinavir (SQV/r) |
2 |
1 |
2 |
Clarification:
Theoretically, drug interactions might occur between certain
ritonavir-boosted protease inhibitors and certain hormonal
contraceptives that might reduce the effectiveness of the
hormonal contraceptive. Any potential effect on contraceptive
effectiveness is likely to be lower with DMPA than with other
POCs because of the higher dose of DMPA. |
|||
vi.
Ritonavir-boosted tipranavir (TPV/r) |
2 |
1 |
2 |
Clarification:
Theoretically, drug interactions might occur between certain
ritonavir-boosted protease inhibitors and certain hormonal
contraceptives that might reduce the effectiveness of the
hormonal contraceptive. Any potential effect on contraceptive
effectiveness is likely to be lower with DMPA than with other
POCs because of the higher dose of DMPA. |
|||
d. Protease
inhibitors
without ritonavir | |||||||
i.
Atazanavir (ATV) |
1 |
1 |
1 |
Comment: When ATV is
administered with cobicistat, theoretical concern exists for a
drug interaction with hormonal contraceptives. Cobicistat is an
inhibitor of CYP3A and CYP2D6 and could theoretically increase
contraceptive hormone levels. However, its effects on CYP
enzymes and drug levels might vary when combined with other
ARVs. |
|||
ii.
Fosamprenavir (FPV) |
2 |
2 |
2 |
Clarification:
Theoretical concern exists that interactions between FPV and
hormonal contraceptives leading to decreased levels of FPV might
diminish effectiveness of the ARV drug. The drug interaction
likely involves CYP3A4 pathways; POCs have less effect on CYP3A4
enzymes than CHCs. |
|||
iii.
Indinavir (IDV) |
1 |
1 |
1 |
— |
|||
iv.
Nelfinavir (NFV) |
2 |
1 |
2 |
Clarification:
Theoretically, drug interactions might occur between certain
protease inhibitors and certain hormonal contraceptives that
might reduce the effectiveness of the hormonal contraceptive.
Any potential effect on contraceptive effectiveness is likely to
be lower with DMPA than with other POCs because of the higher
dose of DMPA. Concern exists that interactions between NFV and
POCs might decrease NFV levels. Evidence: One study found no pregnancies, no ovulations, no change in DMPA concentrations and no change in HIV disease progression with use of DMPA and NFV compared with DMPA alone; NFV concentrations were decreased with concomitant DMPA use (166,168). |
|||
e. CCR5
co-receptor
antagonists | |||||||
i.
Maraviroc (MVC) |
1 |
1 |
1 |
— |
|||
f. HIV
integrase strand transfer
inhibitors | |||||||
i.
Raltegravir (RAL) |
1 |
1 |
1 |
— |
|||
ii.
Dolutegravir (DTG) |
1 |
1 |
1 |
— |
|||
iii.
Elvitegravir (EVG) |
1 |
1 |
1 |
Comment: When EVG is
administered with cobicistat, theoretical concern exists for a
drug interaction with hormonal contraceptives. Cobicistat is an
inhibitor of CYP3A and CYP2D6 and could theoretically increase
contraceptive hormone levels. However, its effects on CYP
enzymes and drug levels might vary when combined with other
ARVs. |
|||
g. Fusion
inhibitors | |||||||
i.
Enfuvirtide |
1 |
1 |
1 |
— |
|||
Anticonvulsant therapy
| |||||||
a. Certain anticonvulsants
(phenytoin, carbamazepine, barbiturates, primidone, topiramate,
and oxcarbazepine) |
2 |
1 |
3 |
Clarification: Although
the interaction of certain anticonvulsants with POPs and
etonogestrel implants is not harmful, it is likely to reduce the
effectiveness of POPs and etonogestrel implants. Whether
increasing the hormone dose of POPs alleviates this concern
remains unclear. Use of other contraceptives should be
encouraged for persons who are long-term users of any of these
drugs. Use of DMPA is a category 1 because its effectiveness is
not decreased by use of certain
anticonvulsants. Evidence: Use of certain anticonvulsants might decrease the effectiveness of POCs (175–178). |
|||
b. Lamotrigine |
1 |
1 |
1 |
Evidence: No drug
interactions have been reported among women with epilepsy
receiving lamotrigine and POCs (178,179). |
|||
Antimicrobial therapy
| |||||||
a. Broad-spectrum
antibiotics |
1 |
1 |
1 |
— |
|||
b. Antifungals |
1 |
1 |
1 |
— |
|||
c.
Antiparasitics |
1 |
1 |
1 |
— |
|||
d. Rifampin or rifabutin
therapy |
2 |
1 |
3 |
Clarification: Although
the interaction of rifampin or rifabutin with POPs and
etonogestrel implants is not harmful, it is likely to reduce the
effectiveness of POPs and etonogestrel implants. Use of other
contraceptives should be encouraged for persons who are
long-term users of any of these drugs. Use of DMPA is a category
1 because its effectiveness is not decreased by use of rifampin
or rifabutin. Whether increasing the hormone dose of POPs
alleviates this concern remains unclear. |
|||
Psychotropic medications
|
Comment: For many common
psychotropic agents, limited or no theoretical concern exits for
clinically significant drug interactions when co-administered
with hormonal contraceptives. However, either no or very limited
data exist examining potential interactions for these classes of
medications. |
||||||
a. Selective serotonin
reuptake inhibitors (SSRIs) |
1 |
1 |
1 |
Evidence: No evidence
specifically examined the use of POCs with SSRIs. Limited
clinical and pharmacokinetic data do not demonstrate concern for
SSRIs decreasing the effectiveness of oral contraceptives.
Limited evidence suggests that for women taking SSRIs, the use
of hormonal contraceptives was not associated with differences
in effectiveness of the SSRI for treatment or in adverse events
when compared with women not taking hormonal contraceptives
(180). Comment: Drugs that are inhibitors of CYP3A4 or CYP2C9 theoretically have the potential to increase levels of contraceptive steroid, which might increase adverse events. Fluvoxamine is an SSRI known to be a moderate inhibitor of both 3A4 and 2C9; however, no clinical or pharmacokinetic studies were identified to explore potential drug-drug interactions. |
|||
St. John’s wort | 2 |
1 |
2 |
Evidence: No evidence
specifically examined the use of POCs with St. John’s
wort. Although clinical data are limited, studies with
pharmacokinetic and pharmacodynamics outcomes raise concern that
St. John’s wort might decrease effectiveness of hormonal
contraceptives, including increased risk for breakthrough
bleeding and ovulation and increased metabolism of estrogen and
progestin. Any interactions might be dependent on the dose of
St. John’s wort, and the concentration of active
ingredients across types of St. John’s wort preparations
might vary (181). Comment: Any potential effect on contraceptive effectiveness is likely to be lower with DMPA than with other POCs because of the higher dose of DMPA. |
Abbreviations: ARV = antiretroviral; BMD = bone mineral density; BMI = body mass index; CHC = combined hormonal contraceptive; CKD = chronic kidney disease; COC = combined oral contraceptive; Cu-IUD = copper intrauterine device; CYP = cytochrome P450; DMPA = depot medroxyprogesterone acetate; DRSP = drospirenone; DVT = deep venous thrombosis; hCG = human chorionic gonadotropin; HDL = high-density lipoprotein; IBD = inflammatory bowel disease; IM = intramuscular; LDL = low-density lipoprotein; LNG = levonorgestrel; LNG-IUD = levonorgestrel intrauterine device; NA = not applicable; PE = pulmonary embolism; PID = pelvic inflammatory disease; POC = progestin-only contraceptive; POP = progestin-only pill; PrEP = pre-exposure prophylaxis; RCT = randomized clinical trial; SLE = systemic lupus erythematosus; STI = sexually transmitted infection; U.S. MEC = U.S. Medical Eligibility Criteria for Contraceptive Use; U.S. SPR = U.S. Selected Practice Recommendations for Contraceptive Use; VTE = venous thromboembolism.
References
- 1.Curtis KM, Nguyen AT, Tepper NK, et al. U.S. selected practice recommendations for contraceptive use, 2024. MMWR Recomm Rep 2024;73(No. RR-3):1–77. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2.Workowski KA, Bachmann LH, Chan PA, et al. Sexually transmitted infections treatment guidelines, 2021. MMWR Recomm Rep 2021;70(No. RR-4):1–187. 10.15585/mmwr.rr7004a1 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 3.CDC. US Public Health Service preexposure prophylaxis for the prevention of HIV infection in the United States—2021 update: a clinical practice guideline. Atlanta, GA: US Department of Health and Human Services, CDC; 2021. https://www.cdc.gov/hiv/pdf/risk/prep/cdc-hiv-prep-guidelines-2021.pdf
- 4.Curtis KM, Martins SL. Progestogen-only contraception and bone mineral density: a systematic review. Contraception 2006;73:470–87. 10.1016/j.contraception.2005.12.010 [DOI] [PubMed] [Google Scholar]
- 5.Lanza LL, McQuay LJ, Rothman KJ, et al. Use of depot medroxyprogesterone acetate contraception and incidence of bone fracture. Obstet Gynecol 2013;121:593–600. 10.1097/AOG.0b013e318283d1a1 [DOI] [PubMed] [Google Scholar]
- 6.Harel Z, Riggs S, Vaz R, Flanagan P, Harel D, Machan JT. Bone accretion in adolescents using the combined estrogen and progestin transdermal contraceptive method Ortho Evra: a pilot study. J Pediatr Adolesc Gynecol 2010;23:23–31. 10.1016/j.jpag.2009.04.008 [DOI] [PubMed] [Google Scholar]
- 7.Kaunitz AM, Miller PD, Rice VM, Ross D, McClung MR. Bone mineral density in women aged 25–35 years receiving depot medroxyprogesterone acetate: recovery following discontinuation. Contraception 2006;74:90–9. 10.1016/j.contraception.2006.03.010 [DOI] [PubMed] [Google Scholar]
- 8.Kaunitz AM, Arias R, McClung M. Bone density recovery after depot medroxyprogesterone acetate injectable contraception use. Contraception 2008;77:67–76. 10.1016/j.contraception.2007.10.005 [DOI] [PubMed] [Google Scholar]
- 9.Kaunitz AM, Darney PD, Ross D, Wolter KD, Speroff L. Subcutaneous DMPA vs. intramuscular DMPA: a 2-year randomized study of contraceptive efficacy and bone mineral density. Contraception 2009;80:7–17. 10.1016/j.contraception.2009.02.005 [DOI] [PubMed] [Google Scholar]
- 10.Lappe JM, Stegman MR, Recker RR. The impact of lifestyle factors on stress fractures in female Army recruits. Osteoporos Int 2001;12:35–42. 10.1007/s001980170155 [DOI] [PubMed] [Google Scholar]
- 11.Lara-Torre E, Edwards CP, Perlman S, Hertweck SP. Bone mineral density in adolescent females using depot medroxyprogesterone acetate. J Pediatr Adolesc Gynecol 2004;17:17–21. 10.1016/j.jpag.2003.11.017 [DOI] [PubMed] [Google Scholar]
- 12.Lopez LM, Chen M, Mullins S, Curtis KM, Helmerhorst FM. Steroidal contraceptives and bone fractures in women: evidence from observational studies. Cochrane Database Syst Rev 2012;8:CD009849. [DOI] [PubMed] [Google Scholar]
- 13.Lopez LM, Grimes DA, Schulz KF, Curtis KM. Steroidal contraceptives: effect on bone fractures in women. Cochrane Database Syst Rev 2011; (7):CD006033. [DOI] [PubMed] [Google Scholar]
- 14.Meier C, Brauchli YB, Jick SS, Kraenzlin ME, Meier CR. Use of depot medroxyprogesterone acetate and fracture risk. J Clin Endocrinol Metab 2010;95:4909–16. 10.1210/jc.2010-0032 [DOI] [PubMed] [Google Scholar]
- 15.Merki-Feld GS, Neff M, Keller PJ. A 2-year prospective study on the effects of depot medroxyprogesterone acetate on bone mass-response to estrogen and calcium therapy in individual users. Contraception 2003;67:79–86. 10.1016/S0010-7824(02)00460-2 [DOI] [PubMed] [Google Scholar]
- 16.Monteiro-Dantas C, Espejo-Arce X, Lui-Filho JF, Fernandes AM, Monteiro I, Bahamondes L. A three-year longitudinal evaluation of the forearm bone density of users of etonogestrel- and levonorgestrel-releasing contraceptive implants. Reprod Health 2007;4:11. 10.1186/1742-4755-4-11 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 17.Naessen T, Olsson SE, Gudmundson J. Differential effects on bone density of progestogen-only methods for contraception in premenopausal women. Contraception 1995;52:35–9. 10.1016/0010-7824(95)00121-P [DOI] [PubMed] [Google Scholar]
- 18.Sanches L, Marchi NM, Castro S, Juliato CT, Villarroel M, Bahamondes L. Forearm bone mineral density in postmenopausal former users of depot medroxyprogesterone acetate. Contraception 2008;78:365–9. 10.1016/j.contraception.2008.07.013 [DOI] [PubMed] [Google Scholar]
- 19.Scholes D, LaCroix AZ, Ichikawa LE, Barlow WE, Ott SM. Injectable hormone contraception and bone density: results from a prospective study. Epidemiology 2002;13:581–7. 10.1097/00001648-200209000-00015 [DOI] [PubMed] [Google Scholar]
- 20.Scholes D, LaCroix AZ, Ichikawa LE, Barlow WE, Ott SM. Change in bone mineral density among adolescent women using and discontinuing depot medroxyprogesterone acetate contraception. Arch Pediatr Adolesc Med 2005;159:139–44. 10.1001/archpedi.159.2.139 [DOI] [PubMed] [Google Scholar]
- 21.Segall-Gutierrez P, Agarwal R, Ge M, Lopez C, Hernandez G, Stanczyk FZ. A pilot study examining short-term changes in bone mineral density among class 3 obese users of depot-medroxyprogesterone acetate. Eur J Contracept Reprod Health Care 2013;18:199–205. 10.3109/13625187.2013.774358 [DOI] [PubMed] [Google Scholar]
- 22.Tang OS, Tang G, Yip PS, Li B. Further evaluation on long-term depot-medroxyprogesterone acetate use and bone mineral density: a longitudinal cohort study. Contraception 2000;62:161–4. 10.1016/S0010-7824(00)00168-2 [DOI] [PubMed] [Google Scholar]
- 23.Vestergaard P, Rejnmark L, Mosekilde L. The effects of depot medroxyprogesterone acetate and intrauterine device use on fracture risk in Danish women. Contraception 2008;78:459–64. 10.1016/j.contraception.2008.07.014 [DOI] [PubMed] [Google Scholar]
- 24.Viola AS, Castro S, Marchi NM, Bahamondes MV, Viola CF, Bahamondes L. Long-term assessment of forearm bone mineral density in postmenopausal former users of depot medroxyprogesterone acetate. Contraception 2011;84:122–7. 10.1016/j.contraception.2010.11.007 [DOI] [PubMed] [Google Scholar]
- 25.Walsh JS, Eastell R, Peel NF. Depot medroxyprogesterone acetate use after peak bone mass is associated with increased bone turnover but no decrease in bone mineral density. Fertil Steril 2010;93:697–701. 10.1016/j.fertnstert.2008.10.004 [DOI] [PubMed] [Google Scholar]
- 26.Wetmore CM, Ichikawa L, LaCroix AZ, Ott SM, Scholes D. Association between caffeine intake and bone mass among young women: potential effect modification by depot medroxyprogesterone acetate use. Osteoporos Int 2008;19:519–27. 10.1007/s00198-007-0473-2 [DOI] [PubMed] [Google Scholar]
- 27.Wong AY, Tang LC, Chin RK. Levonorgestrel-releasing intrauterine system (Mirena) and Depot medroxyprogesterone acetate (Depoprovera) as long-term maintenance therapy for patients with moderate and severe endometriosis: a randomised controlled trial. Aust N Z J Obstet Gynaecol 2010;50:273–9. 10.1111/j.1479-828X.2010.01152.x [DOI] [PubMed] [Google Scholar]
- 28.Yang KY, Kim YS, Ji YI, Jung MH. Changes in bone mineral density of users of the levonorgestrel-releasing intrauterine system. J Nippon Med Sch 2012;79:190–4. 10.1272/jnms.79.190 [DOI] [PubMed] [Google Scholar]
- 29.Zhang MH, Zhang W, Zhang AD, Yang Y, Gai L. Effect of depot medroxyprogesterone acetate on bone mineral density in adolescent women. Chin Med J (Engl) 2013;126:4043–7. 10.3760/cma.j.issn.0366-6999.20130885 [DOI] [PubMed] [Google Scholar]
- 30.Bahamondes MV, Monteiro I, Castro S, Espejo-Arce X, Bahamondes L. Prospective study of the forearm bone mineral density of long-term users of the levonorgestrel-releasing intrauterine system. Hum Reprod 2010;25:1158–64. 10.1093/humrep/deq043 [DOI] [PubMed] [Google Scholar]
- 31.Banks E, Berrington A, Casabonne D. Overview of the relationship between use of progestogen-only contraceptives and bone mineral density. BJOG 2001;108:1214–21. 10.1111/j.1471-0528.2001.00296.x [DOI] [PubMed] [Google Scholar]
- 32.Beerthuizen R, van Beek A, Massai R, Mäkäräinen L, Hout J, Bennink HC. Bone mineral density during long-term use of the progestagen contraceptive implant Implanon compared to a non-hormonal method of contraception. Hum Reprod 2000;15:118–22. 10.1093/humrep/15.1.118 [DOI] [PubMed] [Google Scholar]
- 33.Beksinska ME, Kleinschmidt I, Smit JA, Farley TM. Bone mineral density in adolescents using norethisterone enanthate, depot-medroxyprogesterone acetate or combined oral contraceptives for contraception. Contraception 2007;75:438–43. 10.1016/j.contraception.2007.02.001 [DOI] [PubMed] [Google Scholar]
- 34.Beksinska ME, Kleinschmidt I, Smit JA, Farley TM. Bone mineral density in a cohort of adolescents during use of norethisterone enanthate, depot-medroxyprogesterone acetate or combined oral contraceptives and after discontinuation of norethisterone enanthate. Contraception 2009;79:345–9. 10.1016/j.contraception.2008.11.009 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 35.Berenson AB, Breitkopf CR, Grady JJ, Rickert VI, Thomas A. Effects of hormonal contraception on bone mineral density after 24 months of use. Obstet Gynecol 2004;103:899–906. 10.1097/01.AOG.0000117082.49490.d5 [DOI] [PubMed] [Google Scholar]
- 36.Berenson AB, Rahman M, Breitkopf CR, Bi LX. Effects of depot medroxyprogesterone acetate and 20-microgram oral contraceptives on bone mineral density. Obstet Gynecol 2008;112:788–99. 10.1097/AOG.0b013e3181875b78 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 37.Busen NH, Britt RB, Rianon N. Bone mineral density in a cohort of adolescent women using depot medroxyprogesterone acetate for one to two years. J Adolesc Health 2003;32:257–9. 10.1016/S1054-139X(02)00567-0 [DOI] [PubMed] [Google Scholar]
- 38.Caird LE, Reid-Thomas V, Hannan WJ, Gow S, Glasier AF. Oral progestogen-only contraception may protect against loss of bone mass in breast-feeding women. Clin Endocrinol (Oxf) 1994;41:739–45. 10.1111/j.1365-2265.1994.tb02788.x [DOI] [PubMed] [Google Scholar]
- 39.Clark MK, Sowers M, Levy B, Nichols S. Bone mineral density loss and recovery during 48 months in first-time users of depot medroxyprogesterone acetate. Fertil Steril 2006;86:1466–74. 10.1016/j.fertnstert.2006.05.024 [DOI] [PubMed] [Google Scholar]
- 40.Cromer BA, Lazebnik R, Rome E, et al. Double-blinded randomized controlled trial of estrogen supplementation in adolescent girls who receive depot medroxyprogesterone acetate for contraception. Am J Obstet Gynecol 2005;192:42–7. 10.1016/j.ajog.2004.07.041 [DOI] [PubMed] [Google Scholar]
- 41.Cromer BA, Blair JM, Mahan JD, Zibners L, Naumovski Z. A prospective comparison of bone density in adolescent girls receiving depot medroxyprogesterone acetate (Depo-Provera), levonorgestrel (Norplant), or oral contraceptives. J Pediatr 1996;129:671–6. 10.1016/S0022-3476(96)70148-8 [DOI] [PubMed] [Google Scholar]
- 42.Cromer BA, Bonny AE, Stager M, et al. Bone mineral density in adolescent females using injectable or oral contraceptives: a 24-month prospective study. Fertil Steril 2008;90:2060–7. 10.1016/j.fertnstert.2007.10.070 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 43.Cromer BA, Stager M, Bonny A, et al. Depot medroxyprogesterone acetate, oral contraceptives and bone mineral density in a cohort of adolescent girls. J Adolesc Health 2004;35:434–41. 10.1016/j.jadohealth.2004.07.005 [DOI] [PubMed] [Google Scholar]
- 44.Cundy T, Ames R, Horne A, et al. A randomized controlled trial of estrogen replacement therapy in long-term users of depot medroxyprogesterone acetate. J Clin Endocrinol Metab 2003;88:78–81. 10.1210/jc.2002-020874 [DOI] [PubMed] [Google Scholar]
- 45.Cundy T, Cornish J, Evans MC, Roberts H, Reid IR. Recovery of bone density in women who stop using medroxyprogesterone acetate. BMJ 1994;308:247–8. 10.1136/bmj.308.6923.247 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 46.Cundy T, Cornish J, Roberts H, Reid IR. Menopausal bone loss in long-term users of depot medroxyprogesterone acetate contraception. Am J Obstet Gynecol 2002;186:978–83. 10.1067/mob.2002.122420 [DOI] [PubMed] [Google Scholar]
- 47.Di X, Li Y, Zhang C, Jiang J, Gu S. Effects of levonorgestrel-releasing subdermal contraceptive implants on bone density and bone metabolism. Contraception 1999;60:161–6. 10.1016/S0010-7824(99)00080-3 [DOI] [PubMed] [Google Scholar]
- 48.Díaz S, Reyes MV, Zepeda A, et al. Norplant((R)) implants and progesterone vaginal rings do not affect maternal bone turnover and density during lactation and after weaning. Hum Reprod 1999;14:2499–505. 10.1093/humrep/14.10.2499 [DOI] [PubMed] [Google Scholar]
- 49.Gai L, Zhang J, Zhang H, Gai P, Zhou L, Liu Y. The effect of depot medroxyprogesterone acetate (DMPA) on bone mineral density (BMD) and evaluating changes in BMD after discontinuation of DMPA in Chinese women of reproductive age. Contraception 2011;83:218–22. 10.1016/j.contraception.2010.07.027 [DOI] [PubMed] [Google Scholar]
- 50.Bahamondes L, Espejo-Arce X, Hidalgo MM, Hidalgo-Regina C, Teatin-Juliato C, Petta CA. A cross-sectional study of the forearm bone density of long-term users of levonorgestrel-releasing intrauterine system. Hum Reprod 2006;21:1316–9. 10.1093/humrep/dei457 [DOI] [PubMed] [Google Scholar]
- 51.Bahamondes L, Monteiro-Dantas C, Espejo-Arce X, et al. A prospective study of the forearm bone density of users of etonorgestrel- and levonorgestrel-releasing contraceptive implants. Hum Reprod 2006;21:466–70. 10.1093/humrep/dei358 [DOI] [PubMed] [Google Scholar]
- 52.Pitts SA, Feldman HA, Dorale A, Gordon CM. Bone mineral density, fracture, and vitamin D in adolescents and young women using depot medroxyprogesterone acetate. J Pediatr Adolesc Gynecol 2012;25:23–6. 10.1016/j.jpag.2011.07.014 [DOI] [PubMed] [Google Scholar]
- 53.US Department of Agriculture; US Department of Health and Human Services. Dietary guidelines for Americans, 2020–2025. 9th ed. Washington, DC: US Department of Agriculture and US Department of Health and Human Services; 2020. https://www.dietaryguidelines.gov/sites/default/files/2021-03/Dietary_Guidelines_for_Americans-2020-2025.pdf
- 54.Meek JY, Noble L; Section on Breastfeeding. Policy statement: breastfeeding and the use of human milk. Pediatrics 2022;150:e2022057988. 10.1542/peds.2022-057988 [DOI] [PubMed] [Google Scholar]
- 55.Braga GC, Ferriolli E, Quintana SM, Ferriani RA, Pfrimer K, Vieira CS. Immediate postpartum initiation of etonogestrel-releasing implant: A randomized controlled trial on breastfeeding impact. Contraception 2015;92:536–42. 10.1016/j.contraception.2015.07.009 [DOI] [PubMed] [Google Scholar]
- 56.Phillips SJ, Tepper NK, Kapp N, Nanda K, Temmerman M, Curtis KM. Progestogen-only contraceptive use among breastfeeding women: a systematic review. Contraception 2016;94:226–52. 10.1016/j.contraception.2015.09.010 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 57.Raymond EG, Weaver MA, Louie KS, et al. Effects of depot medroxyprogesterone acetate injection timing on medical abortion efficacy and repeat pregnancy: a randomized controlled trial. Obstet Gynecol 2016;128:739–45. 10.1097/AOG.0000000000001627 [DOI] [PubMed] [Google Scholar]
- 58.Kim C, Nguyen AT, Berry-Bibee E, Ermias Y, Gaffield ME, Kapp N. Systemic hormonal contraception initiation after abortion: a systematic review and meta-analysis. Contraception 2021;103:291–304. 10.1016/j.contraception.2021.01.017 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 59.Beksinska ME, Smit JA, Kleinschmidt I, Milford C, Farley TM. Prospective study of weight change in new adolescent users of DMPA, NET-EN, COCs, nonusers and discontinuers of hormonal contraception. Contraception 2010;81:30–4. 10.1016/j.contraception.2009.07.007 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 60.Bender NM, Segall-Gutierrez P, Najera SO, Stanczyk FZ, Montoro M, Mishell DR Jr. Effects of progestin-only long-acting contraception on metabolic markers in obese women. Contraception 2013;88:418–25. 10.1016/j.contraception.2012.12.007 [DOI] [PubMed] [Google Scholar]
- 61.Berenson AB, Rahman M. Changes in weight, total fat, percent body fat, and central-to-peripheral fat ratio associated with injectable and oral contraceptive use. Am J Obstet Gynecol 2009;200:329.e1–8. 10.1016/j.ajog.2008.12.052 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 62.Bonny AE, Secic M, Cromer B. Early weight gain related to later weight gain in adolescents on depot medroxyprogesterone acetate. Obstet Gynecol 2011;117:793–7. 10.1097/AOG.0b013e31820f387c [DOI] [PMC free article] [PubMed] [Google Scholar]
- 63.Bonny AE, Ziegler J, Harvey R, Debanne SM, Secic M, Cromer BA. Weight gain in obese and nonobese adolescent girls initiating depot medroxyprogesterone, oral contraceptive pills, or no hormonal contraceptive method. Arch Pediatr Adolesc Med 2006;160:40–5. 10.1001/archpedi.160.1.40 [DOI] [PubMed] [Google Scholar]
- 64.Clark MK, Dillon JS, Sowers M, Nichols S. Weight, fat mass, and central distribution of fat increase when women use depot-medroxyprogesterone acetate for contraception. Int J Obes 2005;29:1252–8. 10.1038/sj.ijo.0803023 [DOI] [PubMed] [Google Scholar]
- 65.Gerlach LS, Saldaña SN, Wang Y, Nick TG, Spigarelli MG. Retrospective review of the relationship between weight change and demographic factors following initial depot medroxyprogesterone acetate injection in adolescents. Clin Ther 2011;33:182–7. 10.1016/j.clinthera.2011.02.008 [DOI] [PubMed] [Google Scholar]
- 66.Jain J, Jakimiuk AJ, Bode FR, Ross D, Kaunitz AM. Contraceptive efficacy and safety of DMPA-SC. Contraception 2004;70:269–75. 10.1016/j.contraception.2004.06.011 [DOI] [PubMed] [Google Scholar]
- 67.Kozlowski KJ, Rickert VI, Hendon A, Davis P. Adolescents and Norplant: preliminary findings of side effects. J Adolesc Health 1995;16:373–8. 10.1016/S1054-139X(94)00029-E [DOI] [PubMed] [Google Scholar]
- 68.Le YL, Rahman M, Berenson AB. Early weight gain predicting later weight gain among depot medroxyprogesterone acetate users. Obstet Gynecol 2009;114:279–84. 10.1097/AOG.0b013e3181af68b2 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 69.Leiman G. Depo-medroxyprogesterone acetate as a contraceptive agent: its effect on weight and blood pressure. Am J Obstet Gynecol 1972;114:97–102. 10.1016/0002-9378(72)90296-7 [DOI] [PubMed] [Google Scholar]
- 70.Lopez LM, Grimes DA, Chen M, et al. Hormonal contraceptives for contraception in overweight or obese women. Cochrane Database Syst Rev 2013;4:CD008452. [DOI] [PubMed] [Google Scholar]
- 71.Mangan SA, Larsen PG, Hudson S. Overweight teens at increased risk for weight gain while using depot medroxyprogesterone acetate. J Pediatr Adolesc Gynecol 2002;15:79–82. 10.1016/S1083-3188(01)00147-4 [DOI] [PubMed] [Google Scholar]
- 72.Nyirati CM, Habash DL, Shaffer LE. Weight and body fat changes in postpartum depot-medroxyprogesterone acetate users. Contraception 2013;88:169–76. 10.1016/j.contraception.2012.10.016 [DOI] [PubMed] [Google Scholar]
- 73.Pantoja M, Medeiros T, Baccarin MC, Morais SS, Bahamondes L, dos Santos Fernandes AM. Variations in body mass index of users of depot-medroxyprogesterone acetate as a contraceptive. Contraception 2010;81:107–11. 10.1016/j.contraception.2009.07.008 [DOI] [PubMed] [Google Scholar]
- 74.Risser WL, Gefter LR, Barratt MS, Risser JM. Weight change in adolescents who used hormonal contraception. J Adolesc Health 1999;24:433–6. 10.1016/S1054-139X(98)00151-7 [DOI] [PubMed] [Google Scholar]
- 75.Segall-Gutierrez P, Xiang AH, Watanabe RM, et al. Deterioration in cardiometabolic risk markers in obese women during depot medroxyprogesterone acetate use. Contraception 2012;85:36–41. 10.1016/j.contraception.2011.04.016 [DOI] [PubMed] [Google Scholar]
- 76.Westhoff C, Jain JK, Milsom I, Ray A. Changes in weight with depot medroxyprogesterone acetate subcutaneous injection 104 mg/0.65 mL. Contraception 2007;75:261–7. 10.1016/j.contraception.2006.12.009 [DOI] [PubMed] [Google Scholar]
- 77.Paulen ME, Zapata LB, Cansino C, Curtis KM, Jamieson DJ. Contraceptive use among women with a history of bariatric surgery: a systematic review. Contraception 2010;82:86–94. 10.1016/j.contraception.2010.02.008 [DOI] [PubMed] [Google Scholar]
- 78.World Health Organization Collaborative Study of Cardiovascular Disease and Steroid Hormone Contraception. Cardiovascular disease and use of oral and injectable progestogen-only contraceptives and combined injectable contraceptives. Results of an international, multicenter, case-control study. Contraception 1998;57:315–24. 10.1016/S0010-7824(98)00041-9 [DOI] [PubMed] [Google Scholar]
- 79.Martinelli I, Lensing AW, Middeldorp S, et al. Recurrent venous thromboembolism and abnormal uterine bleeding with anticoagulant and hormone therapy use. Blood 2016;127:1417–25. 10.1182/blood-2015-08-665927 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 80.Sönmezer M, Atabekoğlu C, Cengiz B, Dökmeci F, Cengiz SD. Depot-medroxyprogesterone acetate in anticoagulated patients with previous hemorrhagic corpus luteum. Eur J Contracept Reprod Health Care 2005;10:9–14. 10.1080/13625180400020952 [DOI] [PubMed] [Google Scholar]
- 81.Barbhaiya M, Zuily S, Naden R, et al. ; ACR/EULAR APS Classification Criteria Collaborators. The 2023 ACR/EULAR Antiphospholipid Syndrome Classification Criteria. Arthritis Rheumatol 2023;75:1687–702. 10.1002/art.42624 [DOI] [PubMed] [Google Scholar]
- 82.Bergendal A, Persson I, Odeberg J, et al. Association of venous thromboembolism with hormonal contraception and thrombophilic genotypes. Obstet Gynecol 2014;124:600–9. 10.1097/AOG.0000000000000411 [DOI] [PubMed] [Google Scholar]
- 83.Leon L, Giannoukas AD, Dodd D, Chan P, Labropoulos N. Clinical significance of superficial vein thrombosis. Eur J Vasc Endovasc Surg 2005;29:10–7. 10.1016/j.ejvs.2004.09.021 [DOI] [PubMed] [Google Scholar]
- 84.Tepper NK, Paulen ME, Marchbanks PA, Curtis KM. Safety of contraceptive use among women with peripartum cardiomyopathy: a systematic review. Contraception 2010;82:95–101. 10.1016/j.contraception.2010.02.004 [DOI] [PubMed] [Google Scholar]
- 85.The Criteria Committee of the New York Heart Association. Nomenclature and criteria for diagnosis of diseases of the heart and great vessels. 9th ed. Boston, MA: Little, Brown and Co; 1994. [Google Scholar]
- 86.Folsom AR, Lutsey PL, Astor BC, Wattanakit K, Heckbert SR, Cushman M; Atherosclerosis Risk in Communities Study. Chronic kidney disease and venous thromboembolism: a prospective study. Nephrol Dial Transplant 2010;25:3296–301. 10.1093/ndt/gfq179 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 87.Kayali F, Najjar R, Aswad F, Matta F, Stein PD. Venous thromboembolism in patients hospitalized with nephrotic syndrome. Am J Med 2008;121:226–30. 10.1016/j.amjmed.2007.08.042 [DOI] [PubMed] [Google Scholar]
- 88.Mahmoodi BK, ten Kate MK, Waanders F, et al. High absolute risks and predictors of venous and arterial thromboembolic events in patients with nephrotic syndrome: results from a large retrospective cohort study. Circulation 2008;117:224–30. 10.1161/CIRCULATIONAHA.107.716951 [DOI] [PubMed] [Google Scholar]
- 89.Singhal R, Brimble KS. Thromboembolic complications in the nephrotic syndrome: pathophysiology and clinical management. Thromb Res 2006;118:397–407. 10.1016/j.thromres.2005.03.030 [DOI] [PubMed] [Google Scholar]
- 90.Wattanakit K, Cushman M, Stehman-Breen C, Heckbert SR, Folsom AR. Chronic kidney disease increases risk for venous thromboembolism. J Am Soc Nephrol 2008;19:135–40. 10.1681/ASN.2007030308 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 91.Naylor KL, McArthur E, Leslie WD, et al. The three-year incidence of fracture in chronic kidney disease. Kidney Int 2014;86:810–8. 10.1038/ki.2013.547 [DOI] [PubMed] [Google Scholar]
- 92.Pimentel A, Ureña-Torres P, Zillikens MC, Bover J, Cohen-Solal M. Fractures in patients with CKD-diagnosis, treatment, and prevention: a review by members of the European Calcified Tissue Society and the European Renal Association of Nephrology Dialysis and Transplantation. Kidney Int 2017;92:1343–55. 10.1016/j.kint.2017.07.021 [DOI] [PubMed] [Google Scholar]
- 93.Vilaca T, Salam S, Schini M, et al. Risks of hip and nonvertebral fractures in patients with CKD G3a-G5D: a systematic review and meta-analysis. Am J Kidney Dis 2020;76:521–32. 10.1053/j.ajkd.2020.02.450 [DOI] [PubMed] [Google Scholar]
- 94.Molnar AO, Bota SE, McArthur E, et al. Risk and complications of venous thromboembolism in dialysis patients. Nephrol Dial Transplant 2018;33:874–80. [DOI] [PubMed] [Google Scholar]
- 95.Tveit DP, Hypolite IO, Hshieh P, et al. Chronic dialysis patients have high risk for pulmonary embolism. Am J Kidney Dis 2002;39:1011–7. 10.1053/ajkd.2002.32774 [DOI] [PubMed] [Google Scholar]
- 96.Wang IK, Shen TC, Muo CH, Yen TH, Sung FC. Risk of pulmonary embolism in patients with end-stage renal disease receiving long-term dialysis. Nephrol Dial Transplant 2017;32:1386–93. [DOI] [PubMed] [Google Scholar]
- 97.Alem AM, Sherrard DJ, Gillen DL, et al. Increased risk of hip fracture among patients with end-stage renal disease. Kidney Int 2000;58:396–9. 10.1046/j.1523-1755.2000.00178.x [DOI] [PubMed] [Google Scholar]
- 98.Ball AM, Gillen DL, Sherrard D, et al. Risk of hip fracture among dialysis and renal transplant recipients. JAMA 2002;288:3014–8. 10.1001/jama.288.23.3014 [DOI] [PubMed] [Google Scholar]
- 99.Jadoul M, Albert JM, Akiba T, et al. Incidence and risk factors for hip or other bone fractures among hemodialysis patients in the Dialysis Outcomes and Practice Patterns Study. Kidney Int 2006;70:1358–66. 10.1038/sj.ki.5001754 [DOI] [PubMed] [Google Scholar]
- 100.Bernatsky S, Clarke A, Ramsey-Goldman R, et al. Hormonal exposures and breast cancer in a sample of women with systemic lupus erythematosus. Rheumatology (Oxford) 2004;43:1178–81. 10.1093/rheumatology/keh282 [DOI] [PubMed] [Google Scholar]
- 101.Bernatsky S, Ramsey-Goldman R, Gordon C, et al. Factors associated with abnormal Pap results in systemic lupus erythematosus. Rheumatology (Oxford) 2004;43:1386–9. 10.1093/rheumatology/keh331 [DOI] [PubMed] [Google Scholar]
- 102.Chopra N, Koren S, Greer WL, et al. Factor V Leiden, prothrombin gene mutation, and thrombosis risk in patients with antiphospholipid antibodies. J Rheumatol 2002;29:1683–8. [PubMed] [Google Scholar]
- 103.Esdaile JM, Abrahamowicz M, Grodzicky T, et al. Traditional Framingham risk factors fail to fully account for accelerated atherosclerosis in systemic lupus erythematosus. Arthritis Rheum 2001;44:2331–7. [DOI] [PubMed] [Google Scholar]
- 104.Julkunen HA. Oral contraceptives in systemic lupus erythematosus: side-effects and influence on the activity of SLE. Scand J Rheumatol 1991;20:427–33. 10.3109/03009749109096822 [DOI] [PubMed] [Google Scholar]
- 105.Julkunen HA, Kaaja R, Friman C. Contraceptive practice in women with systemic lupus erythematosus. Br J Rheumatol 1993;32:227–30. 10.1093/rheumatology/32.3.227 [DOI] [PubMed] [Google Scholar]
- 106.Jungers P, Dougados M, Pélissier C, et al. Influence of oral contraceptive therapy on the activity of systemic lupus erythematosus. Arthritis Rheum 1982;25:618–23. 10.1002/art.1780250603 [DOI] [PubMed] [Google Scholar]
- 107.Manzi S, Meilahn EN, Rairie JE, et al. Age-specific incidence rates of myocardial infarction and angina in women with systemic lupus erythematosus: comparison with the Framingham Study. Am J Epidemiol 1997;145:408–15. 10.1093/oxfordjournals.aje.a009122 [DOI] [PubMed] [Google Scholar]
- 108.McAlindon T, Giannotta L, Taub N, D’Cruz D, Hughes G. Environmental factors predicting nephritis in systemic lupus erythematosus. Ann Rheum Dis 1993;52:720–4. 10.1136/ard.52.10.720 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 109.McDonald J, Stewart J, Urowitz MB, Gladman DD. Peripheral vascular disease in patients with systemic lupus erythematosus. Ann Rheum Dis 1992;51:56–60. 10.1136/ard.51.1.56 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 110.Mintz G, Gutiérrez G, Delezé M, Rodríguez E. Contraception with progestagens in systemic lupus erythematosus. Contraception 1984;30:29–38. 10.1016/0010-7824(84)90076-3 [DOI] [PubMed] [Google Scholar]
- 111.Petri M. Musculoskeletal complications of systemic lupus erythematosus in the Hopkins Lupus Cohort: an update. Arthritis Care Res 1995;8:137–45. 10.1002/art.1790080305 [DOI] [PubMed] [Google Scholar]
- 112.Petri M. Lupus in Baltimore: evidence-based ‘clinical pearls’ from the Hopkins Lupus Cohort. Lupus 2005;14:970–3. 10.1191/0961203305lu2230xx [DOI] [PubMed] [Google Scholar]
- 113.Petri M, Kim MY, Kalunian KC, et al. ; OC-SELENA Trial. Combined oral contraceptives in women with systemic lupus erythematosus. N Engl J Med 2005;353:2550–8. 10.1056/NEJMoa051135 [DOI] [PubMed] [Google Scholar]
- 114.Sánchez-Guerrero J, Uribe AG, Jiménez-Santana L, et al. A trial of contraceptive methods in women with systemic lupus erythematosus. N Engl J Med 2005;353:2539–49. 10.1056/NEJMoa050817 [DOI] [PubMed] [Google Scholar]
- 115.Sarabi ZS, Chang E, Bobba R, et al. Incidence rates of arterial and venous thrombosis after diagnosis of systemic lupus erythematosus. Arthritis Rheum 2005;53:609–12. 10.1002/art.21314 [DOI] [PubMed] [Google Scholar]
- 116.Schaedel ZE, Dolan G, Powell MC. The use of the levonorgestrel-releasing intrauterine system in the management of menorrhagia in women with hemostatic disorders. Am J Obstet Gynecol 2005;193:1361–3. 10.1016/j.ajog.2005.05.002 [DOI] [PubMed] [Google Scholar]
- 117.Somers E, Magder LS, Petri M. Antiphospholipid antibodies and incidence of venous thrombosis in a cohort of patients with systemic lupus erythematosus. J Rheumatol 2002;29:2531–6. [PubMed] [Google Scholar]
- 118.Urowitz MB, Bookman AA, Koehler BE, Gordon DA, Smythe HA, Ogryzlo MA. The bimodal mortality pattern of systemic lupus erythematosus. Am J Med 1976;60:221–5. 10.1016/0002-9343(76)90431-9 [DOI] [PubMed] [Google Scholar]
- 119.Culwell KR, Curtis KM, Del Carmen Cravioto M. Safety of contraceptive method use among women with systemic lupus erythematosus: a systematic review. Obstet Gynecol 2009;114:341–53. 10.1097/AOG.0b013e3181ae9c64 [DOI] [PubMed] [Google Scholar]
- 120.Choojitarom K, Verasertniyom O, Totemchokchyakarn K, Nantiruj K, Sumethkul V, Janwityanujit S. Lupus nephritis and Raynaud’s phenomenon are significant risk factors for vascular thrombosis in SLE patients with positive antiphospholipid antibodies. Clin Rheumatol 2008;27:345–51. 10.1007/s10067-007-0721-z [DOI] [PubMed] [Google Scholar]
- 121.Wahl DG, Guillemin F, de Maistre E, Perret C, Lecompte T, Thibaut G. Risk for venous thrombosis related to antiphospholipid antibodies in systemic lupus erythematosus—a meta-analysis. Lupus 1997;6:467–73. 10.1177/096120339700600510 [DOI] [PubMed] [Google Scholar]
- 122.Farr SL, Folger SG, Paulen ME, Curtis KM. Safety of contraceptive methods for women with rheumatoid arthritis: a systematic review. Contraception 2010;82:64–71. 10.1016/j.contraception.2010.02.003 [DOI] [PubMed] [Google Scholar]
- 123.Tepper NK, Whiteman MK, Zapata LB, Marchbanks PA, Curtis KM. Safety of hormonal contraceptives among women with migraine: a systematic review. Contraception 2016;94:630–40. 10.1016/j.contraception.2016.04.016 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 124.Tepper NK, Whiteman MK, Marchbanks PA, James AH, Curtis KM. Progestin-only contraception and thromboembolism: a systematic review. Contraception 2016;94:678–700. 10.1016/j.contraception.2016.04.014 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 125.Headache Classification Committee of the International Headache Society (IHS) The International Classification of Headache Disorders. 3rd edition. Cephalalgia 2018;38:1–211. https://www.ichd-3.org/wp-content/uploads/2018/01/The-International-Classification-of-Headache-Disorders-3rd-Edition-2018.pdf [DOI] [PubMed] [Google Scholar]
- 126.Zapata LB, Oduyebo T, Whiteman MK, Houtchens MK, Marchbanks PA, Curtis KM. Contraceptive use among women with multiple sclerosis: a systematic review. Contraception 2016;94:612–20. 10.1016/j.contraception.2016.07.013 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 127.Pagano HP, Zapata LB, Berry-Bibee EN, Nanda K, Curtis KM. Safety of hormonal contraception and intrauterine devices among women with depressive and bipolar disorders: a systematic review. Contraception 2016;94:641–9. 10.1016/j.contraception.2016.06.012 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 128.Smith JS, Green J, Berrington de Gonzalez A, et al. Cervical cancer and use of hormonal contraceptives: a systematic review. Lancet 2003;361:1159–67. 10.1016/S0140-6736(03)12949-2 [DOI] [PubMed] [Google Scholar]
- 129.Ahmed K, Baeten JM, Beksinska M, et al. ; Evidence for Contraceptive Options and HIV Outcomes (ECHO) Trial Consortium. HIV incidence among women using intramuscular depot medroxyprogesterone acetate, a copper intrauterine device, or a levonorgestrel implant for contraception: a randomized, multicentre, open-label trial. Lancet 2019;394:303–13. 10.1016/S0140-6736(19)31288-7 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 130.Curtis KM, Hannaford PC, Rodriguez MI, Chipato T, Steyn PS, Kiarie JN. Hormonal contraception and HIV acquisition among women: an updated systematic review. BMJ Sex Reprod Health 2020;46:8–16. 10.1136/bmjsrh-2019-200509 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 131.Tepper NK, Curtis KM, Cox S, Whiteman MK. Update to U.S. medical eligibility criteria for contraceptive use, 2016: updated recommendations for the use of contraception among women at high risk for HIV infection. MMWR Morb Mortal Wkly Rep 2020;69:405–10. 10.15585/mmwr.mm6914a3 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 132.Phillips SJ, Curtis KM, Polis CB. Effect of hormonal contraceptive methods on HIV disease progression: a systematic review. AIDS 2013;27:787–94. 10.1097/QAD.0b013e32835bb672 [DOI] [PubMed] [Google Scholar]
- 133.Polis CB, Phillips SJ, Curtis KM. Hormonal contraceptive use and female-to-male HIV transmission: a systematic review of the epidemiologic evidence. AIDS 2013;27:493–505. 10.1097/QAD.0b013e32835ad539 [DOI] [PubMed] [Google Scholar]
- 134.Phillips SJ, Polis CB, Curtis KM. The safety of hormonal contraceptives for women living with HIV and their sexual partners. Contraception 2016;93:11–6. 10.1016/j.contraception.2015.10.002 [DOI] [PubMed] [Google Scholar]
- 135.Tagy AH, Saker ME, Moussa AA, Kolgah A. The effect of low-dose combined oral contraceptive pills versus injectable contraceptive (Depot Provera) on liver function tests of women with compensated bilharzial liver fibrosis. Contraception 2001;64:173–6. 10.1016/S0010-7824(01)00248-7 [DOI] [PubMed] [Google Scholar]
- 136.Pyörälä T, Vähäpassi J, Huhtala M. The effect of lynestrenol and norethindrone on the carbohydrate and lipid metabolism in subjects with gestational diabetes. Ann Chir Gynaecol 1979;68:69–74. [PubMed] [Google Scholar]
- 137.Rådberg T, Gustafson A, Skryten A, Karlsson K. Metabolic studies in gestational diabetic women during contraceptive treatment: effects on glucose tolerance and fatty acid composition of serum lipids. Gynecol Obstet Invest 1982;13:17–29. 10.1159/000299480 [DOI] [PubMed] [Google Scholar]
- 138.Kjos SL, Peters RK, Xiang A, Thomas D, Schaefer U, Buchanan TA. Contraception and the risk of type 2 diabetes mellitus in Latina women with prior gestational diabetes mellitus. JAMA 1998;280:533–8. 10.1001/jama.280.6.533 [DOI] [PubMed] [Google Scholar]
- 139.Nelson AL, Le MH, Musherraf Z, Vanberckelaer A. Intermediate-term glucose tolerance in women with a history of gestational diabetes: natural history and potential associations with breastfeeding and contraception. Am J Obstet Gynecol 2008;198:699.e1–8. 10.1016/j.ajog.2008.03.029 [DOI] [PubMed] [Google Scholar]
- 140.Xiang AH, Kawakubo M, Buchanan TA, Kjos SL. A longitudinal study of lipids and blood pressure in relation to method of contraception in Latino women with prior gestational diabetes mellitus. Diabetes Care 2007;30:1952–8. 10.2337/dc07-0180 [DOI] [PubMed] [Google Scholar]
- 141.Xiang AH, Kawakubo M, Kjos SL, Buchanan TA. Long-acting injectable progestin contraception and risk of type 2 diabetes in Latino women with prior gestational diabetes mellitus. Diabetes Care 2006;29:613–7. 10.2337/diacare.29.03.06.dc05-1940 [DOI] [PubMed] [Google Scholar]
- 142.Diab KM, Zaki MM. Contraception in diabetic women: comparative metabolic study of Norplant, depot medroxyprogesterone acetate, low dose oral contraceptive pill and CuT380A. J Obstet Gynaecol Res 2000;26:17–26. 10.1111/j.1447-0756.2000.tb01195.x [DOI] [PubMed] [Google Scholar]
- 143.Lunt H, Brown LJ. Self-reported changes in capillary glucose and insulin requirements during the menstrual cycle. Diabet Med 1996;13:525–30. [DOI] [PubMed] [Google Scholar]
- 144.Rådberg T, Gustafson A, Skryten A, Karlsson K. Oral contraception in diabetic women. A cross-over study on serum and high density lipoprotein (HDL) lipids and diabetes control during progestogen and combined estrogen/progestogen contraception. Horm Metab Res 1982;14:61–5. [PubMed] [Google Scholar]
- 145.Skouby SO, Mølsted-Pedersen L, Kühl C, Bennet P. Oral contraceptives in diabetic women: metabolic effects of four compounds with different estrogen/progestogen profiles. Fertil Steril 1986;46:858–64. 10.1016/S0015-0282(16)49825-0 [DOI] [PubMed] [Google Scholar]
- 146.Zapata LB, Paulen ME, Cansino C, Marchbanks PA, Curtis KM. Contraceptive use among women with inflammatory bowel disease: a systematic review. Contraception 2010;82:72–85. 10.1016/j.contraception.2010.02.012 [DOI] [PubMed] [Google Scholar]
- 147.Whiteman MK, Oduyebo T, Zapata LB, Walker S, Curtis KM. Contraceptive safety among women with cystic fibrosis: a systematic review. Contraception 2016;94:621–9. 10.1016/j.contraception.2016.05.016 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 148.Brunson A, Keegan T, Mahajan A, White R, Wun T. High incidence of venous thromboembolism recurrence in patients with sickle cell disease. Am J Hematol 2019;94:862–70. 10.1002/ajh.25508 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 149.Naik RP, Streiff MB, Haywood C Jr, Segal JB, Lanzkron S. Venous thromboembolism incidence in the Cooperative Study of Sickle Cell Disease. J Thromb Haemost 2014;12:2010–6. 10.1111/jth.12744 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 150.Noubiap JJ, Temgoua MN, Tankeu R, Tochie JN, Wonkam A, Bigna JJ. Sickle cell disease, sickle trait and the risk for venous thromboembolism: a systematic review and meta-analysis. Thromb J 2018;16:27. 10.1186/s12959-018-0179-z [DOI] [PMC free article] [PubMed] [Google Scholar]
- 151.Ohene-Frempong K, Weiner SJ, Sleeper LA, et al. Cerebrovascular accidents in sickle cell disease: rates and risk factors. Blood 1998;91:288–94. [PubMed] [Google Scholar]
- 152.Anastasilakis AD, Tsourdi E, Makras P, et al. Bone disease following solid organ transplantation: a narrative review and recommendations for management from The European Calcified Tissue Society. Bone 2019;127:401–18. 10.1016/j.bone.2019.07.006 [DOI] [PubMed] [Google Scholar]
- 153.Panel on Treatment of HIV During Pregnancy and Prevention of Perinatal Transmission. Recommendations for the use of antiretroviral drugs during pregnancy and interventions to reduce perinatal HIV transmission in the United States. Washington, DC: US Department of Health and Human Services; 2023. https://clinicalinfo.hiv.gov/en/guidelines/perinatal/recommendations-arv-drugs-pregnancy-overviewhttp:// [Google Scholar]
- 154.Panel on Antiretroviral Guidelines for Adults and Adolescents. Guidelines for the use of antiretroviral agents in adults and adolescents with HIV. Washington, DC: US Department of Health and Human Services; 2023. https://clinicalinfo.hiv.gov/sites/default/files/guidelines/documents/adult-adolescent-arv/guidelines-adult-adolescent-arv.pdf [Google Scholar]
- 155.Aweeka FT, Rosenkranz SL, Segal Y, et al. ; NIAID AIDS Clinical Trials Group. The impact of sex and contraceptive therapy on the plasma and intracellular pharmacokinetics of zidovudine. AIDS 2006;20:1833–41. 10.1097/01.aids.0000244202.18629.36 [DOI] [PubMed] [Google Scholar]
- 156.Kearney BP, Mathias A. Lack of effect of tenofovir disoproxil fumarate on pharmacokinetics of hormonal contraceptives. Pharmacotherapy 2009;29:924–9. 10.1592/phco.29.8.924 [DOI] [PubMed] [Google Scholar]
- 157.Todd CS, Deese J, Wang M, et al. ; FEM-PrEP Study Group. Sino-implant (II) continuation and effect of concomitant tenofovir disoproxil fumarate-emtricitabine use on plasma levonorgestrel concentrations among women in Bondo, Kenya. Contraception 2015;91:248–52. 10.1016/j.contraception.2014.10.008 [DOI] [PubMed] [Google Scholar]
- 158.Murnane PM, Heffron R, Ronald A, et al. ; Partners PrEP Study Team. Pre-exposure prophylaxis for HIV-1 prevention does not diminish the pregnancy prevention effectiveness of hormonal contraception. AIDS 2014;28:1825–30. 10.1097/QAD.0000000000000290 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 159.Kasonde M, Niska RW, Rose C, et al. Bone mineral density changes among HIV-uninfected young adults in a randomised trial of pre-exposure prophylaxis with tenofovir-emtricitabine or placebo in Botswana. PLoS One 2014;9:e90111. 10.1371/journal.pone.0090111 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 160.Callahan R, Nanda K, Kapiga S, et al. ; FEM-PrEP Study Group. Pregnancy and contraceptive use among women participating in the FEM-PrEP trial. J Acquir Immune Defic Syndr 2015;68:196–203. 10.1097/QAI.0000000000000413 [DOI] [PubMed] [Google Scholar]
- 161.Vieira CS, Bahamondes MV, de Souza RM, et al. Effect of antiretroviral therapy including lopinavir/ritonavir or efavirenz on etonogestrel-releasing implant pharmacokinetics in HIV-positive women. J Acquir Immune Defic Syndr 2014;66:378–85. 10.1097/QAI.0000000000000189 [DOI] [PubMed] [Google Scholar]
- 162.Patel RC, Onono M, Gandhi M, et al. Pregnancy rates in HIV-positive women using contraceptives and efavirenz-based or nevirapine-based antiretroviral therapy in Kenya: a retrospective cohort study. Lancet HIV 2015;2:e474–82. 10.1016/S2352-3018(15)00184-8 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 163.Perry SH, Swamy P, Preidis GA, Mwanyumba A, Motsa N, Sarero HN. Implementing the Jadelle implant for women living with HIV in a resource-limited setting: concerns for drug interactions leading to unintended pregnancies. AIDS 2014;28:791–3. 10.1097/QAD.0000000000000177 [DOI] [PubMed] [Google Scholar]
- 164.Scarsi KK, Darin KM, Nakalema S, et al. Unintended pregnancies observed with combined use of the levonorgestrel contraceptive implant and efavirenz-based antiretroviral therapy: a three-arm pharmacokinetic evaluation over 48 weeks. Clin Infect Dis 2016;62:675–82. 10.1093/cid/civ1001 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 165.Pyra M, Heffron R, Mugo NR, et al. ; Partners in Prevention HSVHIV Transmission Study and Partners PrEP Study Teams. Effectiveness of hormonal contraception in HIV-infected women using antiretroviral therapy. AIDS 2015;29:2353–9. 10.1097/QAD.0000000000000827 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 166.Cohn SE, Park JG, Watts DH, et al. ; ACTG A5093 Protocol Team. Depo-medroxyprogesterone in women on antiretroviral therapy: effective contraception and lack of clinically significant interactions. Clin Pharmacol Ther 2007;81:222–7. 10.1038/sj.clpt.6100040 [DOI] [PubMed] [Google Scholar]
- 167.Nanda K, Amaral E, Hays M, Viscola MA, Mehta N, Bahamondes L. Pharmacokinetic interactions between depot medroxyprogesterone acetate and combination antiretroviral therapy. Fertil Steril 2008;90:965–71. 10.1016/j.fertnstert.2007.07.1348 [DOI] [PubMed] [Google Scholar]
- 168.Watts DH, Park JG, Cohn SE, et al. Safety and tolerability of depot medroxyprogesterone acetate among HIV-infected women on antiretroviral therapy: ACTG A5093. Contraception 2008;77:84–90. 10.1016/j.contraception.2007.10.002 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 169.Polis CB, Nakigozi G, Ssempijja V, et al. Effect of injectable contraceptive use on response to antiretroviral therapy among women in Rakai, Uganda. Contraception 2012;86:725–30. 10.1016/j.contraception.2012.05.001 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 170.Hubacher D, Liku J, Kiarie J, et al. Effect of concurrent use of anti-retroviral therapy and levonorgestrel sub-dermal implant for contraception on CD4 counts: a prospective cohort study in Kenya. J Int AIDS Soc 2013;16:18448. 10.7448/IAS.16.1.18448 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 171.Myer L, Carter RJ, Katyal M, Toro P, El-Sadr WM, Abrams EJ. Impact of antiretroviral therapy on incidence of pregnancy among HIV-infected women in Sub-Saharan Africa: a cohort study. PLoS Med 2010;7:e1000229. 10.1371/journal.pmed.1000229 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 172.Day S, Graham SM, Masese LN, et al. A prospective cohort study of the effect of depot medroxyprogesterone acetate on detection of plasma and cervical HIV-1 in women initiating and continuing antiretroviral therapy. J Acquir Immune Defic Syndr 2014;66:452–6. 10.1097/QAI.0000000000000187 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 173.DuBois BN, Atrio J, Stanczyk FZ, Cherala G. Increased exposure of norethindrone in HIV+ women treated with ritonavir-boosted atazanavir therapy. Contraception 2015;91:71–5. 10.1016/j.contraception.2014.08.009 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 174.Luque AE, Cohn SE, Park JG, et al. Depot medroxyprogesterone acetate in combination with a twice-daily lopinavir-ritonavir-based regimen in HIV-infected women showed effective contraception and a lack of clinically significant interactions, with good safety and tolerability: results of the ACTG 5283 study. Antimicrob Agents Chemother 2015;59:2094–101. 10.1128/AAC.04701-14 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 175.Odlind V, Olsson SE. Enhanced metabolism of levonorgestrel during phenytoin treatment in a woman with Norplant implants. Contraception 1986;33:257–61. 10.1016/0010-7824(86)90018-1 [DOI] [PubMed] [Google Scholar]
- 176.Schindlbeck C, Janni W, Friese K. Failure of Implanon contraception in a patient taking carbamazepin for epilepsia. Arch Gynecol Obstet 2006;273:255–6. 10.1007/s00404-005-0064-4 [DOI] [PubMed] [Google Scholar]
- 177.Shane-McWhorter L, Cerveny JD, MacFarlane LL, Osborn C. Enhanced metabolism of levonorgestrel during phenobarbital treatment and resultant pregnancy. Pharmacotherapy 1998;18:1360–4. 10.1002/j.1875-9114.1998.tb03161.x [DOI] [PubMed] [Google Scholar]
- 178.Gaffield ME, Culwell KR, Lee CR. The use of hormonal contraception among women taking anticonvulsant therapy. Contraception 2011;83:16–29. 10.1016/j.contraception.2010.06.013 [DOI] [PubMed] [Google Scholar]
- 179.Reimers A, Helde G, Brodtkorb E. Ethinyl estradiol, not progestogens, reduces lamotrigine serum concentrations. Epilepsia 2005;46:1414–7. 10.1111/j.1528-1167.2005.10105.x [DOI] [PubMed] [Google Scholar]
- 180.Berry-Bibee ENKM, Kim MJ, Simmons KB, et al. Drug interactions between hormonal contraceptives and psychotropic drugs: a systematic review. Contraception 2016;94:650–67. 10.1016/j.contraception.2016.07.011 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 181.Berry-Bibee ENKM, Kim MJ, Tepper NK, Riley HE, Curtis KM. Co-administration of St. John’s wort and hormonal contraceptives: a systematic review. Contraception 2016;94:668–77. 10.1016/j.contraception.2016.07.010 [DOI] [PMC free article] [PubMed] [Google Scholar]
Appendix D. Classifications for Combined Hormonal Contraceptives
Combined hormonal contraceptives (CHCs) include combined oral contraceptives (COCs) (containing a progestin plus ethinyl estradiol [EE] ≤35 μg, estradiol valerate, or estetrol); combined transdermal patches (levonorgestrel/EE or norelgestromin/EE); and combined vaginal rings (etonogestrel/EE or segesterone acetate/EE) (Box D1) (Table D1). Limited information is available about the safety of COCs with estradiol valerate or estetrol, combined transdermal patches, and combined vaginal rings among users with specific medical conditions. Evidence indicates that estradiol valerate and estetrol COCs, combined transdermal patches, and combined vaginal rings provide comparable safety and pharmacokinetic profiles to EE-containing COCs with similar hormone formulations (1–33). Pending further studies, the evidence available for recommendations about EE-containing COCs applies to the recommendations for estradiol valerate and estetrol COCs, the combined transdermal patch, and vaginal rings. Therefore, the estradiol valerate and estetrol COCs, the patches, and the rings should have the same categories as EE-containing COCs, except where noted. The assigned categories should be considered a preliminary best judgment, which will be reevaluated as new data become available.
BOX D1. Categories for classifying combined hormonal contraceptives.
U.S. MEC 1 = A condition for which there is no restriction for the use of the contraceptive method
U.S. MEC 2 = A condition for which the advantages of using the method generally outweigh the theoretical or proven risks
U.S. MEC 3 = A condition for which the theoretical or proven risks usually outweigh the advantages of using the method
U.S. MEC 4 = A condition that represents an unacceptable health risk if the contraceptive method is used
Abbreviation: U.S. MEC = U.S. Medical Eligibility Criteria for Contraceptive Use.
COCs, patches, and rings do not protect against sexually transmitted infections (STIs), including HIV infection, and patients using CHCs should be counseled that consistent and correct use of external (male) latex condoms reduces the risk for STIs, including HIV infection (34). Use of internal (female) condoms can provide protection from transmission of STIs, although data are limited (34). Patients also should be counseled that pre-exposure prophylaxis, when taken as prescribed, is highly effective for preventing HIV infection (35).
TABLE D1. Classifications for combined hormonal contraceptives, including pill, patch, and ring.
Condition | CHC |
Clarification/Evidence/Comment | |
---|---|---|---|
Personal
Characteristics and Reproductive History
| |||
Pregnancy
|
NA |
Clarification: Use of
CHCs is not required. No known harm to the patient, the course
of pregnancy, or the fetus occurs if CHCs are inadvertently used
during pregnancy. |
|
Age
|
Evidence:
Evidence is inconsistent about whether CHC use affects fracture
risk (36–47),
although three recent studies demonstrate no effect (36,37,47). CHC
use might decrease BMD in adolescents, especially in those
choosing very low-dose formulations (COCs containing <30
µg ethinyl estradiol) (48–61). CHC
use has little to no effect on BMD in premenopausal women (62–76) and
might preserve bone mass in those who are perimenopausal (77–85). BMD
is a surrogate marker for fracture risk that might not be valid
for premenopausal women and therefore might not accurately
predict current or future (postmenopausal) fracture risk (86–88). Comment: The risk for cardiovascular disease increases with age and might increase with CHC use. In the absence of other adverse clinical conditions, CHCs can be used until menopause. |
||
a. Menarche to <40
years |
1 |
||
b. ≥40
years |
2 |
||
Parity
| |||
a. Nulliparous |
1 |
— |
|
b. Parous |
1 |
— |
|
Breastfeeding
| |||
a. <21 days
postpartum |
4 |
Clarification
(breastfeeding): Breastfeeding provides important
health benefits for breastfeeding parent and infant. The U.S.
Dietary Guidelines for Americans and American Academy of
Pediatrics recommend that infants be exclusively breastfed for
about the first 6 months with continued breastfeeding while
introducing appropriate complementary foods for 1 year or longer
(89) or up to age 2 years or longer
(90). Evidence (breastfeeding): Clinical studies demonstrate conflicting results regarding effects on breastfeeding continuation or exclusivity in women exposed to COCs during lactation. No consistent effects on infant growth or illness have been reported. Adverse health outcomes or manifestations of exogenous estrogen in infants exposed to CHCs through breast milk have not been demonstrated; however, studies have been inadequately designed to determine whether a risk for either serious or subtle long-term effects exists (91). Evidence: One study examined use of CHCs during the postpartum period and found that VTE rates were higher for CHC users compared with nonusers at all time points postpartum (92). Rates were significantly different only after 13 weeks postpartum; however, the numbers needed to harm were lowest in the first 6 weeks postpartum. VTE risk is increased during pregnancy and the postpartum period; this risk is most pronounced in the first 3 weeks after delivery, decreasing to near baseline levels by 42 days postpartum (93–97). Comment: Risk factors for breastfeeding difficulties include previous breastfeeding difficulties, certain medical conditions, certain perinatal complications, and preterm birth. For all breastfeeding persons, with or without risk factors for breastfeeding difficulties, discussions about contraception should include information about risks, benefits, and alternatives. |
|
b. 21 to
<30 days postpartum | |||
i.
With other risk factors for VTE (e.g., age ≥35 years,
previous VTE, thrombophilia, immobility, transfusion at
delivery, peripartum cardiomyopathy, BMI ≥30
kg/m2, postpartum hemorrhage, postcesarean
delivery, preeclampsia, or smoking) |
3 |
Clarification: For
persons with other risk factors for VTE, these risk factors
might increase the classification to a category
4. Clarification (breastfeeding): Breastfeeding provides important health benefits for breastfeeding parent and infant. The U.S. Dietary Guidelines for Americans and American Academy of Pediatrics recommend that infants be exclusively breastfed for about the first 6 months with continued breastfeeding while introducing appropriate complementary foods for 1 year or longer (89) or up to age 2 years or longer (90). Evidence (breastfeeding): Clinical studies demonstrate conflicting results regarding effects on breastfeeding continuation or exclusivity in women exposed to COCs during lactation. No consistent effects on infant growth or illness have been reported. Adverse health outcomes or manifestations of exogenous estrogen in infants exposed to CHCs through breast milk have not been demonstrated; however, studies have been inadequately designed to determine whether a risk for either serious or subtle long-term effects exists (91). Evidence: One study examined use of CHCs during the postpartum period and found that VTE rates were higher for CHC users compared with nonusers at all time points postpartum (92). Rates were significantly different only after 13 weeks postpartum; however, the numbers needed to harm were lowest in the first 6 weeks postpartum. VTE risk is increased during pregnancy and the postpartum period; this risk is most pronounced in the first 3 weeks after delivery, decreasing to near baseline levels by 42 days postpartum (93–97). Comment: Risk factors for breastfeeding difficulties include previous breastfeeding difficulties, certain medical conditions, certain perinatal complications, and preterm birth. For all breastfeeding persons, with or without risk factors for breastfeeding difficulties, discussions about contraception should include information about risks, benefits, and alternatives. |
|
ii. Without other risk factors for
VTE |
3 |
Clarification
(breastfeeding): Breastfeeding provides important
health benefits for breastfeeding parent and infant. The U.S.
Dietary Guidelines for Americans and American Academy of
Pediatrics recommend that infants be exclusively breastfed for
about the first 6 months with continued breastfeeding while
introducing appropriate complementary foods for 1 year or longer
(89) or up to age 2 years or longer
(90). Evidence (breastfeeding): Clinical studies demonstrate conflicting results regarding effects on breastfeeding continuation or exclusivity in women exposed to COCs during lactation. No consistent effects on infant growth or illness have been reported. Adverse health outcomes or manifestations of exogenous estrogen in infants exposed to CHCs through breast milk have not been demonstrated; however, studies have been inadequately designed to determine whether a risk for either serious or subtle long-term effects exists (91). Evidence: One study examined use of CHCs during the postpartum period and found that VTE rates were higher for CHC users compared with nonusers at all time points postpartum (92). Rates were significantly different only after 13 weeks postpartum; however, the numbers needed to harm were lowest in the first 6 weeks postpartum. VTE risk is increased during pregnancy and the postpartum period; this risk is most pronounced in the first 3 weeks after delivery, decreasing to near baseline levels by 42 days postpartum (93–97). Comment: Risk factors for breastfeeding difficulties include previous breastfeeding difficulties, certain medical conditions, certain perinatal complications, and preterm birth. For all breastfeeding persons, with or without breastfeeding difficulties, discussions about contraception should include information about risks, benefits, and alternatives. |
|
c.
30–42 days postpartum | |||
i.
With other risk factors for VTE (e.g., age ≥35 years,
previous VTE, thrombophilia, immobility, transfusion at
delivery, peripartum cardiomyopathy, BMI ≥30
kg/m2, postpartum hemorrhage, postcesarean
delivery, preeclampsia, or smoking) |
3 |
Clarification: For
persons with other risk factors for VTE, these risk factors
might increase the classification to a category
4. Clarification (breastfeeding): Breastfeeding provides important health benefits for breastfeeding parent and infant. The U.S. Dietary Guidelines for Americans and American Academy of Pediatrics recommend that infants be exclusively breastfed for about the first 6 months with continued breastfeeding while introducing appropriate complementary foods for 1 year or longer (89) or up to age 2 years or longer (90). Evidence (breastfeeding): Clinical studies demonstrate conflicting results regarding effects on breastfeeding continuation or exclusivity in women exposed to COCs during lactation. No consistent effects on infant growth or illness have been reported. Adverse health outcomes or manifestations of exogenous estrogen in infants exposed to CHCs through breast milk have not been demonstrated; however, studies have been inadequately designed to determine whether a risk for either serious or subtle long-term effects exists (91). Evidence: One study examined use of CHCs during the postpartum period and found that VTE rates were higher for CHC users compared with nonusers at all time points postpartum (92). Rates were significantly different only after 13 weeks postpartum; however, the numbers needed to harm were lowest in the first 6 weeks postpartum. VTE risk is increased during pregnancy and the postpartum period; this risk is most pronounced in the first 3 weeks after delivery, decreasing to near baseline levels by 42 days postpartum (93–97). Comment: Risk factors for breastfeeding difficulties include previous breastfeeding difficulties, certain medical conditions, certain perinatal complications, and preterm birth. For all breastfeeding persons, with or without breastfeeding difficulties, discussions about contraception should include information about risks, benefits, and alternatives. |
|
ii. Without other risk factors for
VTE |
2 |
Clarification
(breastfeeding): Breastfeeding provides important
health benefits for breastfeeding parent and infant. The U.S.
Dietary Guidelines for Americans and American Academy of
Pediatrics recommend that infants be exclusively breastfed for
about the first 6 months with continued breastfeeding while
introducing appropriate complementary foods for 1 year or longer
(89) or up to age 2 years or longer
(90). Evidence (breastfeeding): Clinical studies demonstrate conflicting results regarding effects on breastfeeding continuation or exclusivity in women exposed to COCs during lactation. No consistent effects on infant growth or illness have been reported. Adverse health outcomes or manifestations of exogenous estrogen in infants exposed to CHCs through breast milk have not been demonstrated; however, studies have been inadequately designed to determine whether a risk for either serious or subtle long-term effects exists (91). Evidence: One study examined use of CHCs during the postpartum period and found that VTE rates were higher for CHC users compared with nonusers at all time points postpartum (92). Rates were significantly different only after 13 weeks postpartum; however, the numbers needed to harm were lowest in the first 6 weeks postpartum. VTE risk is increased during pregnancy and the postpartum period; this risk is most pronounced in the first 3 weeks after delivery, decreasing to near baseline levels by 42 days postpartum (93–97). Comment: Risk factors for breastfeeding difficulties include previous breastfeeding difficulties, certain medical conditions, certain perinatal complications, and preterm birth. For all breastfeeding persons, with or without breastfeeding difficulties, discussions about contraception should include information about risks, benefits, and alternatives. |
|
d. >42 days
postpartum |
2 |
Clarification
(breastfeeding): Breastfeeding provides important
health benefits for breastfeeding parent and infant. The U.S.
Dietary Guidelines for Americans and American Academy of
Pediatrics recommend that infants be exclusively breastfed for
about the first 6 months with continued breastfeeding while
introducing appropriate complementary foods for 1 year or longer
(89) or up to age 2 years or longer
(90). Evidence: Clinical studies demonstrate conflicting results regarding effects on breastfeeding continuation or exclusivity in women exposed to COCs during lactation. No consistent effects on infant growth or illness have been reported. Adverse health outcomes or manifestations of exogenous estrogen in infants exposed to CHCs through breast milk have not been demonstrated; however, studies have been inadequately designed to determine whether a risk for either serious or subtle long-term effects exists (91). Comment: Risk factors for breastfeeding difficulties include previous breastfeeding difficulties, certain medical conditions, certain perinatal complications, and preterm birth. For all breastfeeding persons, with or without breastfeeding difficulties, discussions about contraception should include information about risks, benefits, and alternatives. |
|
Postpartum (nonbreastfeeding) | |||
a. <21 days
postpartum |
4 |
Evidence: One study
examined use of CHCs during the postpartum period and found that
VTE rates were higher for CHC users compared with nonusers at
all time points postpartum (92). Rates were significantly
different only after 13 weeks postpartum; however, the numbers
needed to harm were lowest in the first 6 weeks postpartum. VTE
risk is increased during pregnancy and the postpartum period;
this risk is most pronounced in the first 3 weeks after
delivery, decreasing to near baseline levels by 42 days
postpartum (93–97). Risk
for pregnancy during the first 21 days postpartum is very low
but increases after that point; ovulation before first menses is
common (98). |
|
b.
21–42 days postpartum | |||
i.
With other risk factors for VTE (e.g., age ≥35 years,
previous VTE, thrombophilia, immobility, transfusion at
delivery, peripartum cardiomyopathy, BMI ≥30
kg/m2 postpartum hemorrhage, postcesarean
delivery, preeclampsia, or smoking) |
3 |
Clarification: For
persons with other risk factors for VTE, these risk factors
might increase the classification to a category
4. Evidence: One study examined use of CHCs during the postpartum period and found that VTE rates were higher for CHC users compared with nonusers at all time points postpartum (92). Rates were significantly different only after 13 weeks postpartum; however, the numbers needed to harm were lowest in the first 6 weeks postpartum. VTE risk is increased during pregnancy and the postpartum period; this risk is most pronounced in the first 3 weeks after delivery, decreasing to near baseline levels by 42 days postpartum (93–97). |
|
ii. Without other risk factors for
VTE |
2 |
Evidence: One study
examined use of CHCs during the postpartum period and found that
VTE rates were higher for CHC users compared with nonusers at
all time points postpartum (92). Rates were significantly
different only after 13 weeks postpartum; however, the numbers
needed to harm were lowest in the first 6 weeks postpartum. VTE
risk is increased during pregnancy and the postpartum period;
this risk is most pronounced in the first 3 weeks after
delivery, decreasing to near baseline levels by 42 days
postpartum (93–97). |
|
c. >42 days
postpartum |
1 |
— |
|
Postabortion (spontaneous or
induced) | |||
a. First
trimester abortion |
Clarification: CHCs may be started immediately
after abortion completion or at time of medication abortion
initiation. Evidence: Evidence suggests that there is no increased risk for adverse events when CHCs are initiated after first trimester procedural or medication abortion (immediately or delayed) (99). Immediate initiation of COCs after first trimester procedural or medication abortion did not cause clinically significant changes in coagulation parameters compared with placebo, a hormonal IUD, a nonhormonal contraceptive method, or delayed COC initiation (100). |
||
i.
Procedural (surgical) |
1 |
||
ii. Medication |
1 |
||
iii. Spontaneous abortion with no
intervention |
1 |
||
b. Second
trimester abortion |
Clarification: CHCs may be started immediately
after abortion completion or at time of medication abortion
initiation. Evidence: Limited evidence suggests that there is no increased risk for adverse events when CHCs are initiated after second trimester procedural abortion (immediately or delayed) (99). |
||
i.
Procedural (surgical) |
1 |
||
ii. Medication |
1 |
||
iii. Spontaneous abortion with no
intervention |
1 |
||
c. Immediate postseptic
abortion |
1 |
Clarification: CHCs may
be started immediately after abortion completion or at time of
medication abortion initiation. |
|
Past ectopic
pregnancy
|
1 |
Comment: The risk for
future ectopic pregnancy is increased among those who have had
an ectopic pregnancy in the past. CHCs protect against pregnancy
in general, including ectopic gestation. |
|
History of pelvic
surgery
|
1 |
— |
|
Smoking
|
|
Evidence: COC
users who smoked were at increased risk for cardiovascular
diseases, especially myocardial infarction, compared with those
who did not smoke. Studies also demonstrated an increased risk
for myocardial infarction with increasing number of cigarettes
smoked per day (101–113). |
|
a. Age <35
years |
2 |
||
b. Age ≥35
years |
|
||
i. <15 cigarettes per
day |
3 |
||
ii. ≥15 cigarettes
per day |
4 |
||
Obesity
|
|
Clarification: Risk for thrombosis increases
with multiple risk factors, such as obesity, older age (e.g.,
≥40 years), diabetes, smoking, family history of
thrombosis, and dyslipidemia. When a person has multiple risk
factors, any of which alone would increase risk for thrombosis,
use of CHCs might increase thrombosis risk to an unacceptable
level. However, a simple addition of categories for multiple
risk factors is not intended; for example, a combination of two
category 2 risk factors might not necessarily warrant a higher
category. Evidence: Although the absolute risk for VTE in healthy women of reproductive age is small, COC use and higher BMI independently increase risk for VTE, with the greatest relative risks among those with both risk factors. From a systematic review, COC users with obesity consistently had a relative risk for VTE of 5–8 times that of nonusers with obesity (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). Research examining the interaction between COCs and BMI on VTE risk is limited, particularly for those in the highest BMI categories (BMI ≥35 kg/m2). Comparative studies on the risk for VTE among contraceptive patch or ring users by weight or BMI were not identified (114–116). Limited evidence suggests that COC users with obesity do not have a higher risk for acute myocardial infarction or stroke than do nonusers with obesity (114) (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). Limited evidence suggests that effectiveness of certain COC formulations might decrease with increasing BMI; however the observed reductions in effectiveness are minimal and evidence is conflicting (117–124). Effectiveness of the patch might be reduced in women with BMI ≥30 kg/m2 or weight >90 kg (125). |
|
a. BMI ≥30
kg/m2 |
2 |
||
b. Menarche to <18
years and BMI ≥30 kg/m2 |
2 |
||
History
of bariatric surgery This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | |||
a. Restrictive procedures:
decrease storage capacity of the stomach (vertical banded
gastroplasty, laparoscopic adjustable gastric band, or
laparoscopic sleeve gastrectomy) |
1 |
Evidence: Limited
evidence demonstrated no substantial decrease in effectiveness
of oral contraceptives among women who underwent laparoscopic
placement of an adjustable gastric band (126). |
|
b. Malabsorptive
procedures: decrease absorption of nutrients and calories by
shortening the functional length of the small intestine
(Roux-en-Y gastric bypass or biliopancreatic
diversion) |
COCs: 3 Patch and ring: 1 |
Evidence: Limited
evidence demonstrated no substantial decrease in effectiveness
of oral contraceptives among women who underwent a
biliopancreatic diversion; however, evidence from
pharmacokinetic studies reported conflicting results of oral
contraceptive effectiveness among women who underwent a
jejunoileal bypass (126). Comment: Bariatric surgical procedures involving a malabsorptive component have the potential to decrease oral contraceptive effectiveness, perhaps further decreased by postoperative complications, such as long-term diarrhea or vomiting. |
|
Surgery
| |||
a. Minor surgery without
immobilization |
1 |
— |
|
b. Major
surgery | |||
ii. Without prolonged
immobilization |
2 |
— |
|
i.
With prolonged immobilization |
4 |
— |
|
Cardiovascular Disease
| |||
Multiple risk
factors for atherosclerotic cardiovascular disease
(e.g., older age, smoking, diabetes, hypertension, low HDL, high
LDL, or high triglyceride levels) |
3/4 |
Clarification: When a
person has multiple major risk factors, any of which alone would
substantially increase risk for cardiovascular disease, use of
CHCs might increase risk to an unacceptable level. However, a
simple addition of categories for multiple risk factors is not
intended; for example, a combination of two category 2 risk
factors might not necessarily warrant a higher
category. Clarification: The recommendations apply to known pre-existing medical conditions or characteristics. Few if any screening tests are needed before initiation of contraception. See U.S. SPR (https://www.cdc.gov/contraception/hcp/usspr/HYPERLINK) (127). |
|
Hypertension Systolic blood pressure ≥160 mm Hg or diastolic blood pressure ≥100 mm Hg are associated with increased risk for adverse health events as a result of pregnancy (Box 3). | |||
a. Adequately controlled
hypertension |
3 |
Clarification: For all
categories of hypertension, classifications are based on the
assumption that no other risk factors exist for cardiovascular
disease. When multiple risk factors do exist, risk for
cardiovascular disease might increase substantially. A single
reading of blood pressure level is not sufficient to classify a
person as hypertensive. Clarification: Persons adequately treated for hypertension are at reduced risk for acute myocardial infarction and stroke compared with untreated persons. Although no data exist, CHC users with adequately controlled and monitored hypertension should be at reduced risk for acute myocardial infarction and stroke compared with untreated hypertensive CHC users. Evidence: Among women with hypertension, COC users were at higher risk than nonusers for stroke, acute myocardial infarction, and peripheral arterial disease (101,103,110–113,128–142). Discontinuation of COCs in women with hypertension might improve blood pressure control (143). |
|
b. Elevated
blood pressure levels
(properly taken
measurements) |
Clarification: For all categories of
hypertension, classifications are based on the assumption that
no other risk factors exist for cardiovascular disease. When
multiple risk factors do exist, risk for cardiovascular disease
might increase substantially. A single reading of blood pressure
level is not sufficient to classify a person as
hypertensive. Evidence: Among women with hypertension, COC users were at higher risk than nonusers for stroke, acute myocardial infarction, and peripheral arterial disease (101,103,110–113,128–142). Discontinuation of COCs in women with hypertension might improve blood pressure control (143). |
||
i.
Systolic 140–159 mm Hg or diastolic 90–99 mm
Hg |
3 |
||
ii. Systolic ≥160 mm Hg or
diastolic ≥100 mm Hg |
4 |
||
c. Vascular
disease |
4 |
||
History of high
blood pressure during pregnancy (when current blood
pressure is measurable and normal) |
2 |
Evidence: Women with a
history of high blood pressure in pregnancy who also used COCs
had a higher risk for myocardial infarction and VTE than did COC
users who did not have a history of high blood pressure during
pregnancy. The absolute risks for acute myocardial infarction
and VTE in this population remained small (112,129,141,142,144–150). |
|
Deep
venous thrombosis/
Pulmonary
embolism This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | |||
a. Current or history of
DVT/PE, receiving anticoagulant therapy (therapeutic dose)
(e.g., acute DVT/PE or long-term therapeutic dose) |
3 |
Clarification: Persons
using anticoagulant therapy are at risk for gynecologic
complications of therapy, such as heavy or prolonged bleeding
and hemorrhagic ovarian cysts. CHCs can be of benefit in
preventing or treating these complications. When a contraceptive
method is used as a therapy, rather than solely to prevent
pregnancy, the risk/benefit ratio might differ and should be
considered on a case-by-case
basis. Clarification: When a patient discontinues therapeutic dose of anticoagulant therapy, careful consideration should be given to transitioning from CHCs to a progestin-only or nonhormonal method, if acceptable to the patient. Evidence: Limited evidence was identified on use of CHCs among women with DVT/PE receiving anticoagulant therapy (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). In one study among women with a history of acute VTE currently receiving therapeutic anticoagulant therapy (i.e., rivaroxaban or enoxaparin/vitamin K antagonist [warfarin or acenocoumarol]), the incidence of recurrent VTE was similar among estrogen users (CHC or estrogen-only pills), POC users, and women not on hormonal therapy (151). |
|
b. History of
DVT/PE, receiving
anticoagulant therapy (prophylactic
dose) |
Clarification: Persons using anticoagulant therapy
are at risk for gynecologic complications of therapy, such as
heavy or prolonged bleeding and hemorrhagic ovarian cysts. CHCs
can be of benefit in preventing or treating these complications.
When a contraceptive method is used as a therapy, rather than
solely to prevent pregnancy, the risk/benefit ratio might differ
and should be considered on a case-by-case basis. |
||
i. Higher risk for
recurrent DVT/PE (one or more risk factors) |
4 |
||
• Thrombophilia (e.g.,
factor V Leiden mutation; prothrombin gene mutation; protein S,
protein C, and antithrombin deficiencies; or antiphospholipid
syndrome) • Active cancer (metastatic, receiving therapy, or within 6 months after clinical remission), excluding nonmelanoma skin cancer • History of recurrent DVT/PE | |||
ii. Lower risk for recurrent DVT/PE (no
risk factors) |
3 |
||
c. History of
DVT/PE, not receiving
anticoagulant therapy | |||
i.
Higher risk for recurrent DVT/PE (one or more risk
factors) |
4 |
— |
|
• History of
estrogen-associated
DVT/PE • Pregnancy-associated DVT/PE • Idiopathic DVT/PE • Thrombophilia (e.g., factor V Leiden mutation; prothrombin gene mutation; protein S, protein C, and antithrombin deficiencies; or antiphospholipid syndrome) • Active cancer (metastatic, receiving therapy, or within 6 months after clinical remission), excluding nonmelanoma skin cancer • History of recurrent DVT/PE | |||
ii. Lower risk for recurrent DVT/PE (no
risk factors) |
3 |
— |
|
d. Family history
(first-degree relatives) |
2 |
Comment: Certain
conditions that increase the risk for DVT/PE are
heritable. |
|
Thrombophilia
(e.g., factor V Leiden mutation; prothrombin gene mutation;
protein S, protein C, and antithrombin deficiencies; or
antiphospholipid syndrome)
This condition is associated
with increased risk for adverse health events as a result of
pregnancy (Box
3). |
4 |
Clarification: Routine
screening in the general population before contraceptive
initiation is not
recommended. Clarification: If a person has current or history of DVT/PE, see recommendations for DVT/PE. Clarification: Classification of antiphospholipid syndrome includes presence of a clinical feature (e.g., thrombosis or obstetric morbidity) and persistently abnormal antiphospholipid antibody test on two or more occasions at least 12 weeks apart (152). Evidence: Among women with factor V Leiden mutation, prothrombin gene mutation, antithrombin deficiency, and protein C deficiency, COC users had an increased risk for venous and arterial thrombosis compared with nonusers. Evidence was inconsistent on risk for thrombosis among women with protein S deficiency using COCs. No evidence was identified on COC use among persons with antiphospholipid syndrome (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). |
|
Superficial venous disorders
| |||
a. Varicose
veins |
1 |
Evidence: One study
suggested that among women with varicose veins, the rate of VTE
and superficial venous thrombosis was higher in oral
contraceptive users compared with nonusers; however, statistical
significance was not reported and the number of events was small
(153). |
|
b. Superficial venous
thrombosis (acute or history) |
3 |
Clarification:
Superficial venous thrombosis might be associated with an
increased risk for VTE. If a person has risk factors for
concurrent DVT (e.g., thrombophilia or cancer) or has current or
history of DVT, see recommendations for DVT/PE. Superficial
venous thrombosis associated with a peripheral intravenous
catheter is less likely to be associated with additional
thrombosis and use of CHCs may be
considered. Evidence: One study demonstrated that among women with superficial venous thrombosis, the risk for VTE was higher in oral contraceptive users compared with nonusers (153). |
|
Current and history
of ischemic heart disease
This condition is
associated with increased risk for adverse health events as a
result of pregnancy (Box
3). |
4 |
— |
|
Stroke
(history of cerebrovascular accident)
This condition is
associated with increased risk for adverse health events as a
result of pregnancy (Box
3). |
4 |
— |
|
Valvular
heart disease Complicated valvular heart disease is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | |||
a. Uncomplicated |
2 |
— |
|
b. Complicated (pulmonary
hypertension, risk for atrial fibrillation, or history of
subacute bacterial endocarditis) |
4 |
Comment: Among persons
with valvular heart disease, CHC use might further increase the
risk for arterial thrombosis; persons with complicated valvular
heart disease are at greatest risk. |
|
Peripartum cardiomyopathy This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
Evidence: No
direct evidence exists about the safety of CHCs among women with
peripartum cardiomyopathy. Limited indirect evidence from
noncomparative studies of women with cardiac disease
demonstrated few cases of hypertension and transient ischemic
attack in women with cardiac disease using COCs. No cases of
heart failure were reported (154). Comment: COCs might increase fluid retention in healthy persons; fluid retention might worsen heart failure in persons with peripartum cardiomyopathy. COCs might induce cardiac arrhythmias in healthy persons; persons with peripartum cardiomyopathy have a high incidence of cardiac arrhythmias. |
||
a. Normal or
mildly impaired cardiac
function (New York Heart
Association
Functional Class I or II: no limitation of
activities or slight, mild limitation
of
activity) (155) | |||
i.
<6 months |
4 |
||
ii. ≥6 months |
3 |
||
b. Moderately or severely
impaired cardiac function (New York Heart Association Functional
Class III or IV: marked limitation of activity or should be at
complete rest) (155) |
4 |
||
Renal
Disease
| |||
Chronic
kidney disease This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | |||
a. Current nephrotic
syndrome |
4 |
Evidence: No direct
evidence was identified on CHC use among persons with CKD with
current nephrotic syndrome (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). Persons
with severe CKD or nephrotic syndrome are at higher risk for
thrombosis than the general population (156–158). Use
of CHCs might further elevate risk for thrombosis among those
with CKD with current nephrotic
syndrome. Comment: A person might have CKD without current nephrotic syndrome but might have other conditions often associated with CKD (e.g., diabetes, hypertension, and SLE). See recommendations for other conditions if they apply. |
|
b. Hemodialysis |
4 |
Evidence: No direct
evidence was identified on CHC use among persons with CKD on
hemodialysis (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). Persons
with CKD on dialysis are at higher risk for thrombosis than the
general population (156–158). Use
of CHCs might further elevate risk for thrombosis among those
with CKD on dialysis. Comment: A person might have CKD without hemodialysis, but might have other conditions often associated with CKD (e.g., diabetes, hypertension, and SLE). See recommendations for other conditions if they apply. |
|
c. Peritoneal
dialysis |
4 |
Evidence: No direct
evidence was identified on CHC use among persons with CKD on
peritoneal dialysis (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). Persons
with CKD on dialysis are at higher risk for thrombosis than the
general population (156–158). Use
of CHCs might further elevate risk for thrombosis among those
with CKD. Comment: A person might have CKD without peritoneal dialysis, but might have other conditions often associated with CKD (e.g., diabetes, hypertension, and SLE). See recommendations for other conditions if they apply. |
|
Rheumatic Diseases
| |||
Systemic
lupus erythematosus This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | |||
a. Positive (or unknown)
antiphospholipid antibodies |
4 |
Clarification: Persons
with SLE are at increased risk for ischemic heart disease,
stroke, and VTE. Categories assigned to such conditions in U.S.
MEC should be the same for persons with SLE who have these
conditions. For all subconditions of SLE, classifications are
based on the assumption that no other risk factors for
cardiovascular disease are present; these classifications
must be modified in the presence of such risk factors (159–177). Evidence: Antiphospholipid antibodies are associated with a higher risk for both arterial and venous thrombosis (178,179). |
|
b. Severe
thrombocytopenia |
2 |
Clarification: Persons
with SLE are at increased risk for ischemic heart disease,
stroke, and VTE. Categories assigned to such conditions in U.S.
MEC should be the same for persons with SLE who have these
conditions. For all subconditions of SLE, classifications are
based on the assumption that no other risk factors for
cardiovascular disease are present; these classifications must
be modified in the presence of such risk factors (159–177). |
|
c. Immunosuppressive
therapy |
2 |
Clarification: Persons
with SLE are at increased risk for ischemic heart disease,
stroke, and VTE. Categories assigned to such conditions in U.S.
MEC should be the same for persons with SLE who have these
conditions. For all subconditions of SLE, classifications are
based on the assumption that no other risk factors for
cardiovascular disease are present; these classifications must
be modified in the presence of such risk factors (159–177). |
|
d. None of the
above |
2 |
Clarification: Persons
with SLE are at increased risk for ischemic heart disease,
stroke, and VTE. Categories assigned to such conditions in U.S.
MEC should be the same for persons with SLE who have these
conditions. For all subconditions of SLE, classifications are
based on the assumption that no other risk factors for
cardiovascular disease are present; these classifications must
be modified in the presence of such risk factors (159–177). |
|
Rheumatoid arthritis
|
Evidence:
Limited evidence demonstrates no consistent pattern of
improvement or worsening of rheumatoid arthritis with use of
oral contraceptives, progesterone, or estrogen (180). |
||
a. Not receiving
immunosuppressive therapy |
2 |
||
b. Receiving
immunosuppressive therapy |
2 |
||
Neurologic Conditions
| |||
Headaches
| |||
a. Nonmigraine
(mild or severe) |
1 |
Clarification:
Classification depends on accurate diagnosis of those severe
headaches that are migraines and those headaches that are not,
as well as diagnosis of ever experiencing aura. Aura is a
specific focal neurologic symptom. For more information about
headache classification see the International Headache
Society’s International Classification of
Headache Disorders, 3rd ed. (https://ichd-3.org) (181). Any new headaches
or marked changes in headaches should be evaluated. |
|
b.
Migraine |
Clarification: Classification depends on
accurate diagnosis of those severe headaches that are migraines
and those headaches that are not, as well as diagnosis of ever
experiencing aura. Aura is a specific focal neurologic symptom.
For more information about headache classification see the
International Headache Society’s International
Classification of Headache Disorders, 3rd ed.
(https://ichd-3.org) (181). Any new headaches
or marked changes in headaches should be
evaluated. Clarification: Classification is for persons without any other risk factors for stroke (e.g., age, hypertension, and smoking). Evidence: Among women with migraine, oral contraceptive use is associated with about a threefold increased risk for ischemic stroke compared with nonuse, although most studies did not specify migraine type or oral contraceptive formulation. The only study to examine migraine type found that the risk for ischemic stroke among women with migraine with aura was increased to a similar level among both oral contraceptive users and nonusers, compared with women without migraine (182). The risk for ischemic stroke is increased among women using COCs, compared with women not using COCs (101,183). The risk for ischemic stroke is also increased among women with migraine with aura, compared with women without migraine (184–186). One older meta-analysis found that migraine without aura was associated with an increased risk for ischemic stroke, while two more recent meta-analyses did not find such an association (184–186). Comment: Menstrual migraine is a subtype of migraine without aura. For more information, see the International Headache Society’s International Classification of Headache Disorders, 3rd ed. (https://ichd-3.org) (181). |
||
i.
Without aura (includes menstrual migraine) |
2 |
||
ii. With aura |
4 |
||
Epilepsy This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
1 |
Clarification: If a
person is taking anticonvulsants, see recommendations for Drug
Interactions. Certain anticonvulsants lower COC effectiveness.
The extent to which patch or ring use is similar to COC use in
this regard remains unclear. |
|
Multiple
sclerosis
|
Evidence:
Limited evidence suggests that use of COCs or oral
contraceptives (type not specified) among women with multiple
sclerosis does not worsen the clinical course of disease (187). Comment: No data exist that evaluate the increased risk for VTE among persons with multiple sclerosis using CHCs. However, persons with multiple sclerosis are at higher risk for VTE than those without multiple sclerosis. |
||
a. Without prolonged
immobility |
1 |
||
b. With prolonged
immobility |
3 |
||
Depressive Disorders
| |||
Depressive
disorders
|
1 |
Clarification: If a
person is receiving psychotropic medications or St.
John’s wort, see recommendations for Drug
Interactions. Evidence: COC use was not associated with increased depressive symptoms in women with depression or scoring above threshold levels on a validated depression screening instrument compared with baseline or with nonusers with depression. One small study of women with bipolar disorder found that oral contraceptives did not significantly change mood across the menstrual cycle (188). |
|
Reproductive Tract Infections and
Disorders
| |||
Vaginal
bleeding patterns
| |||
a. Irregular pattern
without heavy bleeding |
1 |
Comment: Irregular
menstrual bleeding patterns are common among healthy
persons. |
|
b. Heavy or prolonged
bleeding (includes regular and irregular patterns) |
1 |
Clarification: Unusually
heavy bleeding should raise the suspicion of a serious
underlying condition. Evidence: A Cochrane Collaboration Review identified one RCT evaluating the effectiveness of COC use compared with naproxen and danazol in treating menorrhagia. Women with menorrhagia did not report worsening of the condition or any adverse events related to COC use (189). |
|
Unexplained vaginal
bleeding
(suspicious for serious condition)
before evaluation |
2 |
Clarification: If
pregnancy or an underlying pathological condition (e.g., pelvic
malignancy) is suspected, it must be evaluated and the category
adjusted after evaluation. Comment: No conditions that cause vaginal bleeding will be worsened in the short-term by use of CHCs. |
|
Endometriosis
|
1 |
Evidence: A Cochrane
Collaboration Review identified one RCT evaluating the
effectiveness of COC use compared with a gonadotropin-releasing
hormone analog in treating the symptoms of endometriosis. Women
with endometriosis did not report worsening of the condition or
any adverse events related to COC use (190). |
|
Benign ovarian
tumors (including cysts) |
1 |
— |
|
Severe
dysmenorrhea
|
1 |
Evidence: Risk for side
effects with COC use was not higher among women with
dysmenorrhea than among women not using COCs. Certain COC users
had a reduction in pain and bleeding (191,192). |
|
Gestational trophoblastic disease
This
condition is associated with increased
risk for adverse
health events as a result of
pregnancy (Box 3). |
Clarification: For all subconditions of
gestational trophoblastic disease, classifications are based on
the assumption that persons are under close medical supervision
because of the need for monitoring of β-hCG levels for
appropriate disease surveillance. Evidence: After molar pregnancy evacuation, the balance of evidence found COC use did not increase the risk for postmolar trophoblastic disease, and β–hCG levels regressed more rapidly in certain COC users than in nonusers (193). Limited evidence suggests that use of COCs during chemotherapy does not significantly affect the regression or treatment of postmolar trophoblastic disease compared with women who used a nonhormonal contraceptive method or DMPA during chemotherapy (193). |
||
a. Suspected
gestational trophoblastic
disease (immediate
postevacuation) | |||
i.
Uterine size first trimester |
1 |
||
ii. Uterine size second
trimester |
1 |
||
b. Confirmed
gestational trophoblastic
disease (after initial
evacuation and during
monitoring) | |||
i.
Undetectable or nonpregnant β-hCG levels |
1 |
||
ii. Decreasing β-hCG
levels |
1 |
||
iii. Persistently elevated β-hCG
levels or malignant disease, with no evidence or suspicion of
intrauterine disease |
1 |
||
iv. Persistently elevated β-hCG
levels or malignant disease, with evidence or suspicion of
intrauterine disease |
1 |
||
Cervical
ectropion
|
1 |
Comment: Cervical
ectropion is not a risk factor for cervical cancer, and
restriction of CHC use is unnecessary. |
|
Cervical
intraepithelial neoplasia
|
2 |
Evidence: Among women
with persistent human papillomavirus infection, long-term COC
use (≥5 years) might increase the risk for carcinoma in
situ and invasive carcinoma (194). Limited evidence on women
with low-grade squamous intraepithelial lesions found use of the
vaginal ring did not worsen the condition (9). |
|
Cervical
cancer (awaiting treatment) |
2 |
Comment: Theoretical
concern exists that CHC use might affect prognosis of the
existing disease. While awaiting treatment, persons may use
CHCs. In general, treatment of this condition can render a
person infertile. |
|
Breast
disease Breast cancer is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | |||
a. Undiagnosed
mass |
2 |
Clarification: Evaluation
of mass should be pursued as early as possible. |
|
b. Benign breast
disease |
1 |
— |
|
c. Family history of
cancer |
1 |
Evidence: Women with
breast cancer susceptibility genes (e.g., BRCA1
and BRCA2) have a higher baseline risk for
breast cancer than women without these genes. The baseline risk
for breast cancer also is higher among women with a family
history of breast cancer than among those who do not have such a
history. However, evidence does not suggest that the increased
risk for breast cancer among women with either a family history
of breast cancer or breast cancer susceptibility genes is
modified by the use of COCs (195–212). |
|
d. Breast
cancer |
Comment:
Breast cancer is a hormonally sensitive tumor, and the prognosis
for persons with current or recent breast cancer might worsen
with CHC use. |
||
i.
Current |
4 |
||
ii. Past and no evidence of current
disease for 5 years |
3 |
||
Endometrial
hyperplasia
|
1 |
— |
|
Endometrial
cancer This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
1 |
Comment: COC use reduces
the risk for endometrial cancer; whether patch or ring use
reduces the risk for endometrial cancer is not known. While
awaiting treatment, patients may use CHCs. In general, treatment
of this condition can render a person infertile. |
|
Ovarian
cancer This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
1 |
Comment: COC use reduces
the risk for ovarian cancer; whether patch or ring use reduces
the risk for ovarian cancer is not known. While awaiting
treatment, patients may use CHCs. In general, treatment of this
condition can render a person infertile. |
|
Uterine
fibroids
|
1 |
Comment: COCs do not
appear to cause growth of uterine fibroids, and patch and ring
also are not expected to cause growth. |
|
Pelvic
inflammatory disease
|
Comment: COCs
might reduce the risk for PID among persons with STIs but do not
protect against HIV infection or lower genital tract STIs.
Whether use of patch or ring reduces the risk for PID among
persons with STIs is unknown; however, they do not protect
against HIV infection or lower genital tract STIs. |
||
a. Current PID |
1 |
||
b. Past PID |
|
||
i.
With subsequent pregnancy |
1 |
||
ii. Without subsequent
pregnancy |
1 |
||
Sexually
transmitted infections
| |||
a. Current purulent
cervicitis or chlamydial infection or gonococcal
infection |
1 |
— |
|
b. Vaginitis (including
Trichomonas vaginalis and bacterial
vaginosis) |
1 |
— |
|
c. Other factors related
to STIs |
1 |
— |
|
HIV
| |||
High risk for HIV
infection
|
1 |
Evidence:
Low-to-moderate-quality evidence from 11 observational studies
suggested no association between COC use (it was assumed that
studies that did not specify oral contraceptive type examined
mostly, if not exclusively, COC use) and HIV acquisition. No
studies of patch or ring were identified (213,214). |
|
HIV
infection For persons with HIV infection who are not clinically well or not receiving ARV therapy, this condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
1 |
Clarification: Drug
interactions might exist between hormonal contraceptives and ARV
drugs; see recommendations for Drug
Interactions. Evidence: Overall, evidence does not support an association between COC use and progression of HIV. Limited direct evidence does not support an association between COC use and transmission of HIV to noninfected partners; studies measuring genital viral shedding as a proxy for infectivity have had mixed results. Studies measuring whether hormonal contraceptive methods affect plasma HIV viral load generally have found no effect (215–217). |
|
Other
Infections
| |||
Schistosomiasis
Schistosomiasis with
fibrosis of the liver is
associated with increased risk
for adverse
health events as a result of
pregnancy
(Box
3). | |||
a. Uncomplicated |
1 |
Evidence: Among women
with uncomplicated schistosomiasis, COC use had no adverse
effects on liver function (218–224). |
|
b. Fibrosis of the liver
(if severe, see recommendations for Cirrhosis) |
1 |
— |
|
Tuberculosis
This condition is
associated with
increased risk for adverse health
events
as a result of pregnancy (Box 3). |
Clarification: If a person is taking rifampin,
see recommendations for Drug Interactions. Rifampin is likely to
decrease COC effectiveness. The extent to which patch or ring
use is similar to COC use in this regard remains
unclear. |
||
a. Nonpelvic |
1 |
||
b. Pelvic |
1 |
||
Malaria
|
1 |
— |
|
Endocrine Conditions
| |||
Diabetes Insulin-dependent diabetes; diabetes with nephropathy, retinopathy, or neuropathy; diabetes with other vascular disease; or diabetes of >20 years’ duration are associated with increased risk for adverse health events as a result of pregnancy (Box 3). | |||
a. History of gestational
disease |
1 |
Evidence: The development
of non–insulin-dependent diabetes in women with a history
of gestational diabetes is not increased by use of COCs (225–232).
Likewise, lipid levels appear to be unaffected by COC use (233–235). |
|
b. Nonvascular
disease |
Evidence: Among women
with insulin-dependent or non–insulin-dependent diabetes,
COC use had limited effect on daily insulin requirements and no
effect on long-term diabetes control (e.g., glycosylated
hemoglobin levels) or progression to retinopathy. Changes in
lipid profile and hemostatic markers were limited, and most
changes remained within normal values (236–245). |
||
i.
Non-insulin dependent |
2 |
— |
|
ii. Insulin dependent |
2 |
— |
|
c. Nephropathy,
retinopathy, or neuropathy |
3/4 |
Clarification: The
category should be assessed according to the severity of the
condition. |
|
d. Other vascular disease
or diabetes of >20 years’ duration |
3/4 |
Clarification: The
category should be assessed according to the severity of the
condition. |
|
Thyroid
disorders
| |||
a. Simple goiter |
1 |
— |
|
b. Hyperthyroid |
1 |
— |
|
c. Hypothyroid |
1 |
— |
|
Gastrointestinal Conditions
| |||
Inflammatory bowel
disease (ulcerative colitis or Crohn’s
disease) |
2/3 |
Clarification: For
persons with mild IBD and with no other risk factor for VTE, the
benefits of CHC use generally outweigh the risks (category 2).
However, for persons with IBD who are at increased risk for VTE
(e.g., those with active or extensive disease, surgery,
immobilization, corticosteroid use, vitamin deficiencies, or
fluid depletion), the risks of CHC use generally outweigh the
benefits (category 3). Evidence: Risk for disease relapse was not significantly higher among women with IBD using oral contraceptives (most studies did not specify type) than among nonusers (246). Absorption of COCs among women with mild ulcerative colitis and no or small ileal resections was similar to the absorption among healthy women (246). Findings might not apply to women with Crohn’s disease or more extensive bowel resections. No data exist that evaluate the increased risk for VTE among women with IBD using CHCs. However, women with IBD are at higher risk than unaffected women for VTE (246). |
|
Gallbladder disease
|
Comment: CHCs
might cause a small increased risk for gallbladder disease. CHCs
might worsen existing gallbladder disease. |
||
a. Asymptomatic |
2 |
||
b.
Symptomatic | |||
i.
Current |
3 |
||
ii. Treated by
cholecystectomy |
2 |
||
iii. Medically treated |
3 |
||
History
of cholestasis
| |||
a. Pregnancy
related |
2 |
Comment: History of
pregnancy-related cholestasis might predict an increased risk
for COC-related cholestasis. |
|
b. Past COC
related |
3 |
Comment: History of
COC-related cholestasis predicts an increased risk with
subsequent COC use. |
|
Viral
hepatitis
|
Initiation |
Continuation |
— |
a. Acute or
flare |
3/4 |
2 |
Clarification
(initiation): The category should be assessed
according to the severity of the
condition. Evidence: Limited evidence was identified on COC use among persons with acute viral hepatitis. Data suggest that in women with chronic viral hepatitis, COC use does not increase the risk or severity of fibrosis, nor does it increase the risk for hepatocellular carcinoma. For women with chronic viral hepatitis, COC use does not appear to trigger severe liver dysfunction (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). Comment: Hepatic metabolism of exogenous hormones might be impaired in persons with liver dysfunction, which could lead to increased estrogen levels in circulation and estrogen-related side effects and adverse events (e.g., thrombosis). |
b. Chronic |
1 |
1 |
Evidence: Data suggest
that in women with chronic viral hepatitis, COC use does not
increase the risk or severity of fibrosis, nor does it increase
the risk for hepatocellular carcinoma. For women with chronic
viral hepatitis, COC use does not appear to trigger severe liver
dysfunction (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). |
Cirrhosis Decompensated cirrhosis is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | |||
a. Compensated (normal
liver function) |
1 |
Evidence: No direct
evidence was identified on CHC use among persons with
compensated cirrhosis (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). |
|
b. Decompensated (impaired
liver function) |
4 |
Evidence: No direct
evidence was identified on CHC use among persons with
decompensated cirrhosis (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). Comment: Hepatic metabolism of exogenous hormones might be impaired in persons with liver dysfunction, which could lead to increased estrogen levels in circulation and estrogen-related side effects and adverse events (e.g., thrombosis). Any estrogen-related hepatotoxicity might be less tolerated in persons with existing liver dysfunction. |
|
Liver
tumors Hepatocellular adenoma and malignant liver tumors are associated with increased risk for adverse health events as a result of pregnancy (Box 3). | |||
a.
Benign | |||
i.
Focal nodular hyperplasia |
2 |
Evidence: Limited
evidence suggests that COC use does not influence either
progression or regression of focal nodular hyperplasia
(Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). |
|
ii. Hepatocellular adenoma |
4 |
Evidence: Evidence
suggests that COC use is associated with progression of
hepatocellular adenoma growth, while COC discontinuation is
associated with stability or regression (Supplementary Appendix,
https://stacks.cdc.gov/view/cdc/156516). |
|
b. Malignant
(hepatocellular carcinoma) |
4 |
Evidence: No direct
evidence was identified on CHC use among persons with
hepatocellular carcinoma (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). |
|
Respiratory Conditions
| |||
Cystic
fibrosis This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
1 |
Clarification: Persons
with cystic fibrosis are at increased risk for diabetes, liver
disease, gallbladder disease, and VTE (particularly related to
use of central venous catheters) and are frequently prescribed
antibiotics. Categories assigned to such conditions in U.S. MEC
should be the same for persons with cystic fibrosis who have
these conditions. For cystic fibrosis, classifications are based
on the assumption that no other conditions are present; these
classifications must be modified in the presence of such
conditions. Clarification: Certain drugs to treat cystic fibrosis (e.g., lumacaftor) might reduce effectiveness of hormonal contraceptives, including oral, injectable, transdermal, and implantable contraceptives. Evidence: Limited evidence suggests that use of COCs or oral contraceptives (type not specified) among women with cystic fibrosis is not associated with worsening of disease severity. Very limited evidence suggests that cystic fibrosis does not impair the effectiveness of hormonal contraception (247). |
|
Hematologic Conditions
| |||
Thalassemia
|
1 |
Comment: Anecdotal
evidence from countries where thalassemia is prevalent indicates
that COC use does not worsen the condition. |
|
Sickle cell
disease This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
4 |
Evidence: Persons with
sickle cell disease are at higher risk for stroke and venous
thrombosis than the general population (248–251). CHC
use might further elevate risk for thrombosis among persons with
sickle cell disease, but evidence is limited (Supplementary
Appendix, https://stacks.cdc.gov/view/cdc/156516). |
|
Iron deficiency
anemia
|
1 |
Comment: CHC use might
decrease menstrual blood loss. |
|
Solid
Organ Transplantation
| |||
Solid
organ transplantation This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | |||
a. No graft
failure |
2 |
Clarification: Persons
with transplant due to Budd-Chiari syndrome should not use CHCs
because of the increased risk for
thrombosis. Evidence: Limited evidence among CHC users indicated no adverse events and no overall changes in biochemical parameters (e.g., blood pressure, cholesterol) and no pregnancies (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). However, one study reported discontinuations of COC use in two (8%) of 26 women as a result of serious medical complications, including acute graft rejection (Supplementary Appendix, https://stacks.cdc.gov/view/cdc/156516). |
|
b. Graft failure |
4 |
Evidence: Limited
evidence among CHC users indicated no adverse events and no
overall changes in biochemical parameters (e.g., blood pressure,
cholesterol) and no pregnancies (Supplementary Appendix,
https://stacks.cdc.gov/view/cdc/156516).
However, one study reported discontinuations of COC use in two
(8%) of 26 women as a result of serious medical complications,
including acute graft rejection (Supplementary Appendix,
https://stacks.cdc.gov/view/cdc/156516). |
|
Drug
Interactions
| |||
Antiretrovirals used for prevention
(PrEP) or
treatment of HIV infection
|
Comment: These
recommendations generally are for ARV agents used alone.
However, most persons receiving ARV therapy are using multiple
drugs in combination. In general, whether interactions between
ARVs and hormonal contraceptives differ when ARVs are given
alone or in combination is unknown. |
||
See the
following guidelines for the most up-to-date recommendations on
drug-drug interactions between hormonal contraception and ARVs:
1) Recommendations for the Use of Antiretroviral Drugs During
Pregnancy and Interventions to Reduce Perinatal HIV Transmission
in the United States (https://clinicalinfo.hiv.gov/en/guidelines/perinatal/prepregnancy-counseling-childbearing-age-overview?view=full#table-3)
(252) and 2) Guidelines for the Use
of Antiretroviral Agents in Adults and Adolescents with HIV
(https://clinicalinfo.hiv.gov/en/guidelines/hiv-clinical-guidelines-adult-and-adolescent-arv/drug-interactions-overview?view=full)
(253). | |||
a. Nucleoside
reverse transcriptase
inhibitors (NRTIs) | |||
i.
Abacavir (ABC) |
1 |
Evidence:
NRTIs do not appear to have significant risk for interactions
with hormonal contraceptive methods (254–259). |
|
ii. Tenofovir (TDF) |
1 |
||
iii. Zidovudine (AZT) |
1 |
||
iv. Lamivudine (3TC) |
1 |
||
v.
Didanosine (DDI) |
1 |
||
vi. Emtricitabine (FTC) |
1 |
||
vii. Stavudine (D4T) |
1 |
||
b.
Nonnucleoside reverse transcriptase
inhibitors
(NNRTIs) | |||
i.
Efavirenz (EFV) |
2 |
Clarification: Evidence
suggests drug interactions between EFV and certain hormonal
contraceptives. These interactions might reduce the
effectiveness of the hormonal
contraceptive. Evidence: Two studies suggested that pregnancy rates might be higher among women using COCs and EFV compared with COCs alone, although one study found no difference in pregnancy rates (260–262). Two studies found conflicting results on ovulations in women receiving COCs and EFV compared with EFV alone (263,264). Two pharmacokinetic studies demonstrated decreases in ethinyl estradiol and progestin concentrations in women receiving COCs and EFV compared with COCs alone (264,265). Pharmacokinetic studies demonstrated generally no changes in EFV concentrations with concomitant COC use (264–266). |
|
ii. Etravirine (ETR) |
1 |
Evidence: One study
demonstrated no clinically relevant pharmacokinetic or
pharmacodynamic changes in women using COCs and ETR compared
with COCs alone (267). |
|
iii. Nevirapine (NVP) |
1 |
Evidence: Five studies
found no significant differences in pregnancy rates among women
using COCs and NVP compared with women using COCs alone (260–262,266,268).
Three studies reported no ovulations among women receiving COCs
and NVP (263,268,269). Two
pharmacokinetic studies demonstrated decreased concentrations of
ethinyl estradiol and progestin among women using COCs and NVP
compared with COCs alone, and one study found no change in
contraceptive hormone concentrations (263,269,270).
Pharmacokinetic studies demonstrated generally no changes in NVP
concentrations with concomitant COC use (263,270,271). |
|
iv. Rilpivirine (RPV) |
1 |
Evidence: One study
demonstrated no clinical significant pharmacokinetic changes or
adverse events in women using COCs and RPV compared with COCs
alone (272). |
|
c.
Ritonavir-boosted protease inhibitors | |||
i.
Ritonavir-boosted atazanavir (ATV/r) |
2 |
Clarification:
Theoretically, drug interactions might occur between certain
ritonavir-boosted protease inhibitors and certain hormonal
contraceptives that might reduce the effectiveness of the
hormonal contraceptive. Evidence: One pharmacokinetic study demonstrated decreased estrogen but increased progestin concentrations in women using COCs and ATV/r compared with COCs alone (273). |
|
ii. Ritonavir-boosted darunavir
(DRV/r) |
2 |
Clarification:
Theoretically, drug interactions might occur between certain
ritonavir-boosted protease inhibitors and certain hormonal
contraceptives that might reduce the effectiveness of the
hormonal contraceptive. Evidence: One pharmacokinetic study demonstrated no change in follicle-stimulating hormone or luteinizing hormone but decreases in ethinyl estradiol and norethindrone in women using COCs with DRV/r compared with COCs alone (274). |
|
iii. Ritonavir-boosted fosamprenavir
(FPV/r) |
2 |
Clarification:
Theoretically, drug interactions might occur between certain
ritonavir-boosted protease inhibitors and certain hormonal
contraceptives that might reduce the effectiveness of the
hormonal contraceptive. Evidence: Information from the package label states that both ethinyl estradiol and norethindrone concentrations decreased with concurrent administration of COCs and FPV/r (275). |
|
iv. Ritonavir-boosted lopinavir
(LPV/r) |
1 |
Evidence: One study
demonstrated a nonsignificant increase in pregnancy rates among
women using COCs and LPV/r compared with COCs alone (260). One
study demonstrated no ovulations in women using the combined
hormonal patch and LPV/r compared with combined hormonal patch
alone; ethinyl estradiol concentrations for COC and patch users
decreased but norelgestromin concentrations increased with use
of the patch (276). |
|
v.
Ritonavir-boosted saquinavir (SQV/r) |
2 |
Clarification:
Theoretically, drug interactions might occur between certain
ritonavir-boosted protease inhibitors and certain hormonal
contraceptives that might reduce the effectiveness of the
hormonal contraceptive. Evidence: One pharmacokinetic study demonstrated no change in SQV concentrations in women using COC and SQV compared with COCs alone (277). |
|
iv. Ritonavir-boosted tipranavir
(TPV/r) |
2 |
Clarification:
Theoretically, drug interactions might occur between certain
ritonavir-boosted protease inhibitors and certain hormonal
contraceptives that might reduce the effectiveness of the
hormonal contraceptive. Evidence: Information from the package label states that ethinyl estradiol concentrations decrease but norethindrone concentrations increased with concurrent administration of COCs and TPV/r (278). |
|
d. Protease
inhibitors without ritonavir | |||
i.
Atazanavir (ATV) |
2 |
Clarification:
Theoretical concern exists that increased levels of ethinyl
estradiol because of interactions with ATV might increase the
risk for adverse events. Evidence: Information from the package label states that there are inconsistent changes in ethinyl estradiol concentrations and increases in progestin concentrations with concurrent administration of two different COCs and ATV (279). Comment: When ATV is administered with cobicistat, theoretical concern exists for a drug interaction with hormonal contraceptives. Cobicistat is an inhibitor of CYP3A and CYP2D6 and could theoretically increase contraceptive hormone levels. However, its effects on CYP enzymes and drug levels might vary when combined with other ARVs. |
|
ii.
Fosamprenavir (FPV) |
3 |
Clarification: Concern
exists that interactions between FPV and hormonal contraceptives
leading to decreased levels of FPV might diminish effectiveness
of the ARV drug. Evidence: Information from the package label states that amprenavir concentrations decreased with concurrent administration of COCs and amprenavir. Norethindrone concentrations increased and ethinyl estradiol concentrations did not change (275). |
|
iii.
Indinavir (IDV) |
1 |
Evidence: One small study
found no pregnancies in women using COCs and IDV (262). |
|
iv.
Nelfinavir (NFV) |
2 |
Clarification: Evidence
suggests drug interactions between certain protease inhibitors
and certain hormonal contraceptives. These interactions might
reduce the effectiveness of the hormonal
contraceptive. Evidence: One small study suggested that women using COCs and NFV might have had higher pregnancy rates than those using COCs alone (262). |
|
e. CCR5
co-receptor antagonists | |||
i.
Maraviroc (MVC) |
1 |
Evidence: COC
concentrations were not altered by co-administration with MVC
(280). |
|
f. HIV
integrase strand transfer inhibitors | |||
i.
Raltegravir (RAL) |
1 |
Evidence: One
pharmacokinetic study demonstrated increased concentrations of
norgestimate and no change in ethinyl estradiol among women
using COCs and RAL compared with COCs alone (281). |
|
ii.
Dolutegravir (DTG) |
1 |
Evidence: One study
demonstrated no clinically relevant pharmacokinetic or
pharmacodynamic changes in women using COCs and DTG compared
with COCs alone (282). |
|
iii.
Elvitegravir (EVG) |
1 |
Evidence: Information
from the package label states that ethinyl estradiol
concentrations decreased and norgestimate concentrations
increased with concurrent administration of COCs and EVG (283). Comment: When EVG is administered with cobicistat, theoretical concern exists for a drug interaction with hormonal contraceptives. Cobicistat is an inhibitor of CYP3A and CYP2D6 and could theoretically increase contraceptive hormone levels. However, its effects on CYP enzymes and drug levels might vary when combined with other ARVs. |
|
g. Fusion
inhibitors | |||
i.
Enfuvirtide |
1 |
— |
|
Anticonvulsant therapy
| |||
a. Certain anticonvulsants
(phenytoin, carbamazepine, barbiturates, primidone, topiramate,
oxcarbazepine) |
3 |
Clarification: Although
the interaction of certain anticonvulsants with CHCs is not
harmful, it is likely to reduce the effectiveness of CHCs. Use
of other contraceptives should be encouraged for persons who are
long-term users of any of these drugs. When a COC is chosen, a
preparation containing a minimum of 30
μg ethinyl estradiol should be
used. Evidence: Use of certain anticonvulsants might decrease the effectiveness of COCs (284–288). |
|
b. Lamotrigine |
3 |
Clarification: The
recommendation for lamotrigine applies only for situations where
lamotrigine monotherapy is taken concurrently with COCs.
Anticonvulsant treatment regimens that combine lamotrigine and
non–enzyme-inducing antiepileptic drugs (e.g., sodium
valproate) do not interact with
COCs. Evidence: Pharmacokinetic studies demonstrate levels of lamotrigine decrease significantly during COC use (288–293). Certain women who used both COCs and lamotrigine experienced increased seizure activity in one trial (289). |
|
Antimicrobial therapy
| |||
a. Broad-spectrum
antibiotics |
1 |
Evidence: Most
broad-spectrum antibiotics do not affect the contraceptive
effectiveness of COCs (294–330),
patch (331), or ring (332). |
|
b. Antifungals |
1 |
Evidence: Studies of
antifungal agents have demonstrated no clinically significant
pharmacokinetic interactions with COCs (333–342) or
ring (343). |
|
c.
Antiparasitics |
1 |
Evidence: Studies of
antiparasitic agents have demonstrated no clinically significant
pharmacokinetic interactions with COCs (218,344–348). |
|
d. Rifampin or rifabutin
therapy |
3 |
Clarification: Although
the interaction of rifampin or rifabutin therapy with CHCs is
not harmful, it is likely to reduce the effectiveness of CHCs.
Use of other contraceptives should be encouraged for persons who
are long-term users of either of these drugs. When a COC is
chosen, a preparation containing a minimum of 30
μg ethinyl estradiol should be
used. Evidence: The balance of the evidence suggests that rifampin reduces the effectiveness of COCs (349–363). Data on rifabutin are limited, but effects on metabolism of COCs are less than with rifampin, and small studies have not demonstrated evidence of ovulation (351,357). |
|
Psychotropic medications
|
Comment: For many common
psychotropic agents, limited or no theoretical concern exists
for clinically significant drug interactions when
co-administered with hormonal contraceptives. However, either no
or very limited data exist examining potential interactions for
these classes of medications. For psychotropic agents that are
CYP1A2 substrates (e.g., duloxetine, mirtazapine, ziprasidone,
olanzapine, clomipramine, imipramine, and amitriptyline),
co-administration with CHCs could theoretically yield increased
concentrations of the psychotropic drug. For agents with narrow
therapeutic windows (e.g., tricyclic antidepressants), increased
drug concentrations might pose safety concerns that could
necessitate closer monitoring. |
||
a. Selective serotonin
reuptake inhibitors (SSRIs) |
1 |
Evidence: Limited
clinical and pharmacokinetic data do not demonstrate concern for
SSRIs decreasing the effectiveness of oral contraceptives.
Limited evidence suggests that for women taking SSRIs, the use
of hormonal contraceptives was not associated with differences
in effectiveness of the SSRI for treatment or in adverse events
when compared with women not taking hormonal contraceptives
(364). Comment: Drugs that are inhibitors of CYP3A4 or CYP2C9 theoretically have the potential to increase levels of contraceptive steroids which might increase adverse events. Fluvoxamine is an SSRI known to be a moderate inhibitor of both CYP3A4 and CYP2C9; however, no clinical or pharmacokinetic studies were identified to explore potential drug-drug interactions. |
|
St. John’s wort | 2 |
Evidence: Although clinical data are limited, studies with pharmacokinetic and pharmacodynamics outcomes raise concern that St. John’s wort might decrease effectiveness of hormonal contraceptives, including increased risk for breakthrough bleeding and ovulation and increased metabolism of estrogen and progestins. Any interactions might be dependent on the dose of St. John’s wort, and the concentration of active ingredients across types of St. John’s wort preparations might vary (365). |
Abbreviations: ARV = antiretroviral; BMD = bone mineral density; BMI = body mass index; CHC = combined hormonal contraceptive; CKD = chronic kidney disease; COC = combined oral contraceptive; CYP = cytochrome P450; DMPA = depot medroxyprogesterone acetate; DVT = deep venous thrombosis; hCG = human chorionic gonadotropin; HDL = high-density lipoprotein; IBD = inflammatory bowel disease; IUD = intrauterine device; LDL = low-density lipoprotein; NA = not applicable; PE = pulmonary embolism; PID = pelvic inflammatory disease; POC = progestin-only contraceptive; PrEP = pre-exposure prophylaxis; RCT = randomized clinical trial; SLE = systemic lupus erythematosus; SSRI = selective serotonin reuptake inhibitor; STI = sexually transmitted infection; U.S. MEC = U.S. Medical Eligibility Criteria for Contraceptive Use; U.S. SPR = U.S. Selected Practice Recommendations for Contraceptive Use; VTE = venous thromboembolism.
References
- 1.Abrams LS, Skee DM, Natarajan J, Wong FA, Lasseter KC. Multiple-dose pharmacokinetics of a contraceptive patch in healthy women participants. Contraception 2001;64:287–94. 10.1016/S0010-7824(01)00273-6 [DOI] [PubMed] [Google Scholar]
- 2.Ahrendt HJ, Nisand I, Bastianelli C, et al. Efficacy, acceptability and tolerability of the combined contraceptive ring, NuvaRing, compared with an oral contraceptive containing 30 microg of ethinyl estradiol and 3 mg of drospirenone. Contraception 2006;74:451–7. 10.1016/j.contraception.2006.07.004 [DOI] [PubMed] [Google Scholar]
- 3.Audet MC, Moreau M, Koltun WD, et al. ; ORTHO EVRA/EVRA 004 Study Group. Evaluation of contraceptive efficacy and cycle control of a transdermal contraceptive patch vs an oral contraceptive: a randomized controlled trial. JAMA 2001;285:2347–54. 10.1001/jama.285.18.2347 [DOI] [PubMed] [Google Scholar]
- 4.Bjarnadóttir RI, Tuppurainen M, Killick SR. Comparison of cycle control with a combined contraceptive vaginal ring and oral levonorgestrel/ethinyl estradiol. Am J Obstet Gynecol 2002;186:389–95. 10.1067/mob.2002.121103 [DOI] [PubMed] [Google Scholar]
- 5.Boonyarangkul A, Taneepanichskul S. Comparison of cycle control and side effects between transdermal contraceptive patch and an oral contraceptive in women older than 35 years. J Med Assoc Thai 2007;90:1715–9. [PubMed] [Google Scholar]
- 6.Burkman RT. The transdermal contraceptive patch: a new approach to hormonal contraception. Int J Fertil Womens Med 2002;47:69–76. [PubMed] [Google Scholar]
- 7.Cole JA, Norman H, Doherty M, Walker AM. Venous thromboembolism, myocardial infarction, and stroke among transdermal contraceptive system users. Obstet Gynecol 2007;109:339–46. 10.1097/01.AOG.0000250968.82370.04 [DOI] [PubMed] [Google Scholar]
- 8.Devineni D, Skee D, Vaccaro N, et al. Pharmacokinetics and pharmacodynamics of a transdermal contraceptive patch and an oral contraceptive. J Clin Pharmacol 2007;47:497–509. 10.1177/0091270006297919 [DOI] [PubMed] [Google Scholar]
- 9.Dieben TOM, Roumen FJME, Apter D. Efficacy, cycle control, and user acceptability of a novel combined contraceptive vaginal ring. Obstet Gynecol 2002;100:585–93. [DOI] [PubMed] [Google Scholar]
- 10.Dittrich R, Parker L, Rosen JB, Shangold G, Creasy GW, Fisher AC; Ortho Evra/Evra 001 Study Group. Transdermal contraception: evaluation of three transdermal norelgestromin/ethinyl estradiol doses in a randomized, multicenter, dose-response study. Am J Obstet Gynecol 2002;186:15–20. 10.1067/mob.2002.118844 [DOI] [PubMed] [Google Scholar]
- 11.Duijkers I, Killick S, Bigrigg A, Dieben TOM. A comparative study on the effects of a contraceptive vaginal ring NuvaRing and an oral contraceptive on carbohydrate metabolism and adrenal and thyroid function. Eur J Contracept Reprod Health Care 2004;9:131–40. 10.1080/13625180400007199 [DOI] [PubMed] [Google Scholar]
- 12.Duijkers IJ, Klipping C, Verhoeven CH, Dieben TOM. Ovarian function with the contraceptive vaginal ring or an oral contraceptive: a randomized study. Hum Reprod 2004;19:2668–73. 10.1093/humrep/deh493 [DOI] [PubMed] [Google Scholar]
- 13.Elkind-Hirsch KE, Darensbourg C, Ogden B, Ogden LF, Hindelang P. Contraceptive vaginal ring use for women has less adverse metabolic effects than an oral contraceptive. Contraception 2007;76:348–56. 10.1016/j.contraception.2007.08.001 [DOI] [PubMed] [Google Scholar]
- 14.Hedon B, Helmerhorst FM, Cronje HS, et al. ; The EVRA 003 Study Group. Comparison of efficacy, cycle control, compliance and safety in users of a contraceptive patch versus an oral contraceptive. Int J Gynaecol Obstet 2000;70:78. 10.1016/S0020-7292(00)85161-9 [DOI] [Google Scholar]
- 15.Jick S, Kaye JA, Li L, Jick H. Further results on the risk of nonfatal venous thromboembolism in users of the contraceptive transdermal patch compared to users of oral contraceptives containing norgestimate and 35 microg of ethinyl estradiol. Contraception 2007;76:4–7. 10.1016/j.contraception.2007.03.003 [DOI] [PubMed] [Google Scholar]
- 16.Jick SS, Jick H. Cerebral venous sinus thrombosis in users of four hormonal contraceptives: levonorgestrel-containing oral contraceptives, norgestimate-containing oral contraceptives, desogestrel-containing oral contraceptives and the contraceptive patch. Contraception 2006;74:290–2. 10.1016/j.contraception.2006.05.071 [DOI] [PubMed] [Google Scholar]
- 17.Jick SS, Jick H. The contraceptive patch in relation to ischemic stroke and acute myocardial infarction. Pharmacotherapy 2007;27:218–20. 10.1592/phco.27.2.218 [DOI] [PubMed] [Google Scholar]
- 18.Jick SS, Kaye JA, Russmann S, Jick H. Risk of nonfatal venous thromboembolism in women using a contraceptive transdermal patch and oral contraceptives containing norgestimate and 35 microg of ethinyl estradiol. Contraception 2006;73:223–8. 10.1016/j.contraception.2006.01.001 [DOI] [PubMed] [Google Scholar]
- 19.Magnusdóttir EM, Bjarnadóttir RI, Onundarson PT, et al. The contraceptive vaginal ring (NuvaRing) and hemostasis: a comparative study. Contraception 2004;69:461–7. 10.1016/j.contraception.2003.12.010 [DOI] [PubMed] [Google Scholar]
- 20.Massai R, Mäkäräinen L, Kuukankorpi A, Klipping C, Duijkers I, Dieben T. The combined contraceptive vaginal ring and bone mineral density in healthy pre-menopausal women. Hum Reprod 2005;20:2764–8. 10.1093/humrep/dei117 [DOI] [PubMed] [Google Scholar]
- 21.Milsom I, Lete I, Bjertnaes A, et al. Effects on cycle control and bodyweight of the combined contraceptive ring, NuvaRing, versus an oral contraceptive containing 30 microg ethinyl estradiol and 3 mg drospirenone. Hum Reprod 2006;21:2304–11. 10.1093/humrep/del162 [DOI] [PubMed] [Google Scholar]
- 22.Oddsson K, Leifels-Fischer B, de Melo NR, et al. Efficacy and safety of a contraceptive vaginal ring (NuvaRing) compared with a combined oral contraceptive: a 1-year randomized trial. Contraception 2005;71:176–82. 10.1016/j.contraception.2004.09.001 [DOI] [PubMed] [Google Scholar]
- 23.Pierson RA, Archer DF, Moreau M, Shangold GA, Fisher AC, Creasy GW. Ortho Evra/Evra versus oral contraceptives: follicular development and ovulation in normal cycles and after an intentional dosing error. Fertil Steril 2003;80:34–42. 10.1016/S0015-0282(03)00556-9 [DOI] [PubMed] [Google Scholar]
- 24.Radowicki S, Skórzewska K, Szlendak K. [Safety evaluation of a transdermal contraceptive system with an oral contraceptive]. Ginekol Pol 2005;76:884–9. [PubMed] [Google Scholar]
- 25.Sabatini R, Cagiano R. Comparison profiles of cycle control, side effects and sexual satisfaction of three hormonal contraceptives. Contraception 2006;74:220–3. 10.1016/j.contraception.2006.03.022 [DOI] [PubMed] [Google Scholar]
- 26.Smallwood GH, Meador ML, Lenihan JP Jr, Shangold GA, Fisher AC, Creasy GW; ORTHO EVRA/EVRA 002 Study Group. Efficacy and safety of a transdermal contraceptive system. Obstet Gynecol 2001;98:799–805. 10.1097/00006250-200111000-00016 [DOI] [PubMed] [Google Scholar]
- 27.Timmer CJ, Mulders TM. Pharmacokinetics of etonogestrel and ethinylestradiol released from a combined contraceptive vaginal ring. Clin Pharmacokinet 2000;39:233–42. 10.2165/00003088-200039030-00005 [DOI] [PubMed] [Google Scholar]
- 28.Tuppurainen M, Klimscheffskij R, Venhola M, Dieben TOM. The combined contraceptive vaginal ring (NuvaRing) and lipid metabolism: a comparative study. Contraception 2004;69:389–94. 10.1016/j.contraception.2004.01.004 [DOI] [PubMed] [Google Scholar]
- 29.Urdl W, Apter D, Alperstein A, et al. ; ORTHO EVRA/EVRA 003 Study Group. Contraceptive efficacy, compliance and beyond: factors related to satisfaction with once-weekly transdermal compared with oral contraception. Eur J Obstet Gynecol Reprod Biol 2005;121:202–10. 10.1016/j.ejogrb.2005.01.021 [DOI] [PubMed] [Google Scholar]
- 30.van den Heuvel MW, van Bragt AJM, Alnabawy AKM, Kaptein MCJ. Comparison of ethinylestradiol pharmacokinetics in three hormonal contraceptive formulations: the vaginal ring, the transdermal patch and an oral contraceptive. Contraception 2005;72:168–74. 10.1016/j.contraception.2005.03.005 [DOI] [PubMed] [Google Scholar]
- 31.Veres S, Miller L, Burington B. A comparison between the vaginal ring and oral contraceptives. Obstet Gynecol 2004;104:555–63. 10.1097/01.AOG.0000136082.59644.13 [DOI] [PubMed] [Google Scholar]
- 32.White T, Ozel B, Jain JK, Stanczyk FZ. Effects of transdermal and oral contraceptives on estrogen-sensitive hepatic proteins. Contraception 2006;74:293–6. 10.1016/j.contraception.2006.04.005 [DOI] [PubMed] [Google Scholar]
- 33.Zieman M, Guillebaud J, Weisberg E, Shangold GA, Fisher AC, Creasy GW. Contraceptive efficacy and cycle control with the Ortho Evra/Evra transdermal system: the analysis of pooled data. Fertil Steril 2002;77(Suppl 2):S13–8. 10.1016/S0015-0282(01)03275-7 [DOI] [PubMed] [Google Scholar]
- 34.Workowski KA, Bachmann LH, Chan PA, et al. Sexually transmitted infections treatment guidelines, 2021. MMWR Recomm Rep 2021;70(No. RR-4):1–187. 10.15585/mmwr.rr7004a1 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 35.CDC. US Public Health Service preexposure prophylaxis for the prevention of HIV infection in the United States—2021 update: a clinical practice guideline. Atlanta, GA: US Department of Health and Human Services, CDC; 2021. https://www.cdc.gov/hiv/pdf/risk/prep/cdc-hiv-prep-guidelines-2021.pdf
- 36.Memon S, Iversen L, Hannaford PC. Is the oral contraceptive pill associated with fracture in later life? New evidence from the Royal College of General Practitioners Oral Contraception Study. Contraception 2011;84:40–7. 10.1016/j.contraception.2010.11.019 [DOI] [PubMed] [Google Scholar]
- 37.Vestergaard P, Rejnmark L, Mosekilde L. Fracture risk in very young women using combined oral contraceptives. Contraception 2008;78:358–64. 10.1016/j.contraception.2008.06.010 [DOI] [PubMed] [Google Scholar]
- 38.Vestergaard P, Rejnmark L, Mosekilde L. Oral contraceptive use and risk of fractures. Contraception 2006;73:571–6. 10.1016/j.contraception.2006.01.006 [DOI] [PubMed] [Google Scholar]
- 39.Barad D, Kooperberg C, Wactawski-Wende J, Liu J, Hendrix SL, Watts NB. Prior oral contraception and postmenopausal fracture: a Women’s Health Initiative observational cohort study. Fertil Steril 2005;84:374–83. 10.1016/j.fertnstert.2005.01.132 [DOI] [PubMed] [Google Scholar]
- 40.Michaëlsson K, Baron JA, Farahmand BY, Ljunghall S. Influence of parity and lactation on hip fracture risk. Am J Epidemiol 2001;153:1166–72. 10.1093/aje/153.12.1166 [DOI] [PubMed] [Google Scholar]
- 41.Michaëlsson K, Baron JA, Farahmand BY, Persson I, Ljunghall S. Oral-contraceptive use and risk of hip fracture: a case-control study. Lancet 1999;353:1481–4. 10.1016/S0140-6736(98)09044-8 [DOI] [PubMed] [Google Scholar]
- 42.La Vecchia C, Tavani A, Gallus S. Oral contraceptives and risk of hip fractures. Lancet 1999;354:335–6. 10.1016/S0140-6736(05)75239-9 [DOI] [PubMed] [Google Scholar]
- 43.Vessey M, Mant J, Painter R. Oral contraception and other factors in relation to hospital referral for fracture. Findings in a large cohort study. Contraception 1998;57:231–5. 10.1016/S0010-7824(98)00026-2 [DOI] [PubMed] [Google Scholar]
- 44.O’Neill TW, Marsden D, Adams JE, Silman AJ. Risk factors, falls, and fracture of the distal forearm in Manchester, UK. J Epidemiol Community Health 1996;50:288–92. 10.1136/jech.50.3.288 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 45.Mallmin H, Ljunghall S, Persson I, Bergström R. Risk factors for fractures of the distal forearm: a population-based case-control study. Osteoporos Int 1994;4:298–304. 10.1007/BF01622186 [DOI] [PubMed] [Google Scholar]
- 46.Cooper C, Hannaford P, Croft P, Kay CR. Oral contraceptive pill use and fractures in women: a prospective study. Bone 1993;14:41–5. 10.1016/8756-3282(93)90254-8 [DOI] [PubMed] [Google Scholar]
- 47.Meier C, Brauchli YB, Jick SS, Kraenzlin ME, Meier CR. Use of depot medroxyprogesterone acetate and fracture risk. J Clin Endocrinol Metab 2010;95:4909–16. 10.1210/jc.2010-0032 [DOI] [PubMed] [Google Scholar]
- 48.Cibula D, Skrenkova J, Hill M, Stepan JJ. Low-dose estrogen combined oral contraceptives may negatively influence physiological bone mineral density acquisition during adolescence. Eur J Endocrinol 2012;166:1003–11. 10.1530/EJE-11-1047 [DOI] [PubMed] [Google Scholar]
- 49.Gai L, Jia Y, Zhang M, et al. Effect of two kinds of different combined oral contraceptives use on bone mineral density in adolescent women. Contraception 2012;86:332–6. 10.1016/j.contraception.2012.01.009 [DOI] [PubMed] [Google Scholar]
- 50.Scholes D, Hubbard RA, Ichikawa LE, et al. Oral contraceptive use and bone density change in adolescent and young adult women: a prospective study of age, hormone dose, and discontinuation. J Clin Endocrinol Metab 2011;96:E1380–7. 10.1210/jc.2010-3027 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 51.Lattakova M, Borovsky M, Payer J, Killinger Z. Oral contraception usage in relation to bone mineral density and bone turnover in adolescent girls. Eur J Contracept Reprod Health Care 2009;14:207–14. 10.1080/13625180902838828 [DOI] [PubMed] [Google Scholar]
- 52.Beksinska ME, Kleinschmidt I, Smit JA, Farley TMM. Bone mineral density in a cohort of adolescents during use of norethisterone enanthate, depot-medroxyprogesterone acetate or combined oral contraceptives and after discontinuation of norethisterone enanthate. Contraception 2009;79:345–9. 10.1016/j.contraception.2008.11.009 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 53.Pikkarainen E, Lehtonen-Veromaa M, Möttönen T, Kautiainen H, Viikari J. Estrogen-progestin contraceptive use during adolescence prevents bone mass acquisition: a 4-year follow-up study. Contraception 2008;78:226–31. 10.1016/j.contraception.2008.05.002 [DOI] [PubMed] [Google Scholar]
- 54.Cromer BA, Bonny AE, Stager M, et al. Bone mineral density in adolescent females using injectable or oral contraceptives: a 24-month prospective study. Fertil Steril 2008;90:2060–7. 10.1016/j.fertnstert.2007.10.070 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 55.Berenson AB, Rahman M, Breitkopf CR, Bi LX. Effects of depot medroxyprogesterone acetate and 20-microgram oral contraceptives on bone mineral density. Obstet Gynecol 2008;112:788–99. 10.1097/AOG.0b013e3181875b78 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 56.Harel Z, Riggs S, Vaz R, Flanagan P, Harel D, Machan JT. Bone accretion in adolescents using the combined estrogen and progestin transdermal contraceptive method Ortho Evra: a pilot study. J Pediatr Adolesc Gynecol 2010;23:23–31. 10.1016/j.jpag.2009.04.008 [DOI] [PubMed] [Google Scholar]
- 57.Cobb KL, Bachrach LK, Sowers M, et al. The effect of oral contraceptives on bone mass and stress fractures in female runners. Med Sci Sports Exerc 2007;39:1464–73. 10.1249/mss.0b013e318074e532 [DOI] [PubMed] [Google Scholar]
- 58.Beksinska ME, Kleinschmidt I, Smit JA, Farley TMM. Bone mineral density in adolescents using norethisterone enanthate, depot-medroxyprogesterone acetate or combined oral contraceptives for contraception. Contraception 2007;75:438–43. 10.1016/j.contraception.2007.02.001 [DOI] [PubMed] [Google Scholar]
- 59.Lara-Torre E, Edwards CP, Perlman S, Hertweck SP. Bone mineral density in adolescent females using depot medroxyprogesterone acetate. J Pediatr Adolesc Gynecol 2004;17:17–21. 10.1016/j.jpag.2003.11.017 [DOI] [PubMed] [Google Scholar]
- 60.Cromer BA, Blair JM, Mahan JD, Zibners L, Naumovski Z. A prospective comparison of bone density in adolescent girls receiving depot medroxyprogesterone acetate (Depo-Provera), levonorgestrel (Norplant), or oral contraceptives. J Pediatr 1996;129:671–6. 10.1016/S0022-3476(96)70148-8 [DOI] [PubMed] [Google Scholar]
- 61.Polatti F, Perotti F, Filippa N, Gallina D, Nappi RE. Bone mass and long-term monophasic oral contraceptive treatment in young women. Contraception 1995;51:221–4. 10.1016/0010-7824(95)00036-A [DOI] [PubMed] [Google Scholar]
- 62.Sørdal T, Grob P, Verhoeven C. Effects on bone mineral density of a monophasic combined oral contraceptive containing nomegestrol acetate/17β-estradiol in comparison to levonorgestrel/ethinylestradiol. Acta Obstet Gynecol Scand 2012;91:1279–85. 10.1111/j.1600-0412.2012.01498.x [DOI] [PubMed] [Google Scholar]
- 63.Gargano V, Massaro M, Morra I, Formisano C, Di Carlo C, Nappi C. Effects of two low-dose combined oral contraceptives containing drospirenone on bone turnover and bone mineral density in young fertile women: a prospective controlled randomized study. Contraception 2008;78:10–5. 10.1016/j.contraception.2008.01.016 [DOI] [PubMed] [Google Scholar]
- 64.Nappi C, Di Spiezio Sardo A, Greco E, Tommaselli GA, Giordano E, Guida M. Effects of an oral contraceptive containing drospirenone on bone turnover and bone mineral density. Obstet Gynecol 2005;105:53–60. 10.1097/01.AOG.0000148344.26475.fc [DOI] [PubMed] [Google Scholar]
- 65.Berenson AB, Radecki CM, Grady JJ, Rickert VI, Thomas A. A prospective, controlled study of the effects of hormonal contraception on bone mineral density. Obstet Gynecol 2001;98:576–82. 10.1016/S0029-7844(01)01495-8 [DOI] [PubMed] [Google Scholar]
- 66.Berenson AB, Breitkopf CR, Grady JJ, Rickert VI, Thomas A. Effects of hormonal contraception on bone mineral density after 24 months of use. Obstet Gynecol 2004;103:899–906. 10.1097/01.AOG.0000117082.49490.d5 [DOI] [PubMed] [Google Scholar]
- 67.Elgán C, Samsioe G, Dykes AK. Influence of smoking and oral contraceptives on bone mineral density and bone remodeling in young women: a 2-year study. Contraception 2003;67:439–47. 10.1016/S0010-7824(03)00048-9 [DOI] [PubMed] [Google Scholar]
- 68.Elgán C, Dykes AK, Samsioe G. Bone mineral density changes in young women: a two year study. Gynecol Endocrinol 2004;19:169–77. 10.1080/09513590400012119 [DOI] [PubMed] [Google Scholar]
- 69.Endrikat J, Mih E, Düsterberg B, et al. A 3-year double-blind, randomized, controlled study on the influence of two oral contraceptives containing either 20 microg or 30 microg ethinylestradiol in combination with levonorgestrel on bone mineral density. Contraception 2004;69:179–87. 10.1016/j.contraception.2003.10.002 [DOI] [PubMed] [Google Scholar]
- 70.Paoletti AM, Orrù M, Lello S, et al. Short-term variations in bone remodeling markers of an oral contraception formulation containing 3 mg of drospirenone plus 30 microg of ethinyl estradiol: observational study in young postadolescent women. Contraception 2004;70:293–8. 10.1016/j.contraception.2004.04.004 [DOI] [PubMed] [Google Scholar]
- 71.Nappi C, Di Spiezio Sardo A, Acunzo G, et al. Effects of a low-dose and ultra-low-dose combined oral contraceptive use on bone turnover and bone mineral density in young fertile women: a prospective controlled randomized study. Contraception 2003;67:355–9. 10.1016/S0010-7824(03)00025-8 [DOI] [PubMed] [Google Scholar]
- 72.Reed SD, Scholes D, LaCroix AZ, Ichikawa LE, Barlow WE, Ott SM. Longitudinal changes in bone density in relation to oral contraceptive use. Contraception 2003;68:177–82. 10.1016/S0010-7824(03)00147-1 [DOI] [PubMed] [Google Scholar]
- 73.Cobb KL, Kelsey JL, Sidney S, Ettinger B, Lewis CE. Oral contraceptives and bone mineral density in white and black women in CARDIA. Coronary Risk Development in Young Adults. Osteoporos Int 2002;13:893–900. 10.1007/s001980200123 [DOI] [PubMed] [Google Scholar]
- 74.Burr DB, Yoshikawa T, Teegarden D, et al. Exercise and oral contraceptive use suppress the normal age-related increase in bone mass and strength of the femoral neck in women 18–31 years of age. Bone 2000;27:855–63. 10.1016/S8756-3282(00)00403-8 [DOI] [PubMed] [Google Scholar]
- 75.Recker RR, Davies KM, Hinders SM, Heaney RP, Stegman MR, Kimmel DB. Bone gain in young adult women. JAMA 1992;268:2403–8. 10.1001/jama.1992.03490170075028 [DOI] [PubMed] [Google Scholar]
- 76.Mazess RB, Barden HS. Bone density in premenopausal women: effects of age, dietary intake, physical activity, smoking, and birth-control pills. Am J Clin Nutr 1991;53:132–42. 10.1093/ajcn/53.1.132 [DOI] [PubMed] [Google Scholar]
- 77.Gambacciani M, Cappagli B, Lazzarini V, Ciaponi M, Fruzzetti F, Genazzani AR. Longitudinal evaluation of perimenopausal bone loss: effects of different low dose oral contraceptive preparations on bone mineral density. Maturitas 2006;54:176–80. 10.1016/j.maturitas.2005.10.007 [DOI] [PubMed] [Google Scholar]
- 78.Gambacciani M, Spinetti A, Taponeco F, Cappagli B, Piaggesi L, Fioretti P. Longitudinal evaluation of perimenopausal vertebral bone loss: effects of a low-dose oral contraceptive preparation on bone mineral density and metabolism. Obstet Gynecol 1994;83:392–6. [PubMed] [Google Scholar]
- 79.Gambacciani M, Spinetti A, Cappagli B, et al. Hormone replacement therapy in perimenopausal women with a low dose oral contraceptive preparation: effects on bone mineral density and metabolism. Maturitas 1994;19:125–31. 10.1016/0378-5122(94)90062-0 [DOI] [PubMed] [Google Scholar]
- 80.Gambacciani M, Cappagli B, Ciaponi M, Benussi C, Genazzani AR. Hormone replacement therapy in perimenopause: effect of a low dose oral contraceptive preparation on bone quantitative ultrasound characteristics. Menopause 1999;6:43–8. 10.1097/00042192-199906010-00009 [DOI] [PubMed] [Google Scholar]
- 81.Volpe A, Malmusi S, Zanni AL, Landi S, Cagnacci A. Oral contraceptives and bone metabolism. Eur J Contracept Reprod Health Care 1997;2:225–8. 10.3109/13625189709165298 [DOI] [PubMed] [Google Scholar]
- 82.Hansen MA, Overgaard K, Riis BJ, Christiansen C. Potential risk factors for development of postmenopausal osteoporosis—examined over a 12-year period. Osteoporos Int 1991;1:95–102. 10.1007/BF01880450 [DOI] [PubMed] [Google Scholar]
- 83.Shargil AA. Hormone replacement therapy in perimenopausal women with a triphasic contraceptive compound: a three-year prospective study. Int J Fertil 1985;30:15–18–28, 18–28. [PubMed] [Google Scholar]
- 84.Taechakraichana N, Limpaphayom K, Ninlagarn T, Panyakhamlerd K, Chaikittisilpa S, Dusitsin N. A randomized trial of oral contraceptive and hormone replacement therapy on bone mineral density and coronary heart disease risk factors in postmenopausal women. Obstet Gynecol 2000;95:87–94. [DOI] [PubMed] [Google Scholar]
- 85.Taechakraichana N, Jaisamrarn U, Panyakhamlerd K, Chaikittisilpa S, Limpaphayom K. Difference in bone acquisition among hormonally treated postmenopausal women with normal and low bone mass. J Med Assoc Thai 2001;84(Suppl 2):S586–92. [PubMed] [Google Scholar]
- 86.Grimes DA, Schulz KF. Surrogate end points in clinical research: hazardous to your health. Obstet Gynecol 2005;105:1114–8. 10.1097/01.AOG.0000157445.67309.19 [DOI] [PubMed] [Google Scholar]
- 87.Schönau E. The peak bone mass concept: is it still relevant? Pediatr Nephrol 2004;19:825–31. 10.1007/s00467-004-1465-5 [DOI] [PubMed] [Google Scholar]
- 88.Cohen A, Shane E. Treatment of premenopausal women with low bone mineral density. Curr Osteoporos Rep 2008;6:39–46. 10.1007/s11914-008-0007-7 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 89.US Department of Agriculture; US Department of Health and Human Services. Dietary guidelines for Americans, 2020–2025. 9th ed. Washington, DC: US Department of Agriculture and US Department of Health and Human Services; 2020. https://www.dietaryguidelines.gov/sites/default/files/2021-03/Dietary_Guidelines_for_Americans-2020-2025.pdf
- 90.Meek JY, Noble L; Section on Breastfeeding. Policy statement: breastfeeding and the use of human milk. Pediatrics 2022;150:e2022057988. 10.1542/peds.2022-057988 [DOI] [PubMed] [Google Scholar]
- 91.Tepper NK, Phillips SJ, Kapp N, Gaffield ME, Curtis KM. Combined hormonal contraceptive use among breastfeeding women: an updated systematic review. Contraception 2016;94:262–74. 10.1016/j.contraception.2015.05.006 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 92.Petersen JF, Bergholt T, Nielsen AK, Paidas MJ, Løkkegaard EC. Combined hormonal contraception and risk of venous thromboembolism within the first year following pregnancy. Danish nationwide historical cohort 1995–2009. Thromb Haemost 2014;112:73–8. 10.1160/TH13-09-0797 [DOI] [PubMed] [Google Scholar]
- 93.Jackson E, Curtis KM, Gaffield ME. Risk of venous thromboembolism during the postpartum period: a systematic review. Obstet Gynecol 2011;117:691–703. 10.1097/AOG.0b013e31820ce2db [DOI] [PubMed] [Google Scholar]
- 94.Kamel H, Navi BB, Sriram N, Hovsepian DA, Devereux RB, Elkind MS. Risk of a thrombotic event after the 6-week postpartum period. N Engl J Med 2014;370:1307–15. 10.1056/NEJMoa1311485 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 95.Sultan AA, Tata LJ, West J, et al. Risk factors for first venous thromboembolism around pregnancy: a population-based cohort study from the United Kingdom. Blood 2013;121:3953–61. 10.1182/blood-2012-11-469551 [DOI] [PubMed] [Google Scholar]
- 96.Sultan AA, West J, Tata LJ, Fleming KM, Nelson-Piercy C, Grainge MJ. Risk of first venous thromboembolism in and around pregnancy: a population-based cohort study. Br J Haematol 2012;156:366–73. 10.1111/j.1365-2141.2011.08956.x [DOI] [PubMed] [Google Scholar]
- 97.Tepper NK, Boulet SL, Whiteman MK, et al. Postpartum venous thromboembolism: incidence and risk factors. Obstet Gynecol 2014;123:987–96. 10.1097/AOG.0000000000000230 [DOI] [PubMed] [Google Scholar]
- 98.Jackson E, Glasier A. Return of ovulation and menses in postpartum nonlactating women: a systematic review. Obstet Gynecol 2011;117:657–62. 10.1097/AOG.0b013e31820ce18c [DOI] [PubMed] [Google Scholar]
- 99.Kim C, Nguyen AT, Berry-Bibee E, Ermias Y, Gaffield ME, Kapp N. Systemic hormonal contraception initiation after abortion: a systematic review and meta-analysis. Contraception 2021;103:291–304. 10.1016/j.contraception.2021.01.017 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 100.Gaffield ME, Kapp N, Ravi A. Use of combined oral contraceptives post abortion. Contraception 2009;80:355–62. 10.1016/j.contraception.2009.04.005 [DOI] [PubMed] [Google Scholar]
- 101.Gillum LA, Mamidipudi SK, Johnston SC. Ischemic stroke risk with oral contraceptives: A meta-analysis. JAMA 2000;284:72–8. 10.1001/jama.284.1.72 [DOI] [PubMed] [Google Scholar]
- 102.Jick SS, Walker AM, Stergachis A, Jick H. Oral contraceptives and breast cancer. Br J Cancer 1989;59:618–21. 10.1038/bjc.1989.125 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 103.Khader YS, Rice J, John L, Abueita O. Oral contraceptives use and the risk of myocardial infarction: a meta-analysis. Contraception 2003;68:11–7. 10.1016/S0010-7824(03)00073-8 [DOI] [PubMed] [Google Scholar]
- 104.Lawson DH, Davidson JF, Jick H. Oral contraceptive use and venous thromboembolism: absence of an effect of smoking. BMJ 1977;2:729–30. 10.1136/bmj.2.6089.729 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 105.Lidegaard O, Edström B, Kreiner S. Oral contraceptives and venous thromboembolism. A case-control study. Contraception 1998;57:291–301. 10.1016/S0010-7824(98)00033-X [DOI] [PubMed] [Google Scholar]
- 106.Nightingale AL, Lawrenson RA, Simpson EL, Williams TJ, MacRae KD, Farmer RD. The effects of age, body mass index, smoking and general health on the risk of venous thromboembolism in users of combined oral contraceptives. Eur J Contracept Reprod Health Care 2000;5:265–74. 10.1080/13625180008500402 [DOI] [PubMed] [Google Scholar]
- 107.Petitti DB, Wingerd J, Pellegrin F, Ramcharan S. Risk of vascular disease in women. Smoking, oral contraceptives, noncontraceptive estrogens, and other factors. JAMA 1979;242:1150–4. 10.1001/jama.1979.03300110022020 [DOI] [PubMed] [Google Scholar]
- 108.Rosenberg L, Palmer JR, Rao RS, Shapiro S. Low-dose oral contraceptive use and the risk of myocardial infarction. Arch Intern Med 2001;161:1065–70. 10.1001/archinte.161.8.1065 [DOI] [PubMed] [Google Scholar]
- 109.Straneva P, Hinderliter A, Wells E, Lenahan H, Girdler S. Smoking, oral contraceptives, and cardiovascular reactivity to stress. Obstet Gynecol 2000;95:78–83. 10.1016/S0029-7844(99)00497-4 [DOI] [PubMed] [Google Scholar]
- 110.Tanis BC, van den Bosch MA, Kemmeren JM, et al. Oral contraceptives and the risk of myocardial infarction. N Engl J Med 2001;345:1787–93. 10.1056/NEJMoa003216 [DOI] [PubMed] [Google Scholar]
- 111.Van den bosch MAAJ, Kemmeren JM, Tanis BC, et al. The RATIO study: oral contraceptives and the risk of peripheral arterial disease in young women. J Thromb Hemost 2003;1:439–44. 10.1046/j.1538-7836.2003.00079.x [DOI] [PubMed] [Google Scholar]
- 112.World Health Organization Collaborative Study of Cardiovascular Disease and Steroid Hormone Contraception. Venous thromboembolic disease and combined oral contraceptives: results of international multicentre case-control study. Lancet 1995;346:1575–82. 10.1016/S0140-6736(95)91926-0 [DOI] [PubMed] [Google Scholar]
- 113.Collaborative Group for the Study of Stroke in Young Women. Oral contraceptives and stroke in young women. Associated risk factors. JAMA 1975;231:718–22. 10.1001/jama.1975.03240190022010 [DOI] [PubMed] [Google Scholar]
- 114.Horton LG, Simmons KB, Curtis KM. Combined hormonal contraceptive use among obese women and risk for cardiovascular events: a systematic review. Contraception 2016;94:590–604. 10.1016/j.contraception.2016.05.014 [DOI] [PubMed] [Google Scholar]
- 115.Schink T, Princk C, Braitmaier M, Haug U. Use of combined oral contraceptives and risk of venous thromboembolism in young women: a nested case-control analysis using German claims data. BJOG 2022;129:2107–16. 10.1111/1471-0528.17268 [DOI] [PubMed] [Google Scholar]
- 116.Traven SA, McGurk KM, Althoff AD, et al. Resident level involvement affects operative time and surgical complications in lower extremity fracture care. J Surg Educ 2021;78:1755–61. 10.1016/j.jsurg.2021.03.004 [DOI] [PubMed] [Google Scholar]
- 117.Brunner Huber LR, Hogue CJ, Stein AD, Drews C, Zieman M. Body mass index and risk for oral contraceptive failure: a case-cohort study in South Carolina. Ann Epidemiol 2006;16:637–43. 10.1016/j.annepidem.2006.01.001 [DOI] [PubMed] [Google Scholar]
- 118.Brunner Huber LR, Toth JL. Obesity and oral contraceptive failure: findings from the 2002 National Survey of Family Growth. Am J Epidemiol 2007;166:1306–11. 10.1093/aje/kwm221 [DOI] [PubMed] [Google Scholar]
- 119.Brunner LR, Hogue CJ. The role of body weight in oral contraceptive failure: results from the 1995 national survey of family growth. Ann Epidemiol 2005;15:492–9. 10.1016/j.annepidem.2004.10.009 [DOI] [PubMed] [Google Scholar]
- 120.Holt VL, Cushing-Haugen KL, Daling JR. Body weight and risk of oral contraceptive failure. Obstet Gynecol 2002;99:820–7. 10.1016/S0029-7844(02)01939-7 [DOI] [PubMed] [Google Scholar]
- 121.Holt VL, Scholes D, Wicklund KG, Cushing-Haugen KL, Daling JR. Body mass index, weight, and oral contraceptive failure risk. Obstet Gynecol 2005;105:46–52. 10.1097/01.AOG.0000149155.11912.52 [DOI] [PubMed] [Google Scholar]
- 122.Trussell J, Schwarz EB, Guthrie K. Obesity and oral contraceptive pill failure. Contraception 2009;79:334–8. 10.1016/j.contraception.2008.11.017 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 123.Vessey M. Oral contraceptive failures and body weight: findings in a large cohort study. J Fam Plann Reprod Health Care 2001;27:90–1. 10.1783/147118901101195092 [DOI] [PubMed] [Google Scholar]
- 124.Yamazaki M, Dwyer K, Sobhan M, et al. Effect of obesity on the effectiveness of hormonal contraceptives: an individual participant data meta-analysis. Contraception 2015;92:445–52. 10.1016/j.contraception.2015.07.016 [DOI] [PubMed] [Google Scholar]
- 125.Dragoman MV, Simmons KB, Paulen ME, Curtis KM. Combined hormonal contraceptive (CHC) use among obese women and contraceptive effectiveness: a systematic review. Contraception 2017;95:117–29. 10.1016/j.contraception.2016.10.010 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 126.Paulen ME, Zapata LB, Cansino C, Curtis KM, Jamieson DJ. Contraceptive use among women with a history of bariatric surgery: a systematic review. Contraception 2010;82:86–94. 10.1016/j.contraception.2010.02.008 [DOI] [PubMed] [Google Scholar]
- 127.Curtis KM, Nguyen AT, Tepper NK, et al. U.S. selected practice recommendations for contraceptive use, 2024. MMWR Recomm Rep 2024;73(No. RR-3):1–77. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 128.Lidegaard Ø, Edström B, Kreiner S. Oral contraceptives and venous thromboembolism: a five-year national case-control study. Contraception 2002;65:187–96. 10.1016/S0010-7824(01)00307-9 [DOI] [PubMed] [Google Scholar]
- 129.Croft P, Hannaford PC. Risk factors for acute myocardial infarction in women: evidence from the Royal College of General Practitioners’ oral contraception study. BMJ 1989;298:165–8. 10.1136/bmj.298.6667.165 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 130.D’Avanzo B, La Vecchia C, Negri E, Parazzini F, Franceschi S. Oral contraceptive use and risk of myocardial infarction: an Italian case-control study. J Epidemiol Community Health 1994;48:324–5. 10.1136/jech.48.3.324 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 131.Dunn NR, Faragher B, Thorogood M, et al. Risk of myocardial infarction in young female smokers. Heart 1999;82:581–3. 10.1136/hrt.82.5.581 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 132.Hannaford PC, Croft PR, Kay CR. Oral contraception and stroke. Evidence from the Royal College of General Practitioners’ Oral Contraception Study. Stroke 1994;25:935–42. 10.1161/01.STR.25.5.935 [DOI] [PubMed] [Google Scholar]
- 133.Heinemann LA, Lewis MA, Spitzer WO, Thorogood M, Guggenmoos-Holzmann I, Bruppacher R; Transnational Research Group on Oral Contraceptives and the Health of Young Women. Thromboembolic stroke in young women. A European case-control study on oral contraceptives. Contraception 1998;57:29–37. 10.1016/S0010-7824(97)00204-7 [DOI] [PubMed] [Google Scholar]
- 134.Kemmeren JM, Tanis BC, van den Bosch MA, et al. Risk of Arterial Thrombosis in Relation to Oral Contraceptives (RATIO) study: oral contraceptives and the risk of ischemic stroke. Stroke 2002;33:1202–8. 10.1161/01.STR.0000015345.61324.3F [DOI] [PubMed] [Google Scholar]
- 135.Lewis MA, Heinemann LA, Spitzer WO, MacRae KD, Bruppacher R. The use of oral contraceptives and the occurrence of acute myocardial infarction in young women. Results from the Transnational Study on Oral Contraceptives and the Health of Young Women. Contraception 1997;56:129–40. 10.1016/S0010-7824(97)00118-2 [DOI] [PubMed] [Google Scholar]
- 136.Lidegaard O. Oral contraception and risk of a cerebral thromboembolic attack: results of a case-control study. BMJ 1993;306:956–63. 10.1136/bmj.306.6883.956 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 137.Lidegaard O. Oral contraceptives, pregnancy and the risk of cerebral thromboembolism: the influence of diabetes, hypertension, migraine and previous thrombotic disease. Br J Obstet Gynaecol 1995;102:153–9. 10.1111/j.1471-0528.1995.tb09070.x [DOI] [PubMed] [Google Scholar]
- 138.Lubianca JN, Faccin CS, Fuchs FD. Oral contraceptives: a risk factor for uncontrolled blood pressure among hypertensive women. Contraception 2003;67:19–24. 10.1016/S0010-7824(02)00429-8 [DOI] [PubMed] [Google Scholar]
- 139.Narkiewicz K, Graniero GR, D’Este D, Mattarei M, Zonzin P, Palatini P. Ambulatory blood pressure in mild hypertensive women taking oral contraceptives. A case-control study. Am J Hypertens 1995;8:249–53. 10.1016/0895-7061(95)96212-3 [DOI] [PubMed] [Google Scholar]
- 140.Siritho S, Thrift AG, McNeil JJ, You RX, Davis SM, Donnan GA; Melbourne Risk Factor Study (MERFS) Group. Risk of ischemic stroke among users of the oral contraceptive pill: The Melbourne Risk Factor Study (MERFS) Group. Stroke 2003;34:1575–80. 10.1161/01.STR.0000077925.16041.6B [DOI] [PubMed] [Google Scholar]
- 141.WHO Collaborative Study of Cardiovascular Disease and Steroid Hormone Contraception. Ischaemic stroke and combined oral contraceptives: results of an international, multicentre, case-control study. Lancet 1996;348:498–505. 10.1016/S0140-6736(95)12393-8 [DOI] [PubMed] [Google Scholar]
- 142.WHO Collaborative Study of Cardiovascular Disease and Steroid Hormone Contraception. Acute myocardial infarction and combined oral contraceptives: results of an international multicentre case-control study. Lancet 1997;349:1202–9. 10.1016/S0140-6736(97)02358-1 [DOI] [PubMed] [Google Scholar]
- 143.Lubianca JN, Moreira LB, Gus M, Fuchs FD. Stopping oral contraceptives: an effective blood pressure-lowering intervention in women with hypertension. J Hum Hypertens 2005;19:451–5. 10.1038/sj.jhh.1001841 [DOI] [PubMed] [Google Scholar]
- 144.Aberg H, Karlsson L, Melander S. Studies on toxaemia of pregnancy with special reference to blood pressure. II. Results after 6-11 years’ follow-up. Ups J Med Sci 1978;83:97–102. 10.3109/03009737809179119 [DOI] [PubMed] [Google Scholar]
- 145.Carmichael SM, Taylor MM, Ayers CR. Oral contraceptives, hypertension, and toxemia. Obstet Gynecol 1970;35:371–6. [PubMed] [Google Scholar]
- 146.Meinel H, Ihle R, Laschinski M. [Effect of hormonal contraceptives on blood pressure following pregnancy-induced hypertension]. Zentralbl Gynakol 1987;109:527–31. [PubMed] [Google Scholar]
- 147.Pritchard JA, Pritchard SA. Blood pressure response to estrogen-progestin oral contraceptive after pregnancy-induced hypertension. Am J Obstet Gynecol 1977;129:733–9. 10.1016/0002-9378(77)90390-8 [DOI] [PubMed] [Google Scholar]
- 148.Sibai BM, Taslimi MM, el-Nazer A, Amon E, Mabie BC, Ryan GM. Maternal-perinatal outcome associated with the syndrome of hemolysis, elevated liver enzymes, and low platelets in severe preeclampsia-eclampsia. Am J Obstet Gynecol 1986;155:501–9. 10.1016/0002-9378(86)90266-8 [DOI] [PubMed] [Google Scholar]
- 149.Sibai BM, Ramadan MK, Chari RS, Friedman SA. Pregnancies complicated by HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets): subsequent pregnancy outcome and long-term prognosis. Am J Obstet Gynecol 1995;172:125–9. 10.1016/0002-9378(95)90099-3 [DOI] [PubMed] [Google Scholar]
- 150.WHO Collaborative Study of Cardiovascular Disease and Steroid Hormone Contraception. Haemorrhagic stroke, overall stroke risk, and combined oral contraceptives: results of an international, multicentre, case-control study. Lancet 1996;348:505–10. 10.1016/S0140-6736(95)12394-6 [DOI] [PubMed] [Google Scholar]
- 151.Martinelli I, Lensing AW, Middeldorp S, et al. Recurrent venous thromboembolism and abnormal uterine bleeding with anticoagulant and hormone therapy use. Blood 2016;127:1417–25. 10.1182/blood-2015-08-665927 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 152.Barbhaiya M, Zuily S, Naden R, et al. ; ACR/EULAR APS Classification Criteria Collaborators. The 2023 ACR/EULAR Antiphospholipid Syndrome Classification Criteria. Arthritis Rheumatol 2023;75:1687–702. 10.1002/art.42624 [DOI] [PubMed] [Google Scholar]
- 153.Tepper NK, Marchbanks PA, Curtis KM. Superficial venous disease and combined hormonal contraceptives: a systematic review. Contraception 2016;94:275–9. 10.1016/j.contraception.2015.03.010 [DOI] [PubMed] [Google Scholar]
- 154.Tepper NK, Paulen ME, Marchbanks PA, Curtis KM. Safety of contraceptive use among women with peripartum cardiomyopathy: a systematic review. Contraception 2010;82:95–101. 10.1016/j.contraception.2010.02.004 [DOI] [PubMed] [Google Scholar]
- 155.The Criteria Committee of the New York Heart Association. Nomenclature and criteria for diagnosis of diseases of the heart and great vessels. 9th ed. Boston, MA: Little, Brown and Co; 1994. [Google Scholar]
- 156.Molnar AO, Bota SE, McArthur E, et al. Risk and complications of venous thromboembolism in dialysis patients. Nephrol Dial Transplant 2018;33:874–80. 10.1093/ndt/gfx212 [DOI] [PubMed] [Google Scholar]
- 157.Tveit DP, Hypolite IO, Hshieh P, et al. Chronic dialysis patients have high risk for pulmonary embolism. Am J Kidney Dis 2002;39:1011–7. 10.1053/ajkd.2002.32774 [DOI] [PubMed] [Google Scholar]
- 158.Wang IK, Shen TC, Muo CH, Yen TH, Sung FC. Risk of pulmonary embolism in patients with end-stage renal disease receiving long-term dialysis. Nephrol Dial Transplant 2017;32:1386–93. [DOI] [PubMed] [Google Scholar]
- 159.Bernatsky S, Clarke A, Ramsey-Goldman R, et al. Hormonal exposures and breast cancer in a sample of women with systemic lupus erythematosus. Rheumatology (Oxford) 2004;43:1178–81. 10.1093/rheumatology/keh282 [DOI] [PubMed] [Google Scholar]
- 160.Bernatsky S, Ramsey-Goldman R, Gordon C, et al. Factors associated with abnormal Pap results in systemic lupus erythematosus. Rheumatology (Oxford) 2004;43:1386–9. 10.1093/rheumatology/keh331 [DOI] [PubMed] [Google Scholar]
- 161.Chopra N, Koren S, Greer WL, et al. Factor V Leiden, prothrombin gene mutation, and thrombosis risk in patients with antiphospholipid antibodies. J Rheumatol 2002;29:1683–8. [PubMed] [Google Scholar]
- 162.Esdaile JM, Abrahamowicz M, Grodzicky T, et al. Traditional Framingham risk factors fail to fully account for accelerated atherosclerosis in systemic lupus erythematosus. Arthritis Rheum 2001;44:2331–7. [DOI] [PubMed] [Google Scholar]
- 163.Julkunen HA. Oral contraceptives in systemic lupus erythematosus: side-effects and influence on the activity of SLE. Scand J Rheumatol 1991;20:427–33. 10.3109/03009749109096822 [DOI] [PubMed] [Google Scholar]
- 164.Julkunen HA, Kaaja R, Friman C. Contraceptive practice in women with systemic lupus erythematosus. Br J Rheumatol 1993;32:227–30. 10.1093/rheumatology/32.3.227 [DOI] [PubMed] [Google Scholar]
- 165.Jungers P, Dougados M, Pélissier C, et al. Influence of oral contraceptive therapy on the activity of systemic lupus erythematosus. Arthritis Rheum 1982;25:618–23. 10.1002/art.1780250603 [DOI] [PubMed] [Google Scholar]
- 166.Manzi S, Meilahn EN, Rairie JE, et al. Age-specific incidence rates of myocardial infarction and angina in women with systemic lupus erythematosus: comparison with the Framingham Study. Am J Epidemiol 1997;145:408–15. 10.1093/oxfordjournals.aje.a009122 [DOI] [PubMed] [Google Scholar]
- 167.McAlindon T, Giannotta L, Taub N, D’Cruz D, Hughes G. Environmental factors predicting nephritis in systemic lupus erythematosus. Ann Rheum Dis 1993;52:720–4. 10.1136/ard.52.10.720 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 168.McDonald J, Stewart J, Urowitz MB, Gladman DD. Peripheral vascular disease in patients with systemic lupus erythematosus. Ann Rheum Dis 1992;51:56–60. 10.1136/ard.51.1.56 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 169.Mintz G, Gutiérrez G, Delezé M, Rodríguez E. Contraception with progestagens in systemic lupus erythematosus. Contraception 1984;30:29–38. 10.1016/0010-7824(84)90076-3 [DOI] [PubMed] [Google Scholar]
- 170.Petri M. Musculoskeletal complications of systemic lupus erythematosus in the Hopkins Lupus Cohort: an update. Arthritis Care Res 1995;8:137–45. 10.1002/art.1790080305 [DOI] [PubMed] [Google Scholar]
- 171.Petri M. Lupus in Baltimore: evidence-based ‘clinical pearls’ from the Hopkins Lupus Cohort. Lupus 2005;14:970–3. 10.1191/0961203305lu2230xx [DOI] [PubMed] [Google Scholar]
- 172.Petri M, Kim MY, Kalunian KC, et al. ; OC-SELENA Trial. Combined oral contraceptives in women with systemic lupus erythematosus. N Engl J Med 2005;353:2550–8. 10.1056/NEJMoa051135 [DOI] [PubMed] [Google Scholar]
- 173.Sánchez-Guerrero J, Uribe AG, Jiménez-Santana L, et al. A trial of contraceptive methods in women with systemic lupus erythematosus. N Engl J Med 2005;353:2539–49. 10.1056/NEJMoa050817 [DOI] [PubMed] [Google Scholar]
- 174.Sarabi ZS, Chang E, Bobba R, et al. Incidence rates of arterial and venous thrombosis after diagnosis of systemic lupus erythematosus. Arthritis Rheum 2005;53:609–12. 10.1002/art.21314 [DOI] [PubMed] [Google Scholar]
- 175.Schaedel ZE, Dolan G, Powell MC. The use of the levonorgestrel-releasing intrauterine system in the management of menorrhagia in women with hemostatic disorders. Am J Obstet Gynecol 2005;193:1361–3. 10.1016/j.ajog.2005.05.002 [DOI] [PubMed] [Google Scholar]
- 176.Somers E, Magder LS, Petri M. Antiphospholipid antibodies and incidence of venous thrombosis in a cohort of patients with systemic lupus erythematosus. J Rheumatol 2002;29:2531–6. [PubMed] [Google Scholar]
- 177.Urowitz MB, Bookman AA, Koehler BE, Gordon DA, Smythe HA, Ogryzlo MA. The bimodal mortality pattern of systemic lupus erythematosus. Am J Med 1976;60:221–5. 10.1016/0002-9343(76)90431-9 [DOI] [PubMed] [Google Scholar]
- 178.Choojitarom K, Verasertniyom O, Totemchokchyakarn K, Nantiruj K, Sumethkul V, Janwityanujit S. Lupus nephritis and Raynaud’s phenomenon are significant risk factors for vascular thrombosis in SLE patients with positive antiphospholipid antibodies. Clin Rheumatol 2008;27:345–51. 10.1007/s10067-007-0721-z [DOI] [PubMed] [Google Scholar]
- 179.Wahl DG, Guillemin F, de Maistre E, Perret C, Lecompte T, Thibaut G. Risk for venous thrombosis related to antiphospholipid antibodies in systemic lupus erythematosus—a meta-analysis. Lupus 1997;6:467–73. 10.1177/096120339700600510 [DOI] [PubMed] [Google Scholar]
- 180.Farr SL, Folger SG, Paulen ME, Curtis KM. Safety of contraceptive methods for women with rheumatoid arthritis: a systematic review. Contraception 2010;82:64–71. 10.1016/j.contraception.2010.02.003 [DOI] [PubMed] [Google Scholar]
- 181.Headache Classification Committee of the International Headache Society (IHS). The International Classification of Headache Disorders. 3rd edition. Cephalalgia 2018;38:1–211. https://www.ichd-3.org/wp-content/uploads/2018/01/The-International-Classification-of-Headache-Disorders-3rd-Edition-2018.pdf [DOI] [PubMed] [Google Scholar]
- 182.Tepper NK, Whiteman MK, Zapata LB, Marchbanks PA, Curtis KM. Safety of hormonal contraceptives among women with migraine: a systematic review. Contraception 2016;94:630–40. 10.1016/j.contraception.2016.04.016 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 183.Xu Z, Li Y, Tang S, Huang X, Chen T. Current use of oral contraceptives and the risk of first-ever ischemic stroke: a meta-analysis of observational studies. Thromb Res 2015;136:52–60. 10.1016/j.thromres.2015.04.021 [DOI] [PubMed] [Google Scholar]
- 184.Etminan M, Takkouche B, Isorna FC, Samii A. Risk of ischaemic stroke in people with migraine: systematic review and meta-analysis of observational studies. BMJ 2005;330:63. 10.1136/bmj.38302.504063.8F [DOI] [PMC free article] [PubMed] [Google Scholar]
- 185.Schürks M, Rist PM, Bigal ME, Buring JE, Lipton RB, Kurth T. Migraine and cardiovascular disease: systematic review and meta-analysis. BMJ 2009;339(oct27 1):b3914. 10.1136/bmj.b3914 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 186.Spector JT, Kahn SR, Jones MR, Jayakumar M, Dalal D, Nazarian S. Migraine headache and ischemic stroke risk: an updated meta-analysis. Am J Med 2010;123:612–24. 10.1016/j.amjmed.2009.12.021 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 187.Zapata LB, Oduyebo T, Whiteman MK, Houtchens MK, Marchbanks PA, Curtis KM. Contraceptive use among women with multiple sclerosis: a systematic review. Contraception 2016;94:612–20. 10.1016/j.contraception.2016.07.013 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 188.Pagano HP, Zapata LB, Berry-Bibee EN, Nanda K, Curtis KM. Safety of hormonal contraception and intrauterine devices among women with depressive and bipolar disorders: a systematic review. Contraception 2016;94:641–9. 10.1016/j.contraception.2016.06.012 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 189.Iyer V, Farquhar C, Jepson R. Oral contraceptive pills for heavy menstrual bleeding. Cochrane Database Syst Rev 2000;(2):CD000154. 10.1002/14651858.CD000154 [DOI] [PubMed] [Google Scholar]
- 190.Davis L, Kennedy SS, Moore J, Prentice A. Oral contraceptives for pain associated with endometriosis. Cochrane Database Syst Rev 2007;(3):CD001019. 10.1002/14651858.CD001019.pub2 [DOI] [PubMed] [Google Scholar]
- 191.Hendrix SL, Alexander NJ. Primary dysmenorrhea treatment with a desogestrel-containing low-dose oral contraceptive. Contraception 2002;66:393–9. 10.1016/S0010-7824(02)00414-6 [DOI] [PubMed] [Google Scholar]
- 192.Wong CL, Farquhar C, Roberts H. Oral contraceptive pills for primary dysmenorrhoea. Cochrane Database Syst Rev 2001;(2). 10.1002/14651858.CD002120.pub3 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 193.Gaffield ME, Kapp N, Curtis KM. Combined oral contraceptive and intrauterine device use among women with gestational trophoblastic disease. Contraception 2009;80:363–71. 10.1016/j.contraception.2009.03.022 [DOI] [PubMed] [Google Scholar]
- 194.Smith JS, Green J, Berrington de Gonzalez A, et al. Cervical cancer and use of hormonal contraceptives: a systematic review. Lancet 2003;361:1159–67. 10.1016/S0140-6736(03)12949-2 [DOI] [PubMed] [Google Scholar]
- 195.Black MM, Barclay THC, Polednak A, Kwon CS, Leis HP Jr, Pilnik S. Family history, oral contraceptive usage, and breast cancer. Cancer 1983;51:2147–51. [DOI] [PubMed] [Google Scholar]
- 196.Brinton LA, Hoover R, Szklo M, Fraumeni JF Jr. Oral contraceptives and breast cancer. Int J Epidemiol 1982;11:316–22. 10.1093/ije/11.4.316 [DOI] [PubMed] [Google Scholar]
- 197.Brohet RM, Goldgar DE, Easton DF, et al. Oral contraceptives and breast cancer risk in the international BRCA1/2 carrier cohort study: a report from EMBRACE, GENEPSO, GEO-HEBON, and the IBCCS Collaborating Group. J Clin Oncol 2007;25:3831–6. 10.1200/JCO.2007.11.1179 [DOI] [PubMed] [Google Scholar]
- 198.Claus EB, Stowe M, Carter D. Oral contraceptives and the risk of ductal breast carcinoma in situ. Breast Cancer Res Treat 2003;81:129–36. 10.1023/A:1025728524310 [DOI] [PubMed] [Google Scholar]
- 199.Collaborative Group on Hormonal Factors in Breast Cancer. Familial breast cancer: collaborative reanalysis of individual data from 52 epidemiological studies including 58,209 women with breast cancer and 101,986 women without the disease. Lancet 2001;358:1389–99. 10.1016/S0140-6736(01)06524-2 [DOI] [PubMed] [Google Scholar]
- 200.Grabrick DM, Hartmann LC, Cerhan JR, et al. Risk of breast cancer with oral contraceptive use in women with a family history of breast cancer. JAMA 2000;284:1791–8. 10.1001/jama.284.14.1791 [DOI] [PubMed] [Google Scholar]
- 201.Gronwald J, Byrski T, Huzarski T, et al. Influence of selected lifestyle factors on breast and ovarian cancer risk in BRCA1 mutation carriers from Poland. Breast Cancer Res Treat 2006;95:105–9. 10.1007/s10549-005-9051-5 [DOI] [PubMed] [Google Scholar]
- 202.Haile RW, Thomas DC, McGuire V, et al. ; kConFab Investigators; Ontario Cancer Genetics Network Investigators. BRCA1 and BRCA2 mutation carriers, oral contraceptive use, and breast cancer before age 50. Cancer Epidemiol Biomarkers Prev 2006;15:1863–70. 10.1158/1055-9965.EPI-06-0258 [DOI] [PubMed] [Google Scholar]
- 203.Harris NV, Weiss NS, Francis AM, Polissar L. Breast cancer in relation to patterns of oral contraceptive use. Am J Epidemiol 1982;116:643–51. 10.1093/oxfordjournals.aje.a113447 [DOI] [PubMed] [Google Scholar]
- 204.Hennekens CH, Speizer FE, Lipnick RJ, et al. A case-control study of oral contraceptive use and breast cancer. J Natl Cancer Inst 1984;72:39–42. 10.1093/jnci/72.1.39 [DOI] [PubMed] [Google Scholar]
- 205.Jernström H, Loman N, Johannsson OT, Borg A, Olsson H. Impact of teenage oral contraceptive use in a population-based series of early-onset breast cancer cases who have undergone BRCA mutation testing. Eur J Cancer 2005;41:2312–20. 10.1016/j.ejca.2005.03.035 [DOI] [PubMed] [Google Scholar]
- 206.Marchbanks PA, McDonald JA, Wilson HG, et al. Oral contraceptives and the risk of breast cancer. N Engl J Med 2002;346:2025–32. 10.1056/NEJMoa013202 [DOI] [PubMed] [Google Scholar]
- 207.Milne RL, Knight JA, John EM, et al. Oral contraceptive use and risk of early-onset breast cancer in carriers and noncarriers of BRCA1 and BRCA2 mutations. Cancer Epidemiol Biomarkers Prev 2005;14:350–6. 10.1158/1055-9965.EPI-04-0376 [DOI] [PubMed] [Google Scholar]
- 208.Narod SA, Dubé MP, Klijn J, et al. Oral contraceptives and the risk of breast cancer in BRCA1 and BRCA2 mutation carriers. J Natl Cancer Inst 2002;94:1773–9. 10.1093/jnci/94.23.1773 [DOI] [PubMed] [Google Scholar]
- 209.Rosenberg L, Palmer JR, Rao RS, et al. Case-control study of oral contraceptive use and risk of breast cancer. Am J Epidemiol 1996;143:25–37. 10.1093/oxfordjournals.aje.a008654 [DOI] [PubMed] [Google Scholar]
- 210.Silvera SAN, Miller AB, Rohan TE. Oral contraceptive use and risk of breast cancer among women with a family history of breast cancer: a prospective cohort study. Cancer Causes Control 2005;16:1059–63. 10.1007/s10552-005-0343-1 [DOI] [PubMed] [Google Scholar]
- 211.Ursin G, Henderson BE, Haile RW, et al. Does oral contraceptive use increase the risk of breast cancer in women with BRCA1/BRCA2 mutations more than in other women? Cancer Res 1997;57:3678–81. [PubMed] [Google Scholar]
- 212.Ursin G, Ross RK, Sullivan-Halley J, Hanisch R, Henderson B, Bernstein L. Use of oral contraceptives and risk of breast cancer in young women. Breast Cancer Res Treat 1998;50:175–84. 10.1023/A:1006037823178 [DOI] [PubMed] [Google Scholar]
- 213.Curtis KM, Hannaford PC, Rodriguez MI, Chipato T, Steyn PS, Kiarie JN. Hormonal contraception and HIV acquisition among women: an updated systematic review. BMJ Sex Reprod Health 2020;46:8–16. 10.1136/bmjsrh-2019-200509 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 214.Tepper NK, Curtis KM, Cox S, Whiteman MK. Update to U.S. medical eligibility criteria for contraceptive use, 2016: updated recommendations for the use of contraception among women at high risk for HIV infection. MMWR Morb Mortal Wkly Rep 2020;69:405–10. 10.15585/mmwr.mm6914a3 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 215.Polis CB, Phillips SJ, Curtis KM. Hormonal contraceptive use and female-to-male HIV transmission: a systematic review of the epidemiologic evidence. AIDS 2013;27:493–505. 10.1097/QAD.0b013e32835ad539 [DOI] [PubMed] [Google Scholar]
- 216.Phillips SJ, Polis CB, Curtis KM. The safety of hormonal contraceptives for women living with HIV and their sexual partners. Contraception 2016;93:11–6. 10.1016/j.contraception.2015.10.002 [DOI] [PubMed] [Google Scholar]
- 217.Phillips SJ, Curtis KM, Polis CB. Effect of hormonal contraceptive methods on HIV disease progression: a systematic review. AIDS 2013;27:787–94. 10.1097/QAD.0b013e32835bb672 [DOI] [PubMed] [Google Scholar]
- 218.el-Raghy I, Back DJ, Osman F, Orme ML, Fathalla M. Contraceptive steroid concentrations in women with early active schistosomiasis: lack of effect of antischistosomal drugs. Contraception 1986;33:373–7. 10.1016/0010-7824(86)90099-5 [DOI] [PubMed] [Google Scholar]
- 219.Gad-el-Mawla N, Abdallah A. Liver function in bilharzial females receiving contraceptive pills. Acta Hepatosplenol 1969;16:308–10. [PubMed] [Google Scholar]
- 220.Gad-el-Mawla N, el-Roubi O, Sabet S, Abdallah A. Plasma lipids and lipoproteins in bilharzial females during oral contraceptive therapy. J Egypt Med Assoc 1972;55:137–47. [PubMed] [Google Scholar]
- 221.Shaaban MM, Hammad WA, Falthalla MF, et al. Effects of oral contraception on liver function tests and serum proteins in women with active schistosomiasis. Contraception 1982;26:75–82. 10.1016/0010-7824(82)90174-3 [DOI] [PubMed] [Google Scholar]
- 222.Shaaban MM, Ghaneimah SA, Mohamed MA, Abdel-Chani S, Mostafa SA. Effect of oral contraception on serum bile acid. Int J Gynaecol Obstet 1984;22:111–5. 10.1016/0020-7292(84)90023-7 [DOI] [PubMed] [Google Scholar]
- 223.Sy FS, Osteria TS, Opiniano V, Gler S. Effect of oral contraceptive on liver function tests of women with schistosomiasis in the Philippines. Contraception 1986;34:283–94. 10.1016/0010-7824(86)90009-0 [DOI] [PubMed] [Google Scholar]
- 224.Tagy AH, Saker ME, Moussa AA, Kolgah A. The effect of low-dose combined oral contraceptive pills versus injectable contraceptive (Depot Provera) on liver function tests of women with compensated bilharzial liver fibrosis. Contraception 2001;64:173–6. 10.1016/S0010-7824(01)00248-7 [DOI] [PubMed] [Google Scholar]
- 225.Beck P, Wells SA. Comparison of the mechanisms underlying carbohydrate intolerance in subclinical diabetic women during pregnancy and during post-partum oral contraceptive steroid treatment. J Clin Endocrinol Metab 1969;29:807–18. 10.1210/jcem-29-6-807 [DOI] [PubMed] [Google Scholar]
- 226.Kjos SL, Peters RK, Xiang A, Thomas D, Schaefer U, Buchanan TA. Contraception and the risk of type 2 diabetes mellitus in Latina women with prior gestational diabetes mellitus. JAMA 1998;280:533–8. 10.1001/jama.280.6.533 [DOI] [PubMed] [Google Scholar]
- 227.Kung AW, Ma JT, Wong VC, et al. Glucose and lipid metabolism with triphasic oral contraceptives in women with history of gestational diabetes. Contraception 1987;35:257–69. 10.1016/0010-7824(87)90027-8 [DOI] [PubMed] [Google Scholar]
- 228.Rådberg T, Gustafson A, Skryten A, Karlsson K. Metabolic studies in gestational diabetic women during contraceptive treatment: effects on glucose tolerance and fatty acid composition of serum lipids. Gynecol Obstet Invest 1982;13:17–29. 10.1159/000299480 [DOI] [PubMed] [Google Scholar]
- 229.Skouby SO, Andersen O, Kühl C. Oral contraceptives and insulin receptor binding in normal women and those with previous gestational diabetes. Am J Obstet Gynecol 1986;155:802–7. 10.1016/S0002-9378(86)80024-2 [DOI] [PubMed] [Google Scholar]
- 230.Skouby SO, Andersen O, Saurbrey N, Kühl C. Oral contraception and insulin sensitivity: in vivo assessment in normal women and women with previous gestational diabetes. J Clin Endocrinol Metab 1987;64:519–23. 10.1210/jcem-64-3-519 [DOI] [PubMed] [Google Scholar]
- 231.Skouby SO, Mølsted-Pedersen L, Kühl C. Low dosage oral contraception in women with previous gestational diabetes. Obstet Gynecol 1982;59:325–8. [PubMed] [Google Scholar]
- 232.Xiang AH, Kawakubo M, Kjos SL, Buchanan TA. Long-acting injectable progestin contraception and risk of type 2 diabetes in Latino women with prior gestational diabetes mellitus. Diabetes Care 2006;29:613–7. 10.2337/diacare.29.03.06.dc05-1940 [DOI] [PubMed] [Google Scholar]
- 233.Kjos SL, Shoupe D, Douyan S, et al. Effect of low-dose oral contraceptives on carbohydrate and lipid metabolism in women with recent gestational diabetes: results of a controlled, randomized, prospective study. Am J Obstet Gynecol 1990;163:1822–7. 10.1016/0002-9378(90)90757-X [DOI] [PubMed] [Google Scholar]
- 234.Rådberg T, Gustafson A, Skryten A, Karlsson K. Metabolic studies in women with previous gestational diabetes during contraceptive treatment: effects on serum lipids and high density lipoproteins. Acta Endocrinol (Copenh) 1982;101:134–9. 10.1530/acta.0.1010134 [DOI] [PubMed] [Google Scholar]
- 235.Skouby SO, Kühl C, Mølsted-Pedersen L, Petersen K, Christensen MS. Triphasic oral contraception: metabolic effects in normal women and those with previous gestational diabetes. Am J Obstet Gynecol 1985;153:495–500. 10.1016/0002-9378(85)90460-0 [DOI] [PubMed] [Google Scholar]
- 236.Beck P, Arnett DM, Alsever RN, Eaton RP. Effect of contraceptive steroids on arginine-stimulated glucagon and insulin secretion in women. II. Carbohydrate and lipid physiology in insulin-dependent diabetics. Metabolism 1976;25:23–31. 10.1016/0026-0495(76)90156-6 [DOI] [PubMed] [Google Scholar]
- 237.Diab KM, Zaki MM. Contraception in diabetic women: comparative metabolic study of Norplant, depot medroxyprogesterone acetate, low dose oral contraceptive pill and CuT380A. J Obstet Gynaecol Res 2000;26:17–26. 10.1111/j.1447-0756.2000.tb01195.x [DOI] [PubMed] [Google Scholar]
- 238.Garg SK, Chase HP, Marshall G, Hoops SL, Holmes DL, Jackson WE. Oral contraceptives and renal and retinal complications in young women with insulin-dependent diabetes mellitus. JAMA 1994;271:1099–102. 10.1001/jama.1994.03510380055037 [DOI] [PubMed] [Google Scholar]
- 239.Grigoryan OR, Grodnitskaya EE, Andreeva EN, Shestakova MV, Melnichenko GA, Dedov II. Contraception in perimenopausal women with diabetes mellitus. Gynecol Endocrinol 2006;22:198–206. 10.1080/09513590600624317 [DOI] [PubMed] [Google Scholar]
- 240.Margolis KL, Adami H-O, Luo J, Ye W, Weiderpass E. A prospective study of oral contraceptive use and risk of myocardial infarction among Swedish women. Fertil Steril 2007;88:310–6. 10.1016/j.fertnstert.2006.11.206 [DOI] [PubMed] [Google Scholar]
- 241.Petersen KR, Skouby SO, Jespersen J. Balance of coagulation activity with fibrinolysis during use of oral contraceptives in women with insulin-dependent diabetes mellitus. Int J Fertil Menopausal Stud 1995;40(Suppl 2):105–11. [PubMed] [Google Scholar]
- 242.Petersen KR, Skouby SO, Sidelmann J, Jespersen J. Assessment of endothelial function during oral contraception in women with insulin-dependent diabetes mellitus. Metabolism 1994;43:1379–83. 10.1016/0026-0495(94)90031-0 [DOI] [PubMed] [Google Scholar]
- 243.Rådberg T, Gustafson A, Skryten A, Karlsson K. Oral contraception in diabetic women. A cross-over study on serum and high density lipoprotein (HDL) lipids and diabetes control during progestogen and combined estrogen/progestogen contraception. Horm Metab Res 1982;14:61–5. [PubMed] [Google Scholar]
- 244.Skouby SO, Jensen BM, Kühl C, Mølsted-Pedersen L, Svenstrup B, Nielsen J. Hormonal contraception in diabetic women: acceptability and influence on diabetes control and ovarian function of a nonalkylated estrogen/progestogen compound. Contraception 1985;32:23–31. 10.1016/0010-7824(85)90113-1 [DOI] [PubMed] [Google Scholar]
- 245.Skouby SO, Mølsted-Pedersen L, Kühl C, Bennet P. Oral contraceptives in diabetic women: metabolic effects of four compounds with different estrogen/progestogen profiles. Fertil Steril 1986;46:858–64. 10.1016/S0015-0282(16)49825-0 [DOI] [PubMed] [Google Scholar]
- 246.Zapata LB, Paulen ME, Cansino C, Marchbanks PA, Curtis KM. Contraceptive use among women with inflammatory bowel disease: a systematic review. Contraception 2010;82:72–85. 10.1016/j.contraception.2010.02.012 [DOI] [PubMed] [Google Scholar]
- 247.Whiteman MK, Oduyebo T, Zapata LB, Walker S, Curtis KM. Contraceptive safety among women with cystic fibrosis: a systematic review. Contraception 2016;94:621–9. 10.1016/j.contraception.2016.05.016 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 248.Brunson A, Keegan T, Mahajan A, White R, Wun T. High incidence of venous thromboembolism recurrence in patients with sickle cell disease. Am J Hematol 2019;94:862–70. 10.1002/ajh.25508 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 249.Naik RP, Streiff MB, Haywood C Jr, Segal JB, Lanzkron S. Venous thromboembolism incidence in the Cooperative Study of Sickle Cell Disease. J Thromb Haemost 2014;12:2010–6. 10.1111/jth.12744 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 250.Noubiap JJ, Temgoua MN, Tankeu R, Tochie JN, Wonkam A, Bigna JJ. Sickle cell disease, sickle trait and the risk for venous thromboembolism: a systematic review and meta-analysis. Thromb J 2018;16:27. 10.1186/s12959-018-0179-z [DOI] [PMC free article] [PubMed] [Google Scholar]
- 251.Ohene-Frempong K, Weiner SJ, Sleeper LA, et al. Cerebrovascular accidents in sickle cell disease: rates and risk factors. Blood 1998;91:288–94. [PubMed] [Google Scholar]
- 252.Panel on Treatment of HIV During Pregnancy and Prevention of Perinatal Transmission. Recommendations for the use of antiretroviral drugs during pregnancy and interventions to reduce perinatal HIV transmission in the United States. Washington, DC: US Department of Health and Human Services; 2023. https://clinicalinfo.hiv.gov/en/guidelines/perinatal/recommendations-arv-drugs-pregnancy-overview [Google Scholar]
- 253.Panel on Antiretroviral Guidelines for Adults and Adolescents. Guidelines for the use of antiretroviral agents in adults and adolescents with HIV. Washington, DC: US Department of Health and Human Services; 2023. https://clinicalinfo.hiv.gov/sites/default/files/guidelines/documents/adult-adolescent-arv/guidelines-adult-adolescent-arv.pdf [Google Scholar]
- 254.Aweeka FT, Rosenkranz SL, Segal Y, et al. ; NIAID AIDS Clinical Trials Group. The impact of sex and contraceptive therapy on the plasma and intracellular pharmacokinetics of zidovudine. AIDS 2006;20:1833–41. 10.1097/01.aids.0000244202.18629.36 [DOI] [PubMed] [Google Scholar]
- 255.Kearney BP, Mathias A. Lack of effect of tenofovir disoproxil fumarate on pharmacokinetics of hormonal contraceptives. Pharmacotherapy 2009;29:924–9. 10.1592/phco.29.8.924 [DOI] [PubMed] [Google Scholar]
- 256.Todd CS, Deese J, Wang M, et al. ; FEM-PrEP Study Group. Sino-implant (II) continuation and effect of concomitant tenofovir disoproxil fumarate-emtricitabine use on plasma levonorgestrel concentrations among women in Bondo, Kenya. Contraception 2015;91:248–52. 10.1016/j.contraception.2014.10.008 [DOI] [PubMed] [Google Scholar]
- 257.Murnane PM, Heffron R, Ronald A, et al. ; Partners PrEP Study Team. Pre-exposure prophylaxis for HIV-1 prevention does not diminish the pregnancy prevention effectiveness of hormonal contraception. AIDS 2014;28:1825–30. 10.1097/QAD.0000000000000290 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 258.Kasonde M, Niska RW, Rose C, et al. Bone mineral density changes among HIV-uninfected young adults in a randomised trial of pre-exposure prophylaxis with tenofovir-emtricitabine or placebo in Botswana. PLoS One 2014;9:e90111. 10.1371/journal.pone.0090111 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 259.Callahan R, Nanda K, Kapiga S, et al. ; FEM-PrEP Study Group. Pregnancy and contraceptive use among women participating in the FEM-PrEP trial. J Acquir Immune Defic Syndr 2015;68:196–203. 10.1097/QAI.0000000000000413 [DOI] [PubMed] [Google Scholar]
- 260.Patel RC, Onono M, Gandhi M, et al. Pregnancy rates in HIV-positive women using contraceptives and efavirenz-based or nevirapine-based antiretroviral therapy in Kenya: a retrospective cohort study. Lancet HIV 2015;2:e474–82. 10.1016/S2352-3018(15)00184-8 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 261.Pyra M, Heffron R, Mugo NR, et al. ; Partners in Prevention HSVHIV Transmission Study and Partners PrEP Study Teams. Effectiveness of hormonal contraception in HIV-infected women using antiretroviral therapy. AIDS 2015;29:2353–9. 10.1097/QAD.0000000000000827 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 262.Clark RA, Theall K. Population-based study evaluating association between selected antiretroviral therapies and potential oral contraceptive failure. J Acquir Immune Defic Syndr 2004;37:1219–20. 10.1097/01.qai.0000136724.15758.ae [DOI] [PubMed] [Google Scholar]
- 263.Landolt NK, Phanuphak N, Ubolyam S, et al. Efavirenz, in contrast to nevirapine, is associated with unfavorable progesterone and antiretroviral levels when coadministered with combined oral contraceptives. J Acquir Immune Defic Syndr 2013;62:534–9. 10.1097/QAI.0b013e31827e8f98 [DOI] [PubMed] [Google Scholar]
- 264.Sevinsky H, Eley T, Persson A, et al. The effect of efavirenz on the pharmacokinetics of an oral contraceptive containing ethinyl estradiol and norgestimate in healthy HIV-negative women. Antivir Ther 2011;16:149–56. 10.3851/IMP1725 [DOI] [PubMed] [Google Scholar]
- 265.Landolt NK, Phanuphak N, Ubolyam S, et al. Significant decrease of ethinylestradiol with nevirapine, and of etonogestrel with efavirenz in HIV-positive women. J Acquir Immune Defic Syndr 2014;66:e50–2. 10.1097/QAI.0000000000000134 [DOI] [PubMed] [Google Scholar]
- 266.Myer L, Carter RJ, Katyal M, Toro P, El-Sadr WM, Abrams EJ. Impact of antiretroviral therapy on incidence of pregnancy among HIV-infected women in Sub-Saharan Africa: a cohort study. PLoS Med 2010;7:e1000229. 10.1371/journal.pmed.1000229 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 267.Schöller-Gyüre M, Kakuda TN, Woodfall B, et al. Effect of steady-state etravirine on the pharmacokinetics and pharmacodynamics of ethinylestradiol and norethindrone. Contraception 2009;80:44–52. 10.1016/j.contraception.2009.01.009 [DOI] [PubMed] [Google Scholar]
- 268.Nanda K, Delany-Moretlwe S, Dubé K, et al. Nevirapine-based antiretroviral therapy does not reduce oral contraceptive effectiveness. AIDS 2013;27(Suppl 1):S17–25. 10.1097/QAD.0000000000000050 [DOI] [PubMed] [Google Scholar]
- 269.Stuart GS, Moses A, Corbett A, et al. Combined oral contraceptives and antiretroviral PK/PD in Malawian women: pharmacokinetics and pharmacodynamics of a combined oral contraceptive and a generic combined formulation antiretroviral in Malawi. J Acquir Immune Defic Syndr 2011;58:e40–3. 10.1097/QAI.0b013e31822b8bf8 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 270.Mildvan D, Yarrish R, Marshak A, et al. Pharmacokinetic interaction between nevirapine and ethinyl estradiol/norethindrone when administered concurrently to HIV-infected women. J Acquir Immune Defic Syndr 2002;29:471–7. 10.1097/00042560-200204150-00007 [DOI] [PubMed] [Google Scholar]
- 271.Muro E, Droste JAH, Hofstede HT, Bosch M, Dolmans W, Burger DM. Nevirapine plasma concentrations are still detectable after more than 2 weeks in the majority of women receiving single-dose nevirapine: implications for intervention studies. J Acquir Immune Defic Syndr 2005;39:419–21. 10.1097/01.qai.0000167154.37357.f9 [DOI] [PubMed] [Google Scholar]
- 272.Crauwels HM, van Heeswijk RP, Buelens A, Stevens M, Hoetelmans RM. Lack of an effect of rilpivirine on the pharmacokinetics of ethinylestradiol and norethindrone in healthy volunteers. Int J Clin Pharmacol Ther 2014;52:118–28. 10.5414/CP201943 [DOI] [PubMed] [Google Scholar]
- 273.Zhang J, Chung E, Yones C, et al. The effect of atazanavir/ritonavir on the pharmacokinetics of an oral contraceptive containing ethinyl estradiol and norgestimate in healthy women. Antivir Ther 2011;16:157–64. 10.3851/IMP1724 [DOI] [PubMed] [Google Scholar]
- 274.Sekar VJ, Lefebvre E, Guzman SS, et al. Pharmacokinetic interaction between ethinyl estradiol, norethindrone and darunavir with low-dose ritonavir in healthy women. Antivir Ther 2008;13:563–9. 10.1177/135965350801300415 [DOI] [PubMed] [Google Scholar]
- 275.Glaxo Smith Kline. Lexiva (fosamprenavir calcium) [Package insert]. Research Triangle Park, NC:Glaxo Smith Kline; 2015.
- 276.Vogler MA, Patterson K, Kamemoto L, et al. Contraceptive efficacy of oral and transdermal hormones when co-administered with protease inhibitors in HIV-1-infected women: pharmacokinetic results of ACTG trial A5188. J Acquir Immune Defic Syndr 2010;55:473–82. 10.1097/QAI.0b013e3181eb5ff5 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 277.Fröhlich M, Burhenne J, Martin-Facklam M, et al. Oral contraception does not alter single dose saquinavir pharmacokinetics in women. Br J Clin Pharmacol 2004;57:244–52. 10.1111/j.1365-2125.2003.01983.x [DOI] [PMC free article] [PubMed] [Google Scholar]
- 278.Boehringer Ingelheim Pharmaceuticals. Aptivus (tipranavir) [Package insert]. Ridgefield, CT: Boehringer Ingelheim Pharmaceuticals; 2005.
- 279.Bristol-Myers Squibb. Reyataz (atazanavir sulfate) [Package insert]. Princeton, NJ: Bristol-Myers Squibb; 2003.
- 280.Abel S, Russell D, Whitlock LA, Ridgway CE, Muirhead GJ. Effect of maraviroc on the pharmacokinetics of midazolam, lamivudine/zidovudine, and ethinyloestradiol/levonorgestrel in healthy volunteers. Br J Clin Pharmacol 2008;65(Suppl 1):19–26. 10.1111/j.1365-2125.2008.03132.x [DOI] [PMC free article] [PubMed] [Google Scholar]
- 281.Anderson MS, Hanley WD, Moreau AR, et al. Effect of raltegravir on estradiol and norgestimate plasma pharmacokinetics following oral contraceptive administration in healthy women. Br J Clin Pharmacol 2011;71:616–20. 10.1111/j.1365-2125.2010.03885.x [DOI] [PMC free article] [PubMed] [Google Scholar]
- 282.Song IH, Borland J, Chen S, Wajima T, Peppercorn AF, Piscitelli SC. Dolutegravir has no effect on the pharmacokinetics of oral contraceptives with norgestimate and ethinyl estradiol. Ann Pharmacother 2015;49:784–9. 10.1177/1060028015580637 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 283.Gilead Sciences. Vitekta (elvitegravir) [Package insert]. Foster City, CA: Gilead Sciences; 2012.
- 284.Back DJ, Bates M, Bowden A, et al. The interaction of phenobarbital and other anticonvulsants with oral contraceptive steroid therapy. Contraception 1980;22:495–503. 10.1016/0010-7824(80)90102-X [DOI] [PubMed] [Google Scholar]
- 285.Doose DR, Wang SS, Padmanabhan M, Schwabe S, Jacobs D, Bialer M. Effect of topiramate or carbamazepine on the pharmacokinetics of an oral contraceptive containing norethindrone and ethinyl estradiol in healthy obese and nonobese female subjects. Epilepsia 2003;44:540–9. 10.1046/j.1528-1157.2003.55602.x [DOI] [PubMed] [Google Scholar]
- 286.Fattore C, Cipolla G, Gatti G, et al. Induction of ethinylestradiol and levonorgestrel metabolism by oxcarbazepine in healthy women. Epilepsia 1999;40:783–7. 10.1111/j.1528-1157.1999.tb00779.x [DOI] [PubMed] [Google Scholar]
- 287.Rosenfeld WE, Doose DR, Walker SA, Nayak RK. Effect of topiramate on the pharmacokinetics of an oral contraceptive containing norethindrone and ethinyl estradiol in patients with epilepsy. Epilepsia 1997;38:317–23. 10.1111/j.1528-1157.1997.tb01123.x [DOI] [PubMed] [Google Scholar]
- 288.Gaffield ME, Culwell KR, Lee CR. The use of hormonal contraception among women taking anticonvulsant therapy. Contraception 2011;83:16–29. 10.1016/j.contraception.2010.06.013 [DOI] [PubMed] [Google Scholar]
- 289.Christensen J, Petrenaite V, Atterman J, et al. Oral contraceptives induce lamotrigine metabolism: evidence from a double-blind, placebo-controlled trial. Epilepsia 2007;48:484–9. 10.1111/j.1528-1167.2007.00997.x [DOI] [PubMed] [Google Scholar]
- 290.Contin M, Albani F, Ambrosetto G, et al. Variation in lamotrigine plasma concentrations with hormonal contraceptive monthly cycles in patients with epilepsy. Epilepsia 2006;47:1573–5. 10.1111/j.1528-1167.2006.00558.x [DOI] [PubMed] [Google Scholar]
- 291.Reimers A, Helde G, Brodtkorb E. Ethinyl estradiol, not progestogens, reduces lamotrigine serum concentrations. Epilepsia 2005;46:1414–7. 10.1111/j.1528-1167.2005.10105.x [DOI] [PubMed] [Google Scholar]
- 292.Sabers A, Buchholt JM, Uldall P, Hansen EL. Lamotrigine plasma levels reduced by oral contraceptives. Epilepsy Res 2001;47:151–4. 10.1016/S0920-1211(01)00305-9 [DOI] [PubMed] [Google Scholar]
- 293.Sabers A, Ohman I, Christensen J, Tomson T. Oral contraceptives reduce lamotrigine plasma levels. Neurology 2003;61:570–1. 10.1212/01.WNL.0000076485.09353.7A [DOI] [PubMed] [Google Scholar]
- 294.Back DJ, Breckenridge AM, MacIver M, et al. The effects of ampicillin on oral contraceptive steroids in women. Br J Clin Pharmacol 1982;14:43–8. 10.1111/j.1365-2125.1982.tb04932.x [DOI] [PMC free article] [PubMed] [Google Scholar]
- 295.Back DJ, Grimmer SF, Orme ML, Proudlove C, Mann RD, Breckenridge AM. Evaluation of Committee on Safety of Medicines yellow card reports on oral contraceptive-drug interactions with anticonvulsants and antibiotics. Br J Clin Pharmacol 1988;25:527–32. 10.1111/j.1365-2125.1988.tb03341.x [DOI] [PMC free article] [PubMed] [Google Scholar]
- 296.Back DJ, Tjia J, Martin C, et al. The lack of interaction between temafloxacin and combined oral contraceptive steroids. Contraception 1991;43:317–23. 10.1016/0010-7824(91)90070-V [DOI] [PubMed] [Google Scholar]
- 297.Bacon JF, Shenfield GM. Pregnancy attributable to interaction between tetracycline and oral contraceptives. BMJ 1980;280:293. 10.1136/bmj.280.6210.293 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 298.Bainton R. Interaction between antibiotic therapy and contraceptive medication. Oral Surg Oral Med Oral Pathol 1986;61:453–5. 10.1016/0030-4220(86)90385-3 [DOI] [PubMed] [Google Scholar]
- 299.Bollen M. Use of antibiotics when taking the oral contraceptive pill. [comment]. Aust Fam Physician 1995;24:928–9. [PubMed] [Google Scholar]
- 300.Bromham DR, Cartmill RS. Knowledge and use of secondary contraception among patients requesting termination of pregnancy. BMJ 1993;306:556–7. 10.1136/bmj.306.6877.556 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 301.Côté J. Interaction of griseofulvin and oral contraceptives. [Comment]. J Am Acad Dermatol 1990;22:124–5. 10.1016/S0190-9622(08)80010-2 [DOI] [PubMed] [Google Scholar]
- 302.Csemiczky G, Alvendal C, Landgren BM. Risk for ovulation in women taking a low-dose oral contraceptive (Microgynon) when receiving antibacterial treatment with a fluoroquinolone (ofloxacin). Adv Contracept 1996;12:101–9. 10.1007/BF01849631 [DOI] [PubMed] [Google Scholar]
- 303.de Groot AC, Eshuis H, Stricker BH. [Inefficacy of oral contraception during use of minocycline]. Ned Tijdschr Geneeskd 1990;134:1227–9. [PubMed] [Google Scholar]
- 304.DeSano EA Jr, Hurley SC. Possible interactions of antihistamines and antibiotics with oral contraceptive effectiveness. Fertil Steril 1982;37:853–4. 10.1016/S0015-0282(16)46350-8 [DOI] [PubMed] [Google Scholar]
- 305.Donley TG, Smith RF, Roy B. Reduced oral contraceptive effectiveness with concurrent antibiotic use: a protocol for prescribing antibiotics to women of childbearing age. Compendium 1990;11:392–6. [PubMed] [Google Scholar]
- 306.Friedman CI, Huneke AL, Kim MH, Powell J. The effect of ampicillin on oral contraceptive effectiveness. Obstet Gynecol 1980;55:33–7. [PubMed] [Google Scholar]
- 307.Grimmer SF, Allen WL, Back DJ, Breckenridge AM, Orme M, Tjia J. The effect of cotrimoxazole on oral contraceptive steroids in women. Contraception 1983;28:53–9. 10.1016/S0010-7824(83)80005-5 [DOI] [PubMed] [Google Scholar]
- 308.Helms SE, Bredle DL, Zajic J, Jarjoura D, Brodell RT, Krishnarao I. Oral contraceptive failure rates and oral antibiotics. J Am Acad Dermatol 1997;36:705–10. 10.1016/S0190-9622(97)80322-2 [DOI] [PubMed] [Google Scholar]
- 309.Hempel E, Böhm W, Carol W, Klinger G. [Enzyme induction by drugs and hormonal contraception]. Zentralbl Gynakol 1973;95:1451–7. [PubMed] [Google Scholar]
- 310.Hempel E, Zorn C, Graf K. [Effect of chemotherapy agents and antibiotics on hormonal contraception]. Z Arztl Fortbild (Jena) 1978;72:924–6. [PubMed] [Google Scholar]
- 311.Hetényi G. Possible interactions between antibiotics and oral contraceptives. Ther Hung 1989;37:86–9. [PubMed] [Google Scholar]
- 312.Hughes BR, Cunliffe WJ. Interactions between the oral contraceptive pill and antibiotics. [Comment]. Br J Dermatol 1990;122:717–8. 10.1111/j.1365-2133.1990.tb07299.x [DOI] [PubMed] [Google Scholar]
- 313.Joshi JV, Joshi UM, Sankholi GM, et al. A study of interaction of low-dose combination oral contraceptive with ampicillin and metronidazole. Contraception 1980;22:643–52. 10.1016/0010-7824(80)90089-X [DOI] [PubMed] [Google Scholar]
- 314.Kakouris H, Kovacs GT. Pill failure and nonuse of secondary precautions. Br J Fam Plann 1992;18:41–4. [Google Scholar]
- 315.Kakouris H, Kovacs GT. How common are predisposing factors to pill failure among pill users? Br J Fam Plann 1994;20:33–5. [Google Scholar]
- 316.Kovacs GT, Riddoch G, Duncombe P, et al. Inadvertent pregnancies in oral contraceptive users. Med J Aust 1989;150:549–51. 10.5694/j.1326-5377.1989.tb136691.x [DOI] [PubMed] [Google Scholar]
- 317.Lequeux A. [Pregnancy under oral contraceptives after treatment with tetracycline]. Louv Med 1980;99:413–4. [PubMed] [Google Scholar]
- 318.London BM, Lookingbill DP. Frequency of pregnancy in acne patients taking oral antibiotics and oral contraceptives. Arch Dermatol 1994;130:392–3. 10.1001/archderm.1994.01690030128027 [DOI] [PubMed] [Google Scholar]
- 319.Maggiolo F, Puricelli G, Dottorini M, Caprioli S, Bianchi W, Suter F. The effect of ciprofloxacin on oral contraceptive steroid treatments. Drugs Exp Clin Res 1991;17:451–4. [PubMed] [Google Scholar]
- 320.Murphy AA, Zacur HA, Charache P, Burkman RT. The effect of tetracycline on levels of oral contraceptives. Am J Obstet Gynecol 1991;164:28–33. 10.1016/0002-9378(91)90617-Z [DOI] [PubMed] [Google Scholar]
- 321.Neely JL, Abate M, Swinker M, D’Angio R. The effect of doxycycline on serum levels of ethinyl estradiol, norethindrone, and endogenous progesterone. Obstet Gynecol 1991;77:416–20. [PubMed] [Google Scholar]
- 322.Pillans PI, Sparrow MJ. Pregnancy associated with a combined oral contraceptive and itraconazole. [Comment]. N Z Med J 1993;106:436. [PubMed] [Google Scholar]
- 323.Scholten PC, Droppert RM, Zwinkels MG, Moesker HL, Nauta JJ, Hoepelman IM. No interaction between ciprofloxacin and an oral contraceptive. Antimicrob Agents Chemother 1998;42:3266–8. 10.1128/AAC.42.12.3266 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 324.Silber TJ. Apparent oral contraceptive failure associated with antibiotic administration. J Adolesc Health Care 1983;4:287–9. 10.1016/S0197-0070(83)80014-X [DOI] [PubMed] [Google Scholar]
- 325.Sparrow MJ. Pill method failures. N Z Med J 1987;100:102–5. [PubMed] [Google Scholar]
- 326.Sparrow MJ. Pregnancies in reliable pill takers. N Z Med J 1989;102:575–7. [PubMed] [Google Scholar]
- 327.Sparrow MJ. Pill method failures in women seeking abortion: fourteen years experience. N Z Med J 1998;111:386–8. [PubMed] [Google Scholar]
- 328.van Dijke CP, Weber JC. Interaction between oral contraceptives and griseofulvin. Br Med J (Clin Res Ed) 1984;288:1125–6. 10.1136/bmj.288.6424.1125-a [DOI] [PMC free article] [PubMed] [Google Scholar]
- 329.Wermeling DP, Chandler MH, Sides GD, Collins D, Muse KN. Dirithromycin increases ethinyl estradiol clearance without allowing ovulation. Obstet Gynecol 1995;86:78–84. 10.1016/0029-7844(95)00075-3 [DOI] [PubMed] [Google Scholar]
- 330.Young LK, Farquhar CM, McCowan LM, Roberts HE, Taylor J. The contraceptive practices of women seeking termination of pregnancy in an Auckland clinic. N Z Med J 1994;107:189–92. [PubMed] [Google Scholar]
- 331.Abrams LS, Skee D, Natarajan J, Wong FA. Pharmacokinetic overview of Ortho Evra/Evra. Fertil Steril 2002;77(Suppl 2):S3–12. 10.1016/S0015-0282(01)03261-7 [DOI] [PubMed] [Google Scholar]
- 332.Dogterom P, van den Heuvel MW, Thomsen T. Absence of pharmacokinetic interactions of the combined contraceptive vaginal ring NuvaRing with oral amoxicillin or doxycycline in two randomised trials. Clin Pharmacokinet 2005;44:429–38. 10.2165/00003088-200544040-00007 [DOI] [PubMed] [Google Scholar]
- 333.Devenport MH, Crook D, Wynn V, Lees LJ. Metabolic effects of low-dose fluconazole in healthy female users and non-users of oral contraceptives. Br J Clin Pharmacol 1989;27:851–9. 10.1111/j.1365-2125.1989.tb03449.x [DOI] [PMC free article] [PubMed] [Google Scholar]
- 334.Hilbert J, Messig M, Kuye O, Friedman H. Evaluation of interaction between fluconazole and an oral contraceptive in healthy women. Obstet Gynecol 2001;98:218–23. [DOI] [PubMed] [Google Scholar]
- 335.Kovács I, Somos P, Hámori M. Examination of the potential interaction between ketoconazole (Nizoral) and oral contraceptives with special regard to products of low hormone content (Rigevidon, Anteovin). Ther Hung 1986;34:167–70. [PubMed] [Google Scholar]
- 336.Lunell NO, Pschera H, Zador G, Carlström K. Evaluation of the possible interaction of the antifungal triazole SCH 39304 with oral contraceptives in normal healthy women. Gynecol Obstet Invest 1991;32:91–7. 10.1159/000293003 [DOI] [PubMed] [Google Scholar]
- 337.McDaniel PA, Caldroney RD. Oral contraceptives and griseofulvin interactions. Drug Intell Clin Pharm 1986;20:384. 10.1177/106002808602000511 [DOI] [PubMed] [Google Scholar]
- 338.Meyboom RH, van Puijenbroek EP, Vinks MH, Lastdrager CJ. Disturbance of withdrawal bleeding during concomitant use of itraconazole and oral contraceptives. N Z Med J 1997;110:300. [PubMed] [Google Scholar]
- 339.Rieth H, Sauerbrey N. [Interaction studies with fluconazole, a new triazole antifungal drug]. Wien Med Wochenschr 1989;139:370–4. [PubMed] [Google Scholar]
- 340.Sinofsky FE, Pasquale SA. The effect of fluconazole on circulating ethinyl estradiol levels in women taking oral contraceptives. Am J Obstet Gynecol 1998;178:300–4. 10.1016/S0002-9378(98)80016-1 [DOI] [PubMed] [Google Scholar]
- 341.van Puijenbroek EP, Feenstra J, Meyboom RH. [Pill cycle disturbance in simultaneous use of itraconazole and oral contraceptives]. Ned Tijdschr Geneeskd 1998;142:146–9. [PubMed] [Google Scholar]
- 342.Van Puijenbroek EP, Egberts AC, Meyboom RH, Leufkens HG. Signalling possible drug-drug interactions in a spontaneous reporting system: delay of withdrawal bleeding during concomitant use of oral contraceptives and itraconazole. Br J Clin Pharmacol 1999;47:689–93. 10.1046/j.1365-2125.1999.00957.x [DOI] [PMC free article] [PubMed] [Google Scholar]
- 343.Verhoeven CH, van den Heuvel MW, Mulders TM, Dieben TO. The contraceptive vaginal ring, NuvaRing, and antimycotic co-medication. Contraception 2004;69:129–32. 10.1016/j.contraception.2003.10.001 [DOI] [PubMed] [Google Scholar]
- 344.Back DJ, Breckenridge AM, Grimmer SF, Orme ML, Purba HS. Pharmacokinetics of oral contraceptive steroids following the administration of the antimalarial drugs primaquine and chloroquine. Contraception 1984;30:289–95. 10.1016/0010-7824(84)90092-1 [DOI] [PubMed] [Google Scholar]
- 345.Croft AM, Herxheimer A. Adverse effects of the antimalaria drug, mefloquine: due to primary liver damage with secondary thyroid involvement? BMC Public Health 2002;2:6. 10.1186/1471-2458-2-6 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 346.Karbwang J, Looareesuwan S, Back DJ, Migasana S, Bunnag D, Breckenridge AM. Effect of oral contraceptive steroids on the clinical course of malaria infection and on the pharmacokinetics of mefloquine in Thai women. Bull World Health Organ 1988;66:763–7. [PMC free article] [PubMed] [Google Scholar]
- 347.McGready R, Stepniewska K, Seaton E, et al. Pregnancy and use of oral contraceptives reduces the biotransformation of proguanil to cycloguanil. Eur J Clin Pharmacol 2003;59:553–7. 10.1007/s00228-003-0651-x [DOI] [PubMed] [Google Scholar]
- 348.Wanwimolruk S, Kaewvichit S, Tanthayaphinant O, Suwannarach C, Oranratnachai A. Lack of effect of oral contraceptive use on the pharmacokinetics of quinine. Br J Clin Pharmacol 1991;31:179–81. 10.1111/j.1365-2125.1991.tb05509.x [DOI] [PMC free article] [PubMed] [Google Scholar]
- 349.Back DJ, Breckenridge AM, Crawford F, et al. The effect of rifampicin on norethisterone pharmacokinetics. Eur J Clin Pharmacol 1979;15:193–7. 10.1007/BF00563105 [DOI] [PubMed] [Google Scholar]
- 350.Back DJ, Breckenridge AM, Crawford FE, et al. The effect of rifampicin on the pharmacokinetics of ethynylestradiol in women. Contraception 1980;21:135–43. 10.1016/0010-7824(80)90125-0 [DOI] [PubMed] [Google Scholar]
- 351.Barditch-Crovo P, Trapnell CB, Ette E, et al. The effects of rifampin and rifabutin on the pharmacokinetics and pharmacodynamics of a combination oral contraceptive. Clin Pharmacol Ther 1999;65:428–38. 10.1016/S0009-9236(99)70138-4 [DOI] [PubMed] [Google Scholar]
- 352.Bolt HM, Bolt M, Kappus H. Interaction of rifampicin treatment with pharmacokinetics and metabolism of ethinyloestradiol in man. Acta Endocrinol (Copenh) 1977;85:189–97. 10.1530/acta.0.0850189 [DOI] [PubMed] [Google Scholar]
- 353.Gupta KC, Ali MY. Failure of oral contraceptive with rifampicin. Med J Zambia 1980;15:23. [PubMed] [Google Scholar]
- 354.Hirsch A, Tillement JP, Chretien J. Effets contrariants de la rifampicine sur les contraceptifs oraux: a propos de trois grossesses non desiree chez trois malades. Rev Fr Mal Respir 1975;2:174–82. [Google Scholar]
- 355.Joshi JV, Joshi UM, Sankolli GM, et al. A study of interaction of a low-dose combination oral contraceptive with anti-tubercular drugs. Contraception 1980;21:617–29. 10.1016/0010-7824(80)90034-7 [DOI] [PubMed] [Google Scholar]
- 356.Kropp R. [Rifampicin and oral contraceptives (author’s transl)]. Prax Pneumol 1974;28:270–2. [PubMed] [Google Scholar]
- 357.LeBel M, Masson E, Guilbert E, et al. Effects of rifabutin and rifampicin on the pharmacokinetics of ethinylestradiol and norethindrone. J Clin Pharmacol 1998;38:1042–50. 10.1177/009127009803801109 [DOI] [PubMed] [Google Scholar]
- 358.Meyer B, Müller F, Wessels P, Maree J. A model to detect interactions between roxithromycin and oral contraceptives. Clin Pharmacol Ther 1990;47:671–4. 10.1038/clpt.1990.92 [DOI] [PubMed] [Google Scholar]
- 359.Nocke-Finke L, Breuer H, Reimers D. [Effects of rifampicin on the menstrual cycle and on oestrogen excretion in patients taking oral contraceptives]. Dtsch Med Wochenschr 1973;98:1521–3. 10.1055/s-0028-1107071 [DOI] [PubMed] [Google Scholar]
- 360.Piguet B, Muglioni JF, Chaline G. [Letter: Oral contraception and rifampicin]. Nouv Presse Med 1975;04:115–6. [PubMed] [Google Scholar]
- 361.Reimers D, Jezek A. [The simultaneous use of rifampicin and other antitubercular agents with oral contraceptives]. Prax Pneumol 1971;25:255–62. [PubMed] [Google Scholar]
- 362.Skolnick JL, Stoler BS, Katz DB, Anderson WH. Rifampin, oral contraceptives, and pregnancy. JAMA 1976;236:1382. 10.1001/jama.1976.03270130044027 [DOI] [PubMed] [Google Scholar]
- 363.Szoka PR, Edgren RA. Drug interactions with oral contraceptives: compilation and analysis of an adverse experience report database. Fertil Steril 1988;49(Suppl 2):31S–8S. [PubMed] [Google Scholar]
- 364.Berry-Bibee EN, Kim MJ, Simmons KB, et al. Drug interactions between hormonal contraceptives and psychotropic drugs: a systematic review. Contraception 2016;94:650–67. 10.1016/j.contraception.2016.07.011 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 365.Berry-Bibee EN, Kim MJ, Tepper NK, Riley HEM, Curtis KM. Co-administration of St. John’s wort and hormonal contraceptives: a systematic review. Contraception 2016;94:668–77. 10.1016/j.contraception.2016.07.010 [DOI] [PMC free article] [PubMed] [Google Scholar]
Appendix E. Classifications for Barrier Methods
Classifications for barrier contraceptive methods include those for condoms, which include external (male) condoms (latex or synthetic) and internal (female) condoms, spermicide and vaginal pH modulator, and diaphragm with spermicide and cervical cap with spermicide (Box E1) (Table E1).
BOX E1. Categories for classifying barrier methods.
U.S. MEC 1 = A condition for which there is no restriction for the use of the contraceptive method
U.S. MEC 2 = A condition for which the advantages of using the method generally outweigh the theoretical or proven risks
U.S. MEC 3 = A condition for which the theoretical or proven risks usually outweigh the advantages of using the method
U.S. MEC 4 = A condition that represents an unacceptable health risk if the contraceptive method is used
Abbreviation: U.S. MEC = U.S. Medical Eligibility Criteria for Contraceptive Use.
Patients should be counseled that consistent and correct use of external (male) latex condoms reduces the risk for sexually transmitted infections (STIs), including HIV infection (1). Use of internal (female) condoms can provide protection from transmission of STIs, although data are limited (1). Patients also should be counseled that pre-exposure prophylaxis, when taken as prescribed, is highly effective for preventing HIV infection (2).
TABLE E1. Classifications for barrier methods, including condoms, spermicide and vaginal pH modulator, and diaphragm with spermicide and cervical cap with spermicide.
Condition | Category |
Clarification/Evidence/Comment | ||
---|---|---|---|---|
Condom | Spermicide/Vaginal pH modulator | Diaphragm/Cap (with spermicide) | ||
Personal
Characteristics and Reproductive History
| ||||
Pregnancy
|
NA |
NA |
NA |
Clarification: None of
these methods are relevant for contraception during known
pregnancy. However, for persons who remain at risk for STIs or
HIV infection during pregnancy, the correct and consistent use
of condoms is recommended. |
Age
| ||||
a. Menarche to <40
years |
1 |
1 |
1 |
— |
b. ≥40
years |
1 |
1 |
1 |
— |
Parity
| ||||
a. Nulliparous |
1 |
1 |
1 |
— |
b. Parous |
1 |
1 |
2 |
Clarification: Risk for
cervical cap failure is higher in parous persons than in
nulliparous persons. |
Postpartum (breastfeeding
and
nonbreastfeeding) | ||||
a. <6 weeks
postpartum |
1 |
1 |
NA |
Clarification: Diaphragm
and cap are unsuitable until uterine involution is
complete. |
b. ≥6 weeks
postpartum |
1 |
1 |
1 |
— |
Postabortion (spontaneous
or
induced) | ||||
a. First trimester
abortion |
1 |
1 |
1 |
— |
b. Second trimester
abortion |
1 |
1 |
1 |
Clarification: Diaphragm
and cap are unsuitable until 6 weeks after second trimester
abortion. |
c. Immediate postseptic
abortion |
1 |
1 |
1 |
— |
Past ectopic
pregnancy
|
1 |
1 |
1 |
— |
History of
pelvic surgery
|
1 |
1 |
1 |
— |
Smoking
| ||||
a. Age <35
years |
1 |
1 |
1 |
— |
b. Age
≥35 years | ||||
i. <15
cigarettes per day |
1 |
1 |
1 |
— |
ii.
≥15 cigarettes per day |
1 |
1 |
1 |
— |
Obesity
| ||||
a. BMI ≥30
kg/m2 |
1 |
1 |
1 |
— |
b. Menarche to <18
years and BMI ≥30 kg/m2 |
1 |
1 |
1 |
— |
History
of bariatric surgery This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | ||||
a. Restrictive procedures:
decrease storage capacity of the stomach (vertical banded
gastroplasty, laparoscopic adjustable gastric band, or
laparoscopic sleeve gastrectomy) |
1 |
1 |
1 |
— |
b. Malabsorptive
procedures: decrease absorption of nutrients and calories by
shortening the functional length of the small intestine
(Roux-en-Y gastric bypass or biliopancreatic
diversion) |
1 |
1 |
1 |
— |
Surgery
| ||||
a. Minor surgery without
immobilization |
1 |
1 |
1 |
— |
b. Major
surgery | ||||
i.
Without prolonged immobilization |
1 |
1 |
1 |
— |
ii. With prolonged
immobilization |
1 |
1 |
1 |
— |
Cardiovascular Disease
| ||||
Multiple risk
factors for atherosclerotic cardiovascular disease
(e.g., older age, smoking, diabetes, hypertension, low HDL, high
LDL, or high triglyceride levels) |
1 |
1 |
1 |
— |
Hypertension Systolic blood pressure ≥160 mm Hg or diastolic blood pressure ≥100 mm Hg are associated with increased risk for adverse health events as a result of pregnancy (Box 3). | ||||
a. Adequately controlled
hypertension |
1 |
1 |
1 |
— |
b. Elevated
blood pressure levels (properly taken measurements) | ||||
i.
Systolic 140–159 mm Hg or diastolic 90–99
mm Hg |
1 |
1 |
1 |
— |
ii.
Systolic ≥160 mm Hg or diastolic ≥100 mm
Hg |
1 |
1 |
1 |
— |
c. Vascular
disease |
1 |
1 |
1 |
— |
History of high
blood pressure during pregnancy (when current blood
pressure is measurable and normal) |
1 |
1 |
1 |
— |
Deep
venous thrombosis/
Pulmonary
embolism This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | ||||
a. Current or history of
DVT/PE, receiving anticoagulant therapy (therapeutic dose)
(e.g., acute DVT/PE or long-term therapeutic dose) |
1 |
1 |
1 |
— |
b. History of
DVT/PE, receiving
anticoagulant
therapy
(prophylactic dose) | ||||
i. Higher
risk for recurrent DVT/PE (one or more risk factors) |
1 |
1 |
1 |
— |
• Thrombophilia
(e.g., factor V Leiden mutation; prothrombin gene mutation;
protein S, protein C, and antithrombin deficiencies; or
antiphospholipid
syndrome) • Active cancer (metastatic, receiving therapy, or within 6 months after clinical remission), excluding nonmelanoma skin cancer • History of recurrent DVT/PE | ||||
ii. Lower
risk for recurrent DVT/PE (no risk factors) |
1 |
1 |
1 |
— |
c. History of
DVT/PE, not receiving
anticoagulant therapy | ||||
i. Higher
risk for recurrent DVT/PE (one or more risk factors) |
1 |
1 |
1 |
— |
• History of
estrogen-associated
DVT/PE • Pregnancy-associated DVT/PE • Idiopathic DVT/PE • Thrombophilia (e.g., factor V Leiden mutation; prothrombin gene mutation; protein S, protein C, and antithrombin deficiencies; or antiphospholipid syndrome) • Active cancer (metastatic, receiving therapy, or within 6 months after clinical remission), excluding nonmelanoma skin cancer • History of recurrent DVT/PE | ||||
ii. Lower
risk for recurrent DVT/PE (no risk factors) |
1 |
1 |
1 |
— |
d. Family history
(first-degree relatives) |
1 |
1 |
1 |
— |
Thrombophilia
(e.g., factor V Leiden mutation; prothrombin gene mutation;
protein S, protein C, and antithrombin deficiencies; or
antiphospholipid syndrome) This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
1 |
1 |
1 |
Clarification: Routine
screening in the general population before contraceptive
initiation is not recommended. |
Superficial venous disorders
| ||||
a. Varicose
veins |
1 |
1 |
1 |
— |
b. Superficial venous
thrombosis (acute or history) |
1 |
1 |
1 |
— |
Current and history
of ischemic heart disease This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
1 |
1 |
1 |
— |
Stroke
(history of cerebrovascular accident) This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
1 |
1 |
1 |
— |
Valvular
heart disease Complicated valvular heart disease is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | ||||
a. Uncomplicated |
1 |
1 |
1 |
— |
b. Complicated (pulmonary
hypertension, risk for atrial fibrillation, or history of
subacute bacterial endocarditis) |
1 |
1 |
2 |
— |
Peripartum cardiomyopathy This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | ||||
a. Normal or mildly impaired cardiac function (New York Heart Association Functional Class I or II: no limitation of activities or slight, mild limitation of activity) (3) | ||||
i. <6
months |
1 |
1 |
1 |
— |
ii.
≥6 months |
1 |
1 |
1 |
— |
b. Moderately or severely
impaired cardiac function (New York Heart Association Functional
Class III or IV: marked limitation of activity or should be at
complete rest) (3) |
1 |
1 |
1 |
— |
Renal
Disease
| ||||
Chronic
kidney disease This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | ||||
a. Current nephrotic
syndrome |
1 |
1 |
1 |
— |
b. Hemodialysis |
1 |
1 |
1 |
— |
c. Peritoneal
dialysis |
1 |
1 |
1 |
— |
Rheumatic Diseases
| ||||
Systemic
lupus erythematosus This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | ||||
a. Positive (or unknown)
antiphospholipid antibodies |
1 |
1 |
1 |
— |
b. Severe
thrombocytopenia |
1 |
1 |
1 |
— |
c. Immunosuppressive
therapy |
1 |
1 |
1 |
— |
d. None of the
above |
1 |
1 |
1 |
— |
Rheumatoid
arthritis
|
|
|
|
|
a. Not receiving
immunosuppressive therapy |
1 |
1 |
1 |
— |
b. Receiving
immunosuppressive therapy |
1 |
1 |
1 |
— |
Neurologic Conditions
| ||||
Headaches
| ||||
a. Nonmigraine (mild or
severe) |
1 |
1 |
1 |
— |
b.
Migraine | ||||
i. Without
aura (includes menstrual migraine) |
1 |
1 |
1 |
Comment: Menstrual
migraine is a subtype of migraine without aura. For more
information see the International Headache Society’s
International Classification of Headache Disorders,
3rd ed. (https://ichd-3.org) (4). |
ii. With
aura |
1 |
1 |
1 |
— |
Epilepsy This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
1 |
1 |
1 |
— |
Multiple
sclerosis
| ||||
a. Without prolonged
immobility |
1 |
1 |
1 |
— |
b. With prolonged
immobility |
1 |
1 |
1 |
— |
Depressive Disorders
| ||||
Depressive
disorders
|
1 |
1 |
1 |
— |
Reproductive Tract Infections and
Disorders
| ||||
Unexplained vaginal
bleeding
(suspicious for serious condition)
before evaluation |
1 |
1 |
1 |
Clarification: If
pregnancy or an underlying pathological condition (e.g., pelvic
malignancy) is suspected, it must be evaluated and the category
adjusted after evaluation. |
Endometriosis
|
1 |
1 |
1 |
— |
Benign ovarian
tumors (including cysts) |
1 |
1 |
1 |
— |
Severe
dysmenorrhea
|
1 |
1 |
1 |
— |
Gestational trophoblastic disease This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | ||||
a. Suspected
gestational
trophoblastic disease
(immediate
postevacuation) | ||||
i. Uterine
size first trimester |
1 |
1 |
1 |
— |
ii.
Uterine size second trimester |
1 |
1 |
1 |
— |
b. Confirmed
gestational
trophoblastic disease (after
initial
evacuation and
during
monitoring) | ||||
i.
Undetectable or nonpregnant β–hCG levels |
1 |
1 |
1 |
— |
ii.
Decreasing β–hCG levels |
1 |
1 |
1 |
— |
iii.
Persistently elevated β-hCG levels or malignant disease,
with no evidence or suspicion of intrauterine disease |
1 |
1 |
1 |
— |
iv.
Persistently elevated β-hCG levels or malignant disease,
with evidence or suspicion of intrauterine disease |
1 |
1 |
1 |
— |
Cervical
ectropion
|
1 |
1 |
1 |
— |
Cervical
intraepithelial neoplasia
|
1 |
1 |
1 |
Clarification: The cap
should not be used. Diaphragm use has no restrictions. |
Cervical
cancer (awaiting treatment) |
1 |
Vaginal pH modulator:
1 Spermicide: 2 |
1 |
Clarification: The cap
should not be used. Diaphragm use has no
restrictions. Comment: Repeated and high-dose use of the spermicide nonoxynol-9 can cause vaginal and cervical irritation or abrasions. |
Breast
disease Breast cancer is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | ||||
a. Undiagnosed
mass |
1 |
1 |
1 |
— |
b. Benign breast
disease |
1 |
1 |
1 |
— |
c. Family history of
cancer |
1 |
1 |
1 |
— |
d. Breast
cancer | ||||
i.
Current |
1 |
1 |
1 |
— |
ii. Past
and no evidence of current disease for 5 years |
1 |
1 |
1 |
— |
Endometrial
hyperplasia
|
1 |
1 |
1 |
— |
Endometrial
cancer This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
1 |
1 |
1 |
— |
Ovarian
cancer This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
1 |
1 |
1 |
— |
Uterine
fibroids
|
1 |
1 |
1 |
— |
Anatomical
abnormalities
|
1 |
1 |
NA |
Clarification: The
diaphragm cannot be used in certain cases of prolapse. Cap use
is not appropriate for a person with markedly distorted cervical
anatomy. |
Pelvic
inflammatory disease
| ||||
a. Current PID |
1 |
1 |
1 |
— |
b. Past
PID | ||||
i. With
subsequent pregnancy |
1 |
1 |
1 |
— |
ii.
Without subsequent pregnancy |
1 |
1 |
1 |
— |
Sexually
transmitted infections
| ||||
a. Current purulent
cervicitis or chlamydial infection or gonococcal
infection |
1 |
1 |
1 |
— |
b. Vaginitis (including
Trichomonas vaginalis and bacterial
vaginosis) |
1 |
1 |
1 |
— |
c. Other factors related
to STIs |
1 |
1 |
1 |
— |
HIV
| ||||
High risk for HIV
infection
|
1 |
Vaginal pH modulator:
1 Spermicide: 4 |
4 |
Evidence: Repeated and
high-dose use of the spermicide nonoxynol-9 was associated with
increased risk for genital lesions, which might increase the
risk for HIV infection (5). Comment: Diaphragm and cap use is assigned category 4 because of concerns about the spermicide, not the diaphragm or cap. |
HIV
infection For persons with HIV infection who are not clinically well or not receiving ARV therapy, this condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
1 |
Vaginal pH modulator:
1 Spermicide: 3 |
3 |
Comment: Use of
spermicides, including with diaphragms and caps, can disrupt the
cervical mucosa, which might increase viral shedding and HIV
transmission to noninfected sex partners. |
Other
Infections
| ||||
Schistosomiasis
Schistosomiasis with
fibrosis of
the liver is associated with
increased
risk for adverse health
events as a result of
pregnancy
(Box
3). | ||||
a. Uncomplicated |
1 |
1 |
1 |
— |
b. Fibrosis of the
liver |
1 |
1 |
1 |
— |
Tuberculosis This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | ||||
a. Nonpelvic |
1 |
1 |
1 |
— |
b. Pelvic |
1 |
1 |
1 |
— |
Malaria
|
1 |
1 |
1 |
— |
History of toxic
shock syndrome
|
1 |
1 |
3 |
Comment: Toxic shock
syndrome has been reported in association with contraceptive
sponge and diaphragm use. |
Urinary tract
infection
|
1 |
Vaginal pH modulator:
2 Spermicide: 1 |
2 |
Comment: Use of
diaphragms and spermicides might increase risk for urinary tract
infection. |
Endocrine Conditions
| ||||
Diabetes Insulin-dependent diabetes; diabetes with nephropathy, retinopathy, or neuropathy; diabetes with other vascular disease; or diabetes of >20 years’ duration are associated with increased risk for adverse health events as a result of pregnancy (Box 3). | ||||
a. History of gestational
disease |
1 |
1 |
1 |
— |
b. Nonvascular
disease | ||||
i.
Non-insulin dependent |
1 |
1 |
1 |
— |
ii.
Insulin dependent |
1 |
1 |
1 |
— |
c. Nephropathy,
retinopathy, or neuropathy |
1 |
1 |
1 |
— |
d. Other vascular disease
or diabetes of >20 years' duration |
1 |
1 |
1 |
— |
Thyroid
disorders
| ||||
a. Simple goiter |
1 |
1 |
1 |
— |
b. Hyperthyroid |
1 |
1 |
1 |
— |
c. Hypothyroid |
1 |
1 |
1 |
— |
Gastrointestinal Conditions
| ||||
Inflammatory bowel
disease (ulcerative colitis or Crohn’s
disease) |
1 |
1 |
1 |
— |
Gallbladder disease
| ||||
a. Asymptomatic |
1 |
1 |
1 |
— |
b. Symptomatic |
|
|
|
|
i.
Current |
1 |
1 |
1 |
— |
ii.
Treated by cholecystectomy |
1 |
1 |
1 |
— |
iii.
Medically treated |
1 |
1 |
1 |
— |
History
of cholestasis
| ||||
a. Pregnancy
related |
1 |
1 |
1 |
— |
b. Past COC
related |
1 |
1 |
1 |
— |
Viral
hepatitis
|
|
|
|
|
a. Acute or
flare |
1 |
1 |
1 |
— |
b. Chronic |
1 |
1 |
1 |
— |
Cirrhosis Decompensated cirrhosis is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | ||||
a. Compensated (normal
liver function) |
1 |
1 |
1 |
— |
b. Decompensated (impaired
liver function) |
1 |
1 |
1 |
— |
Liver
tumors Hepatocellular adenoma and malignant liver tumors are associated with increased risk for adverse health events as a result of pregnancy (Box 3). | ||||
a.
Benign | ||||
i.
Focal nodular hyperplasia |
1 |
1 |
1 |
— |
ii. Hepatocellular adenoma |
1 |
1 |
1 |
— |
b. Malignant
(hepatocellular carcinoma) |
1 |
1 |
1 |
— |
Respiratory Conditions
| ||||
Cystic
fibrosis This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
1 |
1 |
1 |
— |
Hematologic Conditions
| ||||
Thalassemia
|
1 |
1 |
1 |
— |
Sickle cell
disease This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
1 |
1 |
1 |
— |
Iron deficiency
anemia
|
1 |
1 |
1 |
— |
Solid
Organ Transplantation
| ||||
Solid
organ transplantation This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | ||||
a. No graft
failure |
1 |
1 |
1 |
— |
b. Graft failure |
1 |
1 |
1 |
— |
Drug
Interactions
| ||||
Antiretrovirals used for
prevention (PrEP) or
treatment
of HIV infection
|
Clarification: No drug interaction between ARV
therapy and barrier method use is known. HIV infection is
classified as category 1 for vaginal pH modulator and category 3
for spermicide and diaphragm and cap use (see recommendations
for HIV infection). High risk for HIV infection is classified as
category 1 for vaginal pH modulator and category 4 for
spermicide and diaphragm or cap (see recommendations for High
risk for HIV infection). |
|||
a. Nucleoside
reverse
transcriptase inhibitors (NRTIs) | ||||
i.
Abacavir (ABC) |
1 |
1/3/4 |
3/4 |
|
ii.
Tenofovir (TDF) |
1 |
1/3/4 |
3/4 |
|
iii.
Zidovudine (AZT) |
1 |
1/3/4 |
3/4 |
|
iv.
Lamivudine (3TC) |
1 |
1/3/4 |
3/4 |
|
v.
Didanosine (DDI) |
1 |
1/3/4 |
3/4 |
|
vi.
Emtricitabine (FTC) |
1 |
1/3/4 |
3/4 |
|
vii.
Stavudine (D4T) |
1 |
1/3/4 |
3/4 |
|
b.
Nonnucleoside reverse
transcriptase inhibitors
(NNRTIs) | ||||
i.
Efavirenz (EFV) |
1 |
1/3/4 |
3/4 |
|
ii.
Etravirine (ETR) |
1 |
1/3/4 |
3/4 |
|
iii.
Nevirapine (NVP) |
1 |
1/3/4 |
3/4 |
|
iv.
Rilpivirine (RPV) |
1 |
1/3/4 |
3/4 |
|
c.
Ritonavir-boosted protease
inhibitors | ||||
i.
Ritonavir-boosted atazanavir (ATV/r) |
1 |
1/3/4 |
3/4 |
|
ii.
Ritonavir-boosted darunavir (DRV/r) |
1 |
1/3/4 |
3/4 |
|
iii.
Ritonavir-boosted fosamprenavir (FPV/r) |
1 |
1/3/4 |
3/4 |
|
iv.
Ritonavir-boosted lopinavir (LPV/r) |
1 |
1/3/4 |
3/4 |
|
v.
Ritonavir-boosted saquinavir (SQV/r) |
1 |
1/3/4 |
3/4 |
|
vi.
Ritonavir-boosted tipranavir (TPV/r) |
1 |
1/3/4 |
3/4 |
|
d. Protease
inhibitors without ritonavir | ||||
i.
Atazanavir (ATV) |
1 |
1/3/4 |
3/4 |
|
ii.
Fosamprenavir (FPV) |
1 |
1/3/4 |
3/4 |
|
iii.
Indinavir (IDV) |
1 |
1/3/4 |
3/4 |
|
iv.
Nelfinavir (NFV) |
1 |
1/3/4 |
3/4 |
|
e. CCR5
co-receptor antagonists | ||||
i.
Maraviroc (MVC) |
1 |
1/3/4 |
3/4 |
|
f. HIV
integrase strand transfer
inhibitors | ||||
i.
Raltegravir (RAL) |
1 |
1/3/4 |
3/4 |
|
ii.
Dolutegravir (DTG) |
1 |
1/3/4 |
3/4 |
|
iii.
Elvitegravir (EVG) |
1 |
1/3/4 |
3/4 |
|
g. Fusion
inhibitors | ||||
i.
Enfuvirtide |
1 |
1/3/4 |
3/4 |
|
Anticonvulsant therapy
| ||||
a. Certain anticonvulsants
(phenytoin, carbamazepine, barbiturates, primidone, topiramate,
or oxcarbazepine) |
1 |
1 |
1 |
— |
b. Lamotrigine |
1 |
1 |
1 |
— |
Antimicrobial therapy
| ||||
a. Broad-spectrum
antibiotics |
1 |
1 |
1 |
— |
b. Antifungals |
1 |
1 |
1 |
— |
c.
Antiparasitics |
1 |
1 |
1 |
— |
d. Rifampin or rifabutin
therapy |
1 |
1 |
1 |
— |
Psychotropic medications
| ||||
a. Selective serotonin
reuptake inhibitors (SSRIs) |
1 |
1 |
1 |
— |
St. John’s
wort
|
1 |
1 |
1 |
— |
Allergy to latex | 3 | 1 | 3 | Clarification: The condition of allergy to latex does not apply to plastic condoms or diaphragms. |
Abbreviations: ARV = antiretroviral; BMI = body mass index; COC = combined oral contraceptive; DVT = deep venous thrombosis; hCG = human chorionic gonadotropin; HDL = high-density lipoprotein; LDL = low-density lipoprotein; NA = not applicable; PE = pulmonary embolism; PID = pelvic inflammatory disease; PrEP = pre-exposure prophylaxis; STI = sexually transmitted infection.
References
- 1.Workowski KA, Bachmann LH, Chan PA, et al. Sexually transmitted infections treatment guidelines, 2021. MMWR Recomm Rep 2021;70(No. RR-4):1–187. 10.15585/mmwr.rr7004a1 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2.CDC. US Public Health Service preexposure prophylaxis for the prevention of HIV infection in the United States—2021 update: a clinical practice guideline. Atlanta, GA: US Department of Health and Human Services, CDC; 2021. https://www.cdc.gov/hiv/pdf/risk/prep/cdc-hiv-prep-guidelines-2021.pdf
- 3.The Criteria Committee of the New York Heart Association. Nomenclature and criteria for diagnosis of diseases of the heart and great vessels. 9th ed. Boston, MA: Little, Brown and Co; 1994. [Google Scholar]
- 4.Headache Classification Committee of the International Headache Society (IHS) The International Classification of Headache Disorders. 3rd ed. Cephalalgia 2018;38:1–211. https://www.ichd-3.org/wp-content/uploads/2018/01/The-International-Classification-of-Headache-Disorders-3rd-Edition-2018.pdf [DOI] [PubMed] [Google Scholar]
- 5.Wilkinson D, Ramjee G, Tholandi M, Rutherford G. Nonoxynol-9 for preventing vaginal acquisition of HIV infection by women from men. Cochrane Database Syst Rev 2002;2002:CD003936. 10.1002/14651858.CD003936 [DOI] [PMC free article] [PubMed] [Google Scholar]
Appendix F. Classifications for Fertility Awareness–Based Methods
Fertility awareness–based (FAB) methods involve identifying the fertile days of the menstrual cycle, whether by observing fertility signs, such as cervical secretions and basal body temperature or by monitoring cycle days, and might include use of Food and Drug Administration–cleared contraceptive software applications (Box F1) (Table F1). FAB methods can be used in combination with abstinence or barrier methods during the fertile time. If barrier methods are used, see Classifications for Barrier Methods (Appendix E).
BOX F1. Definitions for terms associated with fertility awareness–based methods.
Symptoms-based methods: FAB methods based on observation of fertility signs (e.g., cervical secretions or basal body temperature) such as the cervical mucus method, the symptothermal method, and the TwoDay method.
Calendar-based methods: FAB methods based on calendar calculations such as the calendar rhythm method and the standard days method.
Accept: No medical reason exists to deny the particular FAB method to a patient in this circumstance.
Caution: The method normally is provided in a routine setting but with extra preparation and precautions. For FAB methods, this usually means that special counseling might be needed to ensure correct use of the method by a patient in this circumstance.
Delay: Use of this method should be delayed until the condition is evaluated or corrected. Alternative temporary methods of contraception should be offered.
Abbreviation: FAB = fertility awareness–based.
No medical conditions worsen because of FAB methods. In general, FAB methods can be used without concern for health effects in persons who choose them. However, multiple conditions make their use more complex. The existence of these conditions suggests that use of these methods should be delayed until the condition is corrected or resolved, or persons using FAB methods need special counseling; and a provider with particular training in use of these methods is generally necessary to ensure correct use.
FAB methods do not protect against sexually transmitted infections (STIs), including HIV infection, and patients using FAB methods should be counseled that consistent and correct use of external (male) latex condoms reduces the risk for STIs, including HIV infection (1). Use of internal (female) condoms can provide protection from transmission of STIs, although data are limited (1). Patients also should be counseled that pre-exposure prophylaxis, when taken as prescribed, is highly effective for preventing HIV infection (2).
TABLE F1. Fertility awareness–based methods, including symptoms-based and calendar-based methods.
Condition | Category |
Clarification/Evidence/Comment | ||
---|---|---|---|---|
Symptoms-based method | Calendar-based method |
|||
Personal
Characteristics and Reproductive History
| ||||
Pregnancy
|
NA |
NA |
Clarification: FAB
methods are not relevant during pregnancy. |
|
Life
stage
|
Comment:
Menstrual irregularities are common in postmenarche and
perimenopause and might complicate the use of FAB
methods. |
|||
a. Postmenarche |
Caution |
Caution |
||
b. Perimenopause |
Caution |
Caution |
||
Breastfeeding
|
Comment: Use of FAB
methods when breastfeeding might be less effective than when not
breastfeeding. |
|||
a. <6 weeks
postpartum |
Delay |
Delay |
Comment:
Persons who are primarily breastfeeding and are amenorrheic are
unlikely to have sufficient ovarian function to produce
detectable fertility signs and hormonal changes during the first
6 months postpartum. However, the likelihood of resumption of
fertility increases with time postpartum and with substitution
of breast milk by other foods. |
|
b. ≥6 weeks
postpartum |
Caution |
Delay |
||
c. After menses
begin |
Caution |
Caution |
Clarification: Once
fertility signs are noted, particularly cervical secretions,
then symptoms-based methods can be used. First postpartum
menstrual cycles while breastfeeding vary significantly in
length. Return to regularity takes several cycles. When there
have been at least three postpartum menses and cycles are
regular again, a calendar-based method can be used. When there
have been at least four postpartum menses and the most recent
cycle lasted 26–32 days, the standard days method can be
used. Before that time, a barrier method should be offered if
the patient plans to use a FAB method later. |
|
Postpartum (nonbreastfeeding) | ||||
a. <4 weeks |
Delay |
Delay |
Clarification:
Nonbreastfeeding persons are not likely to have detectable
fertility signs or hormonal changes before 4 weeks postpartum.
Although the risk for pregnancy is low, ovulation before first
menses is common; therefore, a method appropriate for the
postpartum period should be offered. |
|
b. ≥4
weeks |
Accept |
Delay |
Clarification:
Nonbreastfeeding persons are likely to have sufficient ovarian
function to produce detectable fertility signs, hormonal
changes, or both at this time; likelihood increases rapidly with
time postpartum. Calendar-based methods can be used as soon as
three postpartum menses have been completed. Methods appropriate
for the postpartum period should be offered before that
time. |
|
Postabortion
(spontaneous or induced) |
Caution |
Delay |
Clarification: After
abortion, it is possible for ovarian function to produce
detectable fertility signs, hormonal changes, or both;
likelihood increases with time postabortion. Calendar-based
methods can be used following at least one postabortion menses
(e.g., persons who before this pregnancy primarily had cycles of
26–32 days can then use the standard days method).
Methods appropriate for the postabortion period should be
offered before that time. |
|
Reproductive Tract Infections and
Disorders
| ||||
Irregular vaginal
bleeding
|
Delay |
Delay |
Clarification: Presence
of this condition makes FAB methods unreliable. Therefore,
barrier methods should be recommended until the bleeding pattern
is compatible with proper method use. The condition should be
evaluated and treated as necessary. |
|
Vaginal
discharge
|
Delay |
Accept |
Clarification: Because
vaginal discharge makes recognition of cervical secretions
difficult, the condition should be evaluated and treated if
needed before providing methods based on cervical
secretions. |
|
Other
| ||||
Use of drugs that
affect cycle regularity, hormones, or fertility
signs
|
Caution /Delay |
Caution/Delay |
Clarification: Use of
certain mood-altering drugs (e.g., lithium, tricyclic
antidepressants, and antianxiety therapies), as well as certain
antibiotics and anti-inflammatory drugs, might alter cycle
regularity or affect fertility signs. The condition should be
carefully evaluated and a barrier method offered until the
degree of effect has been determined or the drug is no longer
being used. |
|
Diseases
that elevate
body temperature
| ||||
a. Chronic
diseases |
Caution |
Accept |
Clarification: Elevated temperatures might make basal body temperature difficult to interpret but have no effect on cervical secretions. Thus, use of a method that relies on temperature should be delayed until the acute febrile disease abates. Temperature-based methods are not appropriate for persons with chronically elevated temperatures. In addition, certain chronic diseases interfere with cycle regularity, making calendar-based methods difficult to interpret. | |
b. Acute diseases | Delay |
Accept |
Abbreviations: FAB = fertility awareness–based; NA = not applicable.
References
- 1.Workowski KA, Bachmann LH, Chan PA, et al. Sexually transmitted infections treatment guidelines, 2021. MMWR Recomm Rep 2021;70(No. RR-4):1–187. 10.15585/mmwr.rr7004a1 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2.CDC. US Public Health Service preexposure prophylaxis for the prevention of HIV infection in the United States—2021 update: a clinical practice guideline. Atlanta, GA: US Department of Health and Human Services, CDC; 2021. https://www.cdc.gov/hiv/pdf/risk/prep/cdc-hiv-prep-guidelines-2021.pdf
Appendix G. Lactational Amenorrhea Method
The Bellagio Consensus provided the scientific basis for defining the conditions under which breastfeeding can be used safely and effectively for birth-spacing purposes; programmatic guidelines were developed at a meeting of family planning experts for its use as a method of contraception, and the method was then named the lactational amenorrhea method (LAM) (1–3). These guidelines include the following three criteria, all of which must be met to ensure adequate protection from pregnancy: 1) amenorrhea, 2) fully or nearly fully breastfeeding (intervals between feedings not exceeding 4 hours during the day or 6 hours at night), and 3) <6 months postpartum (4–6).
The U.S. Dietary Guidelines for Americans recommend that infants be exclusively breastfed for about the first 6 months, with continued breastfeeding while introducing appropriate complementary foods for 1 year or longer (7). The American Academy of Pediatrics (AAP) recommends exclusive breastfeeding for about the first 6 months, with continued breastfeeding along with introducing appropriate complementary foods for up to age 2 years or longer (8).
No medical conditions exist for which use of LAM for contraception is restricted. However, breastfeeding might not be recommended for persons or infants with certain conditions.
LAM does not protect against sexually transmitted infections (STIs), including HIV infection, and patients using LAM should be counseled that consistent and correct use of external (male) latex condoms reduces the risk for STIs, including HIV infection (9). Use of internal (female) condoms can provide protection from transmission of STIs, although data are limited (9). Patients also should be counseled that pre-exposure prophylaxis, when taken as prescribed, is highly effective for preventing HIV infection (10).
HIV Infection. HIV transmission can occur during breastfeeding. For breastfeeding persons on antiretroviral therapy with a sustained undetectable HIV viral load during pregnancy, the risk for transmission through breastfeeding is <1%, but not zero. Patients with HIV infection should receive evidence-based, person-centered counseling to support shared decision-making about infant feeding. For comprehensive information, refer to Infant Feeding for Individuals with HIV in the United States (https://clinicalinfo.hiv.gov/en/guidelines/perinatal/counseling-and-managing-individuals-with-hiv-united-states-who-desire-breastfeed). These recommendations are included within the U.S. Department of Health and Human Services’s Recommendations for the Use of Antiretroviral Drugs During Pregnancy and Interventions to Reduce Perinatal HIV Transmission in the United States (https://clinicalinfo.hiv.gov/en/guidelines/perinatal/whats-new-guidelines) (11).
Other Medical Conditions. CDC and AAP also recommend against both breastfeeding and feeding expressed milk for persons with untreated brucellosis, positivity for human T-cell lymphotropic virus types I or II, herpes simplex lesions on a breast, Ebola virus disease, or mpox. In addition, infants with classic galactosemia should not breastfeed (8,12,13) (https://www.cdc.gov/breastfeeding-special-circumstances/hcp/contraindications/index.html).
Medication Used During Breastfeeding. Although many medications do pass into breast milk, most have little or no effect on milk supply or on infant well-being. Few medications are contraindicated while breastfeeding. More information about specific medications and radioactive compounds is provided by AAP (14), LactMed (https://www.ncbi.nlm.nih.gov/books/NBK501922), Mother to Baby (http://www.mothertobaby.org), and InfantRisk Center (https://www.infantrisk.com/category/breastfeeding).
References
- 1.Kennedy KI, Rivera R, McNeilly AS. Consensus statement on the use of breastfeeding as a family planning method. Contraception 1989;39:477–96. 10.1016/0010-7824(89)90103-0 [DOI] [PubMed] [Google Scholar]
- 2.Labbok M, Cooney K, Coly S. Guidelines: breastfeeding, family planning, and the lactational amenorrhea method—LAM. Washington, DC: Institute for Reproductive Health, 1994. [Google Scholar]
- 3.Labbok MH, Perez A, Valdes V, et al. The lactational amenorrhea method (LAM): a postpartum introductory family planning method with policy and program implications. Adv Contracept 1994;10:93–109. 10.1007/BF01978103 [DOI] [PubMed] [Google Scholar]
- 4.Hight-Laukaran V, Labbok MH, Peterson AE, Fletcher V, von Hertzen H, Van Look PF. Multicenter study of the lactational amenorrhea method (LAM): II. Acceptability, utility, and policy implications. Contraception 1997;55:337–46. 10.1016/S0010-7824(97)00041-3 [DOI] [PubMed] [Google Scholar]
- 5.Labbok MH, Hight-Laukaran V, Peterson AE, Fletcher V, von Hertzen H, Van Look PF. Multicenter study of the lactational amenorrhea method (LAM): I. Efficacy, duration, and implications for clinical application. Contraception 1997;55:327–36. 10.1016/S0010-7824(97)00040-1 [DOI] [PubMed] [Google Scholar]
- 6.Peterson AE, Peŕez-Escamilla R, Labbok MH, Hight V, von Hertzen H, Van Look P. Multicenter study of the lactational amenorrhea method (LAM) III: effectiveness, duration, and satisfaction with reduced client-provider contact. Contraception 2000;62:221–30. 10.1016/S0010-7824(00)00171-2 [DOI] [PubMed] [Google Scholar]
- 7.US Department of Agriculture; US Department of Health and Human Services. Dietary guidelines for Americans, 2020–2025. 9th ed. Washington, DC: US Department of Agriculture and US Department of Health and Human Services; 2020. https://www.dietaryguidelines.gov/sites/default/files/2021-03/Dietary_Guidelines_for_Americans-2020-2025.pdf
- 8.Meek JY, Noble L; Section on Breastfeeding. Policy statement: breastfeeding and the use of human milk. Pediatrics 2022;150:e2022057988. 10.1542/peds.2022-057988 [DOI] [PubMed] [Google Scholar]
- 9.Workowski KA, Bachmann LH, Chan PA, et al. Sexually transmitted infections treatment guidelines, 2021. MMWR Recomm Rep 2021;70(No. RR-4):1–187. 10.15585/mmwr.rr7004a1 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 10.CDC. US Public Health Service preexposure prophylaxis for the prevention of HIV infection in the United States—2021 update: a clinical practice guideline. Atlanta, GA: US Department of Health and Human Services, CDC; 2021. https://www.cdc.gov/hiv/pdf/risk/prep/cdc-hiv-prep-guidelines-2021.pdf
- 11.Panel on Treatment of HIV During Pregnancy and Prevention of Perinatal Transmission. Recommendations for the use of antiretroviral drugs during pregnancy and interventions to reduce perinatal HIV transmission in the United States. Washington, DC: US Department of Health and Human Services; 2023. https://clinicalinfo.hiv.gov/en/guidelines/perinatal/recommendations-arv-drugs-pregnancy-overview [Google Scholar]
- 12.Meek JY, Noble L. Technical report: breastfeeding and the use of human milk. Pediatrics 2022;150:e2022057989. 10.1542/peds.2022-057989 [DOI] [PubMed] [Google Scholar]
- 13.CDC. Contraindications to breastfeeding or feeding expressed breast milk to infants; 2023. https://www.cdc.gov/breastfeeding-special-circumstances/hcp/contraindications/index.html
- 14.Sachs HC, Frattarelli DAC, Galinkin JL, et al. ; Committee on Drugs. The transfer of drugs and therapeutics into human breast milk: an update on selected topics. Pediatrics 2013;132:e796–809. 10.1542/peds.2013-1985 [DOI] [PubMed] [Google Scholar]
Appendix H. Coitus Interruptus (Withdrawal)
Coitus interruptus, also known as withdrawal, is a contraceptive method in which the penis is completely removed from the vagina and away from the external genitalia before ejaculation. Coitus interruptus prevents sperm from entering the vagina, thereby preventing contact between spermatozoa and the ovum.
Coitus interruptus has no directly associated health risks. Coitus interruptus does not protect against sexually transmitted infections (STIs), including HIV infection, and patients using coitus interruptus should be counseled that consistent and correct use of external (male) latex condoms reduces the risk for STIs, including HIV infection (1). Use of internal (female) condoms can provide protection from transmission of STIs, although data are limited (1). Patients also should be counseled that pre-exposure prophylaxis, when taken as prescribed, is highly effective for preventing HIV infection (2).
References
- 1.Workowski KA, Bachmann LH, Chan PA, et al. Sexually transmitted infections treatment guidelines, 2021. MMWR Recomm Rep 2021;70(No. RR-4):1–187. 10.15585/mmwr.rr7004a1 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2.CDC. US Public Health Service preexposure prophylaxis for the prevention of HIV infection in the United States—2021 update: a clinical practice guideline. Atlanta, GA: US Department of Health and Human Services, CDC; 2021. https://www.cdc.gov/hiv/pdf/risk/prep/cdc-hiv-prep-guidelines-2021.pdf
Appendix I. Permanent Contraception
Tubal surgery (including laparoscopic and abdominal approaches) and vasectomy are methods of permanent contraception available in the United States. In general, no medical conditions absolutely restrict a person’s eligibility for permanent contraception (with the exception of known allergy or hypersensitivity to any materials used to complete the permanent contraception procedure). However, certain conditions might increase a person’s surgical risk during tubal surgery; in these cases, careful consideration can be given to the risks and benefits of other acceptable long-acting or permanent alternatives, including intrauterine device, implant, and vasectomy.
Patients should be appropriately counseled that permanent contraception is intended to be irreversible and about the availability of highly effective, long-acting reversible methods of contraception. Most persons who choose permanent contraception remain satisfied with their decision. However, a small proportion of women regret this decision (1%–26% from different studies, with higher rates of regret reported by women who were younger at time of permanent contraception procedure) (1,2). Regret among men about vasectomy has been reported to be approximately 5% (3), similar to the proportion of women who report regretting their husbands’ vasectomy (6%) (4).
Permanent contraception does not protect against sexually transmitted infections (STIs), including HIV infection, and patients using permanent contraception should be counseled that consistent and correct use of external (male) latex condoms reduces the risk for STIs, including HIV infection (5). Use of internal (female) condoms can provide protection from transmission of STIs, although data are limited (5). Patients also should be counseled that pre-exposure prophylaxis, when taken as prescribed, is highly effective for preventing HIV infection (6).
References
- 1.Hillis SD, Marchbanks PA, Tylor LR, Peterson HB. Poststerilization regret: findings from the United States Collaborative Review of Sterilization. Obstet Gynecol 1999;93:889–95. 10.1097/00006250-199906000-00001 [DOI] [PubMed] [Google Scholar]
- 2.Peterson HB. Sterilization. Obstet Gynecol 2008;111:189–203. 10.1097/01.AOG.0000298621.98372.62 [DOI] [PubMed] [Google Scholar]
- 3.Ehn BE, Liljestrand J. A long-term follow-up of 108 vasectomized men. Good counselling routines are important. Scand J Urol Nephrol 1995;29:477–81. 10.3109/00365599509180030 [DOI] [PubMed] [Google Scholar]
- 4.Jamieson DJ, Kaufman SC, Costello C, Hillis SD, Marchbanks PA, Peterson HB; US Collaborative Review of Sterilization Working Group. A comparison of women’s regret after vasectomy versus tubal sterilization. Obstet Gynecol 2002;99:1073–9. 10.1016/S0029-7844(02)01981-6 [DOI] [PubMed] [Google Scholar]
- 5.Workowski KA, Bachmann LH, Chan PA, et al. Sexually transmitted infections treatment guidelines, 2021. MMWR Recomm Rep 2021;70(No. RR-4):1–187. 10.15585/mmwr.rr7004a1 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 6.CDC. US Public Health Service preexposure prophylaxis for the prevention of HIV infection in the United States—2021 update: a clinical practice guideline. Atlanta, GA: US Department of Health and Human Services, CDC; 2021. https://www.cdc.gov/hiv/pdf/risk/prep/cdc-hiv-prep-guidelines-2021.pdf
Appendix. J: Classifications for Emergency Contraception
Classifications are given for the copper intrauterine device (Cu-IUD) as emergency contraception. The Cu-IUD can be placed within 5 days of the first act of unprotected intercourse as emergency contraception. In addition, when the day of ovulation can be estimated, the Cu-IUD can be placed beyond 5 days after sexual intercourse, as long as the placement does not occur >5 days after ovulation. The eligibility criteria for interval Cu-IUD placement also apply for the placement of Cu-IUDs as emergency contraception (Box J1) (Table J1) (1).
Classifications for emergency contraceptive pills (ECPs) are given for ulipristal acetate (UPA), levonorgestrel (LNG), and combined oral contraceptives (COCs). ECPs should be taken as soon as possible within 5 days of unprotected sexual intercourse (1).
Cu-IUDs, UPA, LNG, and COCs do not protect against sexually transmitted infections (STIs), including HIV infection, and patients using these methods should be counseled that consistent and correct use of external (male) latex condoms reduces the risk for STIs, including HIV infection (2). Use of internal (female) condoms can provide protection from transmission of STIs, although data are limited (2). Patients also should be counseled that pre-exposure prophylaxis, when taken as prescribed, is highly effective for preventing HIV infection (3).
BOX. J1. Categories for classifying emergency contraception.
U.S. MEC 1 = A condition for which there is no restriction for the use of the contraceptive method.
U.S. MEC 2 = A condition for which the advantages of using the method generally outweigh the theoretical or proven risks.
U.S. MEC 3 = A condition for which the theoretical or proven risks usually outweigh the advantages of using the method.
U.S. MEC 4 = A condition that represents an unacceptable health risk if the contraceptive method is used.
Abbreviation: U.S. Medical Eligibility Criteria for Contraceptive Use.
TABLE. J1. Classifications for emergency contraception, including the copper intrauterine device, ulipristal acetate, levonorgestrel, and combined oral contraceptives.
Condition | Category |
Clarification/Evidence/Comment | |||
---|---|---|---|---|---|
Cu-IUD | UPA | LNG | COC | ||
Personal Characteristics and Reproductive
History
| |||||
Pregnancy
|
4 |
NA |
NA |
NA |
Clarification (IUD):
The IUD is not indicated during pregnancy and should not be
used because of the risk for serious pelvic infection and
septic spontaneous
abortion. Clarification (ECPs): Although this method is not indicated for a patient with a known or suspected pregnancy, no harm to the patient, the course of pregnancy, or the fetus if ECPs are inadvertently used is known to exist. Evidence: Evidence suggests that poor pregnancy outcomes are rare among pregnant women who used ECPs during conception cycle or early in pregnancy (4). |
Breastfeeding
|
1 |
1 |
1 |
1 |
Evidence:
Breastfeeding outcomes do not seem to differ between women
exposed to LNG and those who are not exposed (4). One
pharmacokinetic study demonstrated that LNG passes to breast
milk but in minimal quantities (4). UPA and its active
metabolite, monodemethyl-ulipristal acetate, are present in
human milk in small amounts; no evidence is available on
effects of UPA emergency contraception exposure on infants
or children who are breastfed (5). |
Past ectopic
pregnancy
|
1 |
1 |
1 |
1 |
— |
Obesity (BMI
≥30 kg/m2)
|
1 |
2 |
2 |
2 |
Clarification
(ECPs): ECPs might be less effective among
persons with BMI ≥30 kg/m2 than among
persons with BMI <25 kg/m2. Despite this, no
safety concerns exist. Evidence: Limited evidence from secondary data analyses suggests that women with BMI ≥30 kg/m2 experience an increased risk for pregnancy after use of LNG compared with women with BMI <25 kg/m2. Two analyses suggest that women with obesity might also experience an increased risk for pregnancy after use of UPA compared with those without obesity, although this increase was not significant in one study (6). |
History of bariatric surgery This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | |||||
a. Restrictive
procedures: decrease storage capacity of the stomach
(vertical banded gastroplasty, laparoscopic adjustable
gastric band, or laparoscopic sleeve gastrectomy) |
1 |
1 |
1 |
1 |
— |
b. Malabsorptive
procedures: decrease absorption of nutrients and calories by
shortening the functional length of the small intestine
(Roux-en-Y gastric bypass or biliopancreatic
diversion) |
1 |
1 |
1 |
1 |
Comment: Bariatric
surgical procedures involving a malabsorptive component have
the potential to decrease oral contraceptive effectiveness,
perhaps further decreased by postoperative complications
such as long-term diarrhea, vomiting, or both. Because of
these malabsorptive concerns, an emergency IUD might be more
appropriate than ECPs. |
Cardiovascular Disease
| |||||
History of
severe cardiovascular disease (ischemic heart
disease, cerebrovascular attack, or other thromboembolic
conditions) This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
1 |
2 |
2 |
2 |
Comment: The duration
of ECP use is less than that of regular use of COCs or POPs
and thus would be expected to have less clinical
impact. |
Rheumatic Diseases
| |||||
Rheumatoid arthritis
| |||||
a. Not receiving
immunosuppressive therapy |
1 |
1 |
1 |
1 |
— |
b. Receiving
immunosuppressive therapy |
2 |
1 |
1 |
1 |
— |
Neurologic Conditions
| |||||
Migraine
|
1 |
1 |
1 |
2 |
Comment: The duration
of ECP use is less than that of regular use of COCs and thus
would be expected to have less clinical impact. |
Gastrointestinal Conditions
| |||||
Inflammatory
bowel disease (ulcerative colitis or
Crohn’s disease) |
1 |
1 |
1 |
1 |
— |
Severe liver
disease (including jaundice) This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
1 |
2 |
2 |
2 |
Comment: The duration
of ECP use is less than that of regular use of COCs or POPs
and thus would be expected to have less clinical
impact. |
Solid Organ Transplantation
| |||||
Solid organ transplantation This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | |||||
a. No graft
failure |
1 |
1 |
1 |
1 |
— |
b. Graft
failure |
2 |
1 |
1 |
1 |
— |
Other
| |||||
Repeated ECP
use
|
— |
1 |
1 |
1 |
Clarification (ECPs):
Frequently repeated ECP use might be harmful for persons
with conditions classified as category 2, 3, or 4 for CHC or
POC use. Evidence: In one case-control study, risk for ectopic pregnancy compared with intrauterine pregnancy did not increase after repeated use of LNG ECPs compared with nonuse (4). |
Sexual
assault
|
2 |
1 |
1 |
1 |
Clarification (IUD):
Persons who have experienced sexual assault are at increased
risk for STIs, including HIV infection. According to CDC STI
treatment guidelines, routine presumptive treatment of
chlamydia, gonorrhea, and trichomonas is recommended after
sexual assault (2). Persons with current
purulent cervicitis, chlamydial infection, or gonococcal
infection should not undergo IUD placement (category
4). |
CYP3A4 inducers (e.g., bosentan, carbamazepine, felbamate, griseofulvin, oxcarbazepine, phenytoin, rifampin, St. John’s wort, topiramate, efavirenz, and lumacaftor) | 1 | 2 | 2 | 2 |
Clarification (ECPs):
Strong CYP3A4 inducers might reduce the effectiveness of
ECPs. Evidence: According to labelling information, rifampin markedly decreases UPA levels by ≥90%, which might decrease its efficacy (5). Therefore, theoretical concerns extend to use of other CYP3A4 inducers as well as to COC and LNG ECPs, which have metabolic pathways similar to those of UPA. A small pharmacokinetic study found that concomitant efavirenz use decreased LNG levels in women taking LNG ECPs (1.5 mg) by 56% compared with LNG ECPs alone (7). |
Abbreviations: BMI = body mass index; CHC = combined hormonal contraceptive; COC = combined hormonal contraceptive; Cu-IUD = copper intrauterine device; CYP = cytochrome P450; ECP = emergency contraceptive pill; IUD = intrauterine device; LNG = levonorgestrel; NA = not applicable; POC = progestin-only contraceptive; POP = progestin-only pill; STI = sexually transmitted infection; UPA = ulipristal acetate.
References
- 1.Curtis KM, Nguyen AT, Tepper NK, et al. U.S. selected practice recommendations for contraceptive use, 2024. MMWR Recomm Rep 2024;73(No. RR-3):1–77. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2.Workowski KA, Bachmann LH, Chan PA, et al. Sexually transmitted infections treatment guidelines, 2021. MMWR Recomm Rep 2021;70(No. RR-4):1–187. 10.15585/mmwr.rr7004a1 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 3.CDC. US Public Health Service preexposure prophylaxis for the prevention of HIV infection in the United States—2021 update: a clinical practice guideline. Atlanta, GA: US Department of Health and Human Services, CDC; 2021. https://www.cdc.gov/hiv/pdf/risk/prep/cdc-hiv-prep-guidelines-2021.pdf
- 4.Jatlaoui TC, Riley H, Curtis KM. Safety data for levonorgestrel, ulipristal acetate and Yuzpe regimens for emergency contraception. Contraception 2016;93:93–112. 10.1016/j.contraception.2015.11.001 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 5.HRA Pharma America. Ella [Package insert]. Morristown, NJ: HRA Pharma America; 2021. [Google Scholar]
- 6.Jatlaoui TC, Curtis KM. Safety and effectiveness data for emergency contraceptive pills among women with obesity: a systematic review. Contraception 2016;94:605–11. 10.1016/j.contraception.2016.05.002 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 7.Carten ML, Kiser JJ, Kwara A, Mawhinney S, Cu-Uvin S. Pharmacokinetic interactions between the hormonal emergency contraception, levonorgestrel (Plan B), and efavirenz. Infect Dis Obstet Gynecol 2012;2012:137192. 10.1155/2012/137192 [DOI] [PMC free article] [PubMed] [Google Scholar]
Appendix. K: Summary of Classifications for Hormonal Contraceptive Methods and Intrauterine Devices
Health care providers can use the summary table as a quick reference guide to the classifications for hormonal contraceptive methods and intrauterine contraception to compare classifications across these methods (Box K1) (Table K1). See the respective appendix for each method for clarifications to the numeric categories, as well as for summaries of the evidence and additional comments. Hormonal contraceptives and intrauterine devices do not protect against sexually transmitted infections (STIs), including HIV infection, and patients using these methods should be counseled that consistent and correct use of external (male) latex condoms reduces the risk for STIs, including HIV infection (1). Use of internal (female) condoms can provide protection from transmission of STIs, although data are limited (1). Patients also should be counseled that pre-exposure prophylaxis, when taken as prescribed, is highly effective for preventing HIV infection (2).
BOX. K1. Categories for classifying hormonal contraceptives and intrauterine devices.
U.S. MEC 1 = A condition for which there is no restriction for the use of the contraceptive method
U.S. MEC 2 = A condition for which the advantages of using the method generally outweigh the theoretical or proven risks
U.S. MEC 3 = A condition for which the theoretical or proven risks usually outweigh the advantages of using the method
U.S. MEC 4 = A condition that represents an unacceptable health risk if the contraceptive method is used
Abbreviation: U.S. MEC = U.S. Medical Eligibility Criteria.
TABLE. K1. Summary of classifications for hormonal contraceptive methods and intrauterine devices.
Condition | Cu-IUD |
LNG-IUD |
Implant |
DMPA |
POP |
CHC |
||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|
Personal Characteristics and Reproductive
History
| ||||||||||||
Pregnancy
|
4* |
4* |
NA* |
NA* |
NA* |
NA* |
||||||
Age
|
Menarche to
<20 years: 2 |
Menarche to
<20 years: 2 |
Menarche to
<18 years: 1 |
Menarche to
<18 years: 2 |
Menarche to
<18 years: 1 |
Menarche to
<40 years: 1 |
||||||
≥20 years: 1 |
≥20 years: 1 |
18–45 years:
1 |
18–45 years:
1 |
18–45 years:
1 |
≥40 years: 2 |
|||||||
>45
years: 1 |
>45 years:
2 |
>45 years:
1 |
||||||||||
Parity
| ||||||||||||
a.
Nulliparous |
2 |
2 |
1 |
1 |
1 |
1 |
||||||
b. Parous |
1 |
1 |
1 |
1 |
1 |
1 |
||||||
Breastfeeding
| ||||||||||||
a. <21 days
postpartum |
— |
— |
2* |
2* |
2* |
4* |
||||||
b. 21 to
<30 days postpartum | ||||||||||||
i.
With other risk factors for VTE (e.g., age ≥35 years,
previous VTE, thrombophilia, immobility, transfusion at
delivery, peripartum cardiomyopathy, BMI ≥30
kg/m2, postpartum hemorrhage, postcesarean
delivery, preeclampsia, or smoking) |
— |
— |
2* |
2* |
2* |
3* |
||||||
ii.
Without other risk factors for VTE |
— |
— |
2* |
2* |
2* |
3* |
||||||
c.
30–42 days postpartum | ||||||||||||
i.
With other risk factors for VTE (e.g., age ≥35 years,
previous VTE, thrombophilia, immobility, transfusion at
delivery, peripartum cardiomyopathy, BMI ≥30
kg/m2, postpartum hemorrhage, postcesarean
delivery, preeclampsia, or smoking) |
— |
— |
1* |
2* |
1* |
3* |
||||||
ii.
Without other risk factors for VTE |
— |
— |
1* |
1* |
1* |
2* |
||||||
d. >42 days
postpartum |
— |
— |
1* |
1* |
1* |
2* |
||||||
Postpartum (nonbreastfeeding) | ||||||||||||
a. <21 days
postpartum |
— |
— |
1 |
2 |
1 |
4 |
||||||
b.
21–42 days postpartum | ||||||||||||
i.
With other risk factors for VTE (e.g., age ≥35 years,
previous VTE, thrombophilia, immobility, transfusion at
delivery, peripartum cardiomyopathy, BMI ≥30
kg/m2, postpartum hemorrhage, postcesarean
delivery, preeclampsia, or smoking) |
— |
— |
1 |
2 |
1 |
3* |
||||||
ii.
Without other risk factors for VTE |
— |
— |
1 |
1 |
1 |
2 |
||||||
c. >42 days
postpartum |
— |
— |
1 |
1 |
1 |
1 |
||||||
Postpartum (including cesarean delivery,
breastfeeding,
or nonbreastfeeding) | ||||||||||||
a. <10 minutes
after delivery of the placenta |
2* |
2* |
— |
— |
— |
— |
||||||
b. 10 minutes after
delivery of the placenta to <4 weeks |
2* |
2* |
— |
— |
— |
— |
||||||
c. ≥4
weeks |
1* |
1* |
— |
— |
— |
— |
||||||
d. Postpartum
sepsis |
4 |
4 |
— |
— |
— |
— |
||||||
Postabortion (spontaneous or
induced) | ||||||||||||
a. First
trimester abortion | ||||||||||||
i.
Procedural (surgical) |
1* |
1* |
1* |
1* |
1* |
1* |
||||||
ii.
Medication |
1* |
1* |
1* |
1/2* |
1* |
1* |
||||||
iii.
Spontaneous abortion with no intervention |
1* |
1* |
1* |
1* |
1* |
1* |
||||||
b. Second
trimester abortion | ||||||||||||
i.
Procedural (surgical) |
2* |
2* |
1* |
1* |
1* |
1* |
||||||
ii.
Medication |
2* |
2* |
1* |
1* |
1* |
1* |
||||||
iii.
Spontaneous abortion with no intervention |
2* |
2* |
1* |
1* |
1* |
1* |
||||||
c. Immediate
postseptic abortion |
4 |
4 |
1* |
1* |
1* |
1* |
||||||
Past ectopic
pregnancy
|
1 |
1 |
1 |
1 |
2 |
1 |
||||||
History of
pelvic surgery (see recommendations for
Postpartum [including cesarean delivery]) |
1 |
1 |
1 |
1 |
1 |
1 |
||||||
Smoking
| ||||||||||||
a. Age <35
years |
1 |
1 |
1 |
1 |
1 |
2 |
||||||
b. Age
≥35 years | ||||||||||||
i.
<15 cigarettes per day |
1 |
1 |
1 |
1 |
1 |
3 |
||||||
ii.
≥15 cigarettes per day |
1 |
1 |
1 |
1 |
1 |
4 |
||||||
Obesity
| ||||||||||||
a. BMI ≥30
kg/m2 |
1 |
1 |
1 |
1 |
1 |
2* |
||||||
b. Menarche to <18
years and BMI ≥30 kg/m2 |
1 |
1 |
1 |
2 |
1 |
2* |
||||||
History of bariatric surgery This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | ||||||||||||
a. Restrictive
procedures: decrease storage capacity of the stomach
(vertical banded gastroplasty, laparoscopic adjustable
gastric band, or laparoscopic sleeve gastrectomy) |
1 |
1 |
1 |
1 |
1 |
1 |
||||||
b. Malabsorptive
procedures: decrease absorption of nutrients and calories by
shortening the functional length of the small intestine
(Roux-en-Y gastric bypass or biliopancreatic
diversion) |
1 |
1 |
1 |
1 |
3 |
COCs: 3 Patch and ring: 1 |
||||||
Surgery
| ||||||||||||
a. Minor surgery
without immobilization |
1 |
1 |
1 |
1 |
1 |
1 |
||||||
b. Major
surgery | ||||||||||||
i.
Without prolonged immobilization |
1 |
1 |
1 |
1 |
1 |
2 |
||||||
ii.
With prolonged immobilization |
1 |
1 |
1 |
2 |
1 |
4 |
||||||
Cardiovascular Disease
| ||||||||||||
Multiple risk
factors for atherosclerotic cardiovascular
disease (e.g., older age, smoking, diabetes,
hypertension, low HDL, high LDL, or high triglyceride
levels) |
1 |
2 |
2* |
3* |
2* |
3/4* |
||||||
Hypertension Systolic blood pressure ≥160 mm Hg or diastolic blood pressure ≥100 mm Hg are associated with increased risk for adverse health events as a result of pregnancy (Box 3). | ||||||||||||
a. Adequately
controlled hypertension |
1* |
1* |
1* |
2* |
1* |
3* |
||||||
b.
Elevated blood pressure levels (properly
taken
measurements) | ||||||||||||
i.
Systolic 140–159 mm Hg or diastolic 90–99 mm
Hg |
1* |
1* |
1* |
2* |
1* |
3* |
||||||
ii.
Systolic ≥160 mm Hg or diastolic ≥100 mm
Hg |
1* |
2* |
2* |
3* |
2* |
4* |
||||||
c. Vascular
disease |
1* |
2* |
2* |
3* |
2* |
4* |
||||||
History of high
blood pressure during pregnancy (when current
blood pressure is measurable and normal) |
1 |
1 |
1 |
1 |
1 |
2 |
||||||
Deep venous thrombosis/Pulmonary
embolism This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | ||||||||||||
a. Current or history
of DVT/PE, receiving anticoagulant therapy (therapeutic
dose) (e.g., acute DVT/PE or long-term therapeutic
dose) |
2* |
2* |
2* |
2* |
2* |
3* |
||||||
b.
History of DVT/PE, receiving anticoagulant
therapy
(prophylactic dose) | ||||||||||||
i.
Higher risk for recurrent DVT/PE (one or more risk
factors) |
2* |
2* |
2* |
3* |
2* |
4* |
||||||
•
Thrombophilia (e.g., factor V Leiden mutation; prothrombin
gene mutation; protein S, protein C, and antithrombin
deficiencies; or antiphospholipid
syndrome) • Active cancer (metastatic, receiving therapy, or within 6 months after clinical remission), excluding nonmelanoma skin cancer • History of recurrent DVT/PE | ||||||||||||
ii.
Lower risk for recurrent DVT/PE (no risk factors) |
2* |
2* |
2* |
2* |
2* |
3* |
||||||
c.
History of DVT/PE, not receiving anticoagulant
therapy | ||||||||||||
i.
Higher risk for recurrent DVT/PE (one or more risk
factors |
1 |
2 |
2 |
3 |
2 |
4 |
||||||
• History of
estrogen-associated
DVT/PE • Pregnancy-associated DVT/PE • Idiopathic DVT/PE • Thrombophilia (e.g., factor V Leiden mutation; prothrombin gene mutation; protein S, protein C, and antithrombin deficiencies; or antiphospholipid syndrome) • Active cancer (metastatic, receiving therapy, or within 6 months after clinical remission), excluding nonmelanoma skin cancer • History of recurrent DVT/PE | ||||||||||||
ii.
Lower risk for recurrent DVT/PE (no risk factors) |
1 |
2 |
2 |
2 |
2 |
3 |
||||||
d. Family history
(first-degree relatives) |
1 |
1 |
1 |
1 |
1 |
2 |
||||||
Thrombophilia (e.g., factor V Leiden
mutation; prothrombin gene mutation; protein S, protein C,
and antithrombin deficiencies; or antiphospholipid
syndrome) This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
1* |
2* |
2* |
3* |
2* |
4* |
||||||
Superficial venous disorders
| ||||||||||||
a. Varicose
veins |
1 |
1 |
1 |
1 |
1 |
1 |
||||||
b. Superficial venous
thrombosis (acute or history) |
1 |
1 |
1 |
2 |
1 |
3* |
||||||
Current and history of ischemic heart
disease This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
1 |
Initiation |
Continuation |
Initiation |
Continuation |
3 |
Initiation |
Continuation |
4 |
|||
2 |
3 |
2 |
3 |
2 |
3 |
|||||||
Stroke (history of cerebrovascular
accident)
This condition is associated with increased
risk for adverse health events as a result of pregnancy
(Box
3). |
1 |
2 |
Initiation |
Continuation |
3 |
Initiation |
Continuation |
4 |
||||
2 |
3 |
2 |
3 |
|||||||||
Valvular heart disease Complicated valvular heart disease is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | ||||||||||||
a.
Uncomplicated |
1 |
1 |
1 |
1 |
1 |
2 |
||||||
b. Complicated
(pulmonary hypertension, risk for atrial fibrillation, or
history of subacute bacterial endocarditis) |
1 |
1 |
1 |
2 |
1 |
4 |
||||||
Peripartum cardiomyopathy This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | ||||||||||||
a. Normal
or mildly impaired cardiac function (New
York Heart
Association Functional Class I or II: no
limitation
of activities or slight, mild limitation
of activity)
(3) | ||||||||||||
i.
<6 months |
2 |
2 |
1 |
2 |
1 |
4 |
||||||
ii.
≥6 months |
2 |
2 |
1 |
2 |
1 |
3 |
||||||
b. Moderately or
severely impaired cardiac function (New York Heart
Association Functional Class III or IV: marked limitation of
activity or should be at complete rest) (3) |
2 |
2 |
2 |
3 |
2 |
4 |
||||||
Renal Disease
| ||||||||||||
Chronic kidney
disease This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
Initiation |
Continuation |
Initiation |
Continuation |
— |
|||||||
a. Current nephrotic
syndrome |
1 |
1 |
2 |
2 |
2 |
3 |
2* DRSP POP with known hyperkalemia: 4* |
4 |
||||
b.
Hemodialysis |
1 |
1 |
2 |
2 |
2 |
3 |
2* DRSP POP with known hyperkalemia: 4* |
4 |
||||
c. Peritoneal
dialysis |
2 |
1 |
2 |
2 |
2 |
3 |
2* DRSP POP with known hyperkalemia: 4* |
4 |
||||
Rheumatic Diseases
| ||||||||||||
Systemic lupus
erythematosus This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
Initiation |
Continuation |
— |
Initiation |
Continuation |
— |
||||||
a. Positive (or
unknown) antiphospholipid antibodies |
1* |
1* |
2* |
2* |
3* |
3* |
2* |
4* |
||||
b. Severe
thrombocytopenia |
3* |
2* |
2* |
2* |
3* |
2* |
2* |
2* |
||||
c. Immunosuppressive
therapy |
2* |
1* |
2* |
2* |
2* |
2* |
2* |
2* |
||||
d. None of the
above |
1* |
1* |
2* |
2* |
2* |
2* |
2* |
2* |
||||
Rheumatoid
arthritis
|
Initiation |
Continuation |
Initiation |
Continuation |
— |
|||||||
a. Not receiving
immunosuppressive therapy |
1 |
1 |
1 |
1 |
1 |
2 |
1 |
2 |
||||
b. Receiving
immunosuppressive therapy |
2 |
1 |
2 |
1 |
1 |
2/3* |
1 |
2 |
||||
Neurologic Conditions
| ||||||||||||
Headaches
| ||||||||||||
a. Nonmigraine (mild
or severe) |
1 |
1 |
1 |
1 |
1 |
1* |
||||||
b.
Migraine | ||||||||||||
i.
Without aura (includes menstrual migraine) |
1 |
1 |
1 |
1 |
1 |
2* |
||||||
ii.
With aura |
1 |
1 |
1 |
1 |
1 |
4* |
||||||
Epilepsy This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
1 |
1 |
1* |
1* |
1* |
1* |
||||||
Multiple sclerosis
| ||||||||||||
a. Without prolonged
immobility |
1 |
1 |
1 |
2 |
1 |
1 |
||||||
b. With prolonged
immobility |
1 |
1 |
1 |
2 |
1 |
3 |
||||||
Depressive Disorders
| ||||||||||||
Depressive
disorders
|
1* |
1* |
1* |
1* |
1* |
1* |
||||||
Reproductive Tract Infections and
Disorders
| ||||||||||||
Vaginal bleeding patterns
|
Initiation |
Continuation |
— |
|||||||||
a. Irregular pattern
without heavy bleeding |
1 |
1 |
1 |
2 |
2 |
2 |
1 |
|||||
b. Heavy or prolonged
bleeding (includes regular and irregular patterns) |
2* |
1* |
2* |
2* |
2* |
2* |
1* |
|||||
Unexplained vaginal
bleeding (suspicious for serious condition) before evaluation |
Initiation |
Continuation |
Initiation |
Continuation |
— |
|||||||
4* |
2* |
4* |
2* |
3* |
3* |
2* |
2* |
|||||
Endometriosis
|
2 |
1 |
1 |
1 |
1 |
1 |
||||||
Benign ovarian
tumors (including cysts) |
1 |
1 |
1 |
1 |
1 |
1 |
||||||
Severe
dysmenorrhea
|
2 |
1 |
1 |
1 |
1 |
1 |
||||||
Gestational trophoblastic
disease This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | ||||||||||||
a.
Suspected gestational trophoblastic
disease
(immediate postevacuation) | ||||||||||||
i.
Uterine size first trimester |
1* |
1* |
1* |
1* |
1* |
1* |
||||||
ii.
Uterine size second trimester |
2* |
2* |
1* |
1* |
1* |
1* |
||||||
b. Confirmed
gestational trophoblastic disease (after initial evacuation
and during monitoring) |
Initiation |
Continuation |
Initiation |
Continuation |
— |
|||||||
i.
Undetectable or nonpregnant β-hCG levels |
1* |
1* |
1* |
1* |
1* |
1* |
1* |
1* |
||||
ii.
Decreasing β-hCG levels |
2* |
1* |
2* |
1* |
1* |
1* |
1* |
1* |
||||
iii.
Persistently elevated β-hCG levels or malignant
disease, with no evidence or suspicion of intrauterine
disease |
2* |
1* |
2* |
1* |
1* |
1* |
1* |
1* |
||||
iv.
Persistently elevated β-hCG levels or malignant
disease, with evidence or suspicion of intrauterine
disease |
4* |
2* |
4* |
2* |
1* |
1* |
1* |
1* |
||||
Cervical
ectropion
|
1 |
1 |
1 |
1 |
1 |
1 |
||||||
Cervical
intraepithelial neoplasia
|
1 |
2 |
2 |
2 |
1 |
2 |
||||||
Cervical cancer (awaiting
treatment) |
Initiation |
Continuation |
Initiation |
Continuation |
— |
|||||||
4 |
2 |
4 |
2 |
2 |
2 |
1 |
2 |
|||||
Breast disease Breast cancer is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | ||||||||||||
a. Undiagnosed
mass |
1 |
2* |
2* |
2* |
2* |
2* |
||||||
b. Benign breast
disease |
1 |
1 |
1 |
1 |
1 |
1 |
||||||
c. Family history of
cancer |
1 |
1 |
1 |
1 |
1 |
1 |
||||||
d. Breast
cancer | ||||||||||||
i.
Current |
1 |
4 |
4 |
4 |
4 |
4 |
||||||
ii.
Past and no evidence of current disease for 5
years |
1 |
3 |
3 |
3 |
3 |
3 |
||||||
Endometrial
hyperplasia
|
1 |
1 |
1 |
1 |
1 |
1 |
||||||
Endometrial cancer This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
Initiation |
Continuation |
Initiation |
Continuation |
— |
|||||||
4 |
2 |
4 |
2 |
1 |
1 |
1 |
1 |
|||||
Ovarian
cancer This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
1 |
1 |
1 |
1 |
1 |
1 |
||||||
Uterine
fibroids
|
2 |
2 |
1 |
1 |
1 |
1 |
||||||
Anatomical abnormalities
| ||||||||||||
a. Distorted uterine
cavity (any congenital or acquired uterine abnormality
distorting the uterine cavity in a manner that is
incompatible with IUD placement) |
4 |
4 |
— |
|||||||||
b. Other abnormalities
(including cervical stenosis or cervical lacerations) not
distorting the uterine cavity or interfering with IUD
placement |
2 |
2 |
||||||||||
Pelvic
inflammatory disease
|
Initiation |
Continuation |
Initiation |
Continuation |
— |
|||||||
a. Current
PID |
4 |
2* |
4 |
2* |
1 |
1 |
1 |
1 |
||||
b. Past
PID | ||||||||||||
i.
With subsequent pregnancy |
1 |
1 |
1 |
1 |
1 |
1 |
1 |
1 |
||||
ii.
Without subsequent pregnancy |
2 |
2 |
2 |
2 |
1 |
1 |
1 |
1 |
||||
Sexually
transmitted infections
|
Initiation |
Continuation |
Initiation |
Continuation |
— |
|||||||
a. Current purulent
cervicitis or chlamydial infection or gonococcal
infection |
4 |
2* |
4 |
2* |
1 |
1 |
1 |
1 |
||||
b. Vaginitis
(including Trichomonas vaginalis and
bacterial vaginosis) |
2 |
2 |
2 |
2 |
1 |
1 |
1 |
1 |
||||
c. Other factors
related to STIs |
2* |
2 |
2* |
2 |
1 |
1 |
1 |
1 |
||||
HIV
| ||||||||||||
High
risk for HIV infection
|
Initiation |
Continuation |
Initiation |
Continuation |
— |
|||||||
1* |
1* |
1* |
1* |
1 |
1 |
1 |
1 |
|||||
HIV
infection For persons with HIV infection who are not clinically well or not receiving ARV therapy, this condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
— |
— |
— |
— |
1* |
1* |
1* |
1* |
||||
a. Clinically well
receiving ARV therapy |
1 |
1 |
1 |
1 |
— |
— |
— |
— |
||||
b. Not clinically well
or not receiving ARV therapy |
2 |
1 |
2 |
1 |
— |
— |
— |
— |
||||
Other Infections
| ||||||||||||
Schistosomiasis Schistosomiasis with fibrosis of the liver is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | ||||||||||||
a.
Uncomplicated |
1 |
1 |
1 |
1 |
1 |
1 |
||||||
b. Fibrosis of the
liver (if severe, see recommendations for
Cirrhosis) |
1 |
1 |
1 |
1 |
1 |
1 |
||||||
Tuberculosis This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
Initiation |
Continuation |
Initiation |
Continuation |
— |
|||||||
a. Nonpelvic |
1 |
1 |
1 |
1 |
1* |
1* |
1* |
1* |
||||
b. Pelvic |
4 |
3 |
4 |
3 |
1* |
1* |
1* |
1* |
||||
Malaria
|
1 |
1 |
1 |
1 |
1 |
1 |
||||||
Endocrine Conditions
| ||||||||||||
Diabetes Insulin-dependent diabetes; diabetes with nephropathy, retinopathy, or neuropathy; diabetes with other vascular disease; or diabetes of >20 years’ duration are associated with increased risk for adverse health events as a result of pregnancy (Box 3). | ||||||||||||
a. History of
gestational disease |
1 |
1 |
1 |
1 |
1 |
1 |
||||||
b.
Nonvascular disease | ||||||||||||
i.
Non-insulin dependent |
1 |
2 |
2 |
2 |
2 |
2 |
||||||
ii.
Insulin dependent |
1 |
2 |
2 |
2 |
2 |
2 |
||||||
c. Nephropathy,
retinopathy, or neuropathy |
1 |
2 |
2 |
3 |
2 |
3/4* |
||||||
d. Other vascular
disease or diabetes of >20 years’
duration |
1 |
2 |
2 |
3 |
2 |
3/4* |
||||||
Thyroid disorders
| ||||||||||||
a. Simple
goiter |
1 |
1 |
1 |
1 |
1 |
1 |
||||||
b.
Hyperthyroid |
1 |
1 |
1 |
1 |
1 |
1 |
||||||
c.
Hypothyroid |
1 |
1 |
1 |
1 |
1 |
1 |
||||||
Gastrointestinal Conditions
| ||||||||||||
Inflammatory
bowel disease (ulcerative colitis or
Crohn’s disease) |
1 |
1 |
1 |
2 |
2 |
2/3* |
||||||
Gallbladder disease
| ||||||||||||
a.
Asymptomatic |
1 |
2 |
2 |
2 |
2 |
2 |
||||||
b.
Symptomatic | ||||||||||||
i.
Current |
1 |
2 |
2 |
2 |
2 |
3 |
||||||
ii.
Treated by cholecystectomy |
1 |
2 |
2 |
2 |
2 |
2 |
||||||
iii.
Medically treated |
1 |
2 |
2 |
2 |
2 |
3 |
||||||
History of cholestasis
| ||||||||||||
a. Pregnancy
related |
1 |
1 |
1 |
1 |
1 |
2 |
||||||
b. Past COC
related |
1 |
2 |
2 |
2 |
2 |
3 |
||||||
Viral hepatitis
|
Initiation |
Continuation |
||||||||||
a. Acute or
flare |
1 |
1 |
1 |
1 |
1 |
3/4* |
2 |
|||||
b. Chronic |
1 |
1 |
1 |
1 |
1 |
1 |
1 |
|||||
Cirrhosis Decompensated cirrhosis is associated with increased risk for adverse health events as a result of pregnancy (Box 3). | ||||||||||||
a. Compensated (normal
liver function) |
1 |
1 |
1 |
1 |
1 |
1 |
||||||
b. Decompensated
(impaired liver function) |
1 |
2 |
2 |
3 |
2 |
4 |
||||||
Liver tumors Hepatocellular adenoma and malignant liver tumors are associated with increased risk for adverse health events as a result of pregnancy (Box 3). | ||||||||||||
a.
Benign | ||||||||||||
i.
Focal nodular hyperplasia |
1 |
2 |
2 |
2 |
2 |
2 |
||||||
ii.
Hepatocellular adenoma |
1 |
2 |
2 |
3 |
2 |
4 |
||||||
b. Malignant
(hepatocellular carcinoma) |
1 |
3 |
3 |
3 |
3 |
4 |
||||||
Respiratory Conditions
| ||||||||||||
Cystic
fibrosis This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
1* |
1* |
1* |
2* |
1* |
1* |
||||||
Hematologic Conditions
| ||||||||||||
Thalassemia
|
2 |
1 |
1 |
1 |
1 |
1 |
||||||
Sickle cell
disease This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
2 |
1 |
1 |
2/3* |
1 |
4 |
||||||
Iron-deficiency
anemia
|
2 |
1 |
1 |
1 |
1 |
1 |
||||||
Solid Organ Transplantation
| ||||||||||||
Solid organ
transplantation This condition is associated with increased risk for adverse health events as a result of pregnancy (Box 3). |
Initiation |
Continuation |
Initiation |
Continuation |
— |
|||||||
a. No graft
failure |
1 |
1 |
1 |
1 |
2 |
2/3* |
2 |
2* |
||||
b. Graft
failure |
2 |
1 |
2 |
1 |
2 |
2/3* |
2 |
4 |
||||
Drug Interactions
| ||||||||||||
Antiretrovirals used for prevention
(PrEP)
or treatment of HIV
infection
| ||||||||||||
See the
following guidelines for the most up-to-date recommendations
on drug-drug interactions between hormonal contraception and
antiretrovirals: 1) Recommendations for the Use of
Antiretroviral Drugs During Pregnancy and Interventions to
Reduce Perinatal HIV Transmission in the United (https://clinicalinfo.hiv.gov/en/guidelines/perinatal/prepregnancy-counseling-childbearing-age-overview?view=full#table-3)
(4) and 2) Guidelines for the
Use of Antiretroviral Agents in Adults and Adolescents with
HIV (https://clinicalinfo.hiv.gov/en/guidelines/hiv-clinical-guidelines-adult-and-adolescent-arv/drug-interactions-overview?view=full)
(5). | ||||||||||||
a. Nucleoside reverse
transcriptase inhibitors (NRTIs) |
Initiation |
Continuation |
Initiation |
Continuation |
— |
|||||||
i.
Abacavir (ABC) |
1/2* |
1* |
1/2* |
1* |
1 |
1 |
1 |
1 |
||||
ii.
Tenofovir (TDF) |
1/2* |
1* |
1/2* |
1* |
1 |
1 |
1 |
1 |
||||
iii.
Zidovudine (AZT) |
1/2* |
1* |
1/2* |
1* |
1 |
1 |
1 |
1 |
||||
iv.
Lamivudine (3TC) |
1/2* |
1* |
1/2* |
1* |
1 |
1 |
1 |
1 |
||||
v.
Didanosine (DDI) |
1/2* |
1* |
1/2* |
1* |
1 |
1 |
1 |
1 |
||||
vi.
Emtricitabine (FTC) |
1/2* |
1* |
1/2* |
1* |
1 |
1 |
1 |
1 |
||||
vii.
Stavudine (D4T) |
1/2* |
1* |
1/2* |
1* |
1 |
1 |
1 |
1 |
||||
b.
Nonnucleoside reverse transcriptase inhibitors
(NNRTIs) | ||||||||||||
i.
Efavirenz (EFV) |
1/2* |
1* |
1/2* |
1* |
2* |
1* |
2* |
2* |
||||
ii.
Etravirine (ETR) |
1/2* |
1* |
1/2* |
1* |
1 |
1 |
1 |
1 |
||||
iii.
Nevirapine (NVP) |
1/2* |
1* |
1/2* |
1* |
1 |
1 |
1 |
1 |
||||
iv.
Rilpivirine (RPV) |
1/2* |
1* |
1/2* |
1* |
1 |
1 |
1 |
1 |
||||
c.
Ritonavir-boosted protease inhibitors | ||||||||||||
i.
Ritonavir-boosted atazanavir (ATV/r) |
1/2* |
1* |
1/2* |
1* |
2* |
1* |
2* |
2* |
||||
ii.
Ritonavir-boosted darunavir (DRV/r) |
1/2* |
1* |
1/2* |
1* |
2* |
1* |
2* |
2* |
||||
iii.
Ritonavir-boosted fosamprenavir (FPV/r) |
1/2* |
1* |
1/2* |
1* |
2* |
1* |
2* |
2* |
||||
iv.
Ritonavir-boosted lopinavir (LPV/r) |
1/2* |
1* |
1/2* |
1* |
1 |
1 |
1 |
1 |
||||
v.
Ritonavir-boosted saquinavir (SQV/r) |
1/2* |
1* |
1/2* |
1* |
2* |
1* |
2* |
2* |
||||
vi.
Ritonavir-boosted tipranavir (TPV/r) |
1/2* |
1* |
1/2* |
1* |
2* |
1* |
2* |
2* |
||||
d.
Protease inhibitors without ritonavir | ||||||||||||
i.
Atazanavir (ATV) |
1/2* |
1* |
1/2* |
1* |
1 |
1 |
1 |
2* |
||||
ii.
Fosamprenavir (FPV) |
1/2* |
1* |
1/2* |
1* |
2* |
2* |
2* |
3* |
||||
iii.
Indinavir (IDV) |
1/2* |
1* |
1/2* |
1* |
1 |
1 |
1 |
1 |
||||
iv.
Nelfinavir (NFV) |
1/2* |
1* |
1/2* |
1* |
2* |
1* |
2* |
2* |
||||
e. CCR5
co-receptor antagonists | ||||||||||||
i.
Maraviroc (MVC) |
1/2* |
1* |
1/2* |
1* |
1 |
1 |
1 |
1 |
||||
f. HIV
integrase strand transfer inhibitors | ||||||||||||
i.
Raltegravir (RAL) |
1/2* |
1* |
1/2* |
1* |
1 |
1 |
1 |
1 |
||||
ii.
Dolutegravir (DTG) |
1/2* |
1* |
1/2* |
1* |
1 |
1 |
1 |
1 |
||||
iii.
Elvitegravir (EVG) |
1/2* |
1* |
1/2* |
1* |
1 |
1 |
1 |
1 |
||||
g. Fusion
inhibitors | ||||||||||||
i.
Enfuvirtide |
1/2* |
1* |
1/2* |
1* |
1 |
1 |
1 |
1 |
||||
Anticonvulsant therapy
| ||||||||||||
a. Certain
anticonvulsants (phenytoin, carbamazepine, barbiturates,
primidone, topiramate, and oxcarbazepine) |
1 |
1 |
2* |
1* |
3* |
3* |
||||||
b.
Lamotrigine |
1 |
1 |
1 |
1 |
1 |
3* |
||||||
Antimicrobial therapy
| ||||||||||||
a. Broad-spectrum
antibiotics |
1 |
1 |
1 |
1 |
1 |
1 |
||||||
b.
Antifungals |
1 |
1 |
1 |
1 |
1 |
1 |
||||||
c.
Antiparasitics |
1 |
1 |
1 |
1 |
1 |
1 |
||||||
d. Rifampin or
rifabutin therapy |
1 |
1 |
2* |
1* |
3* |
3* |
||||||
Psychotropic medications
| ||||||||||||
a. Selective serotonin
reuptake inhibitors (SSRIs) |
1 |
1 |
1 |
1 |
1 |
1 |
||||||
St. John’s wort | 1 |
1 |
2 |
1 |
2 |
2 |
Abbreviations: ARV = antiretroviral; BMI = body mass index; CHC = combined hormonal contraceptive; COC = combined oral contraceptive; Cu-IUD = copper intrauterine device; DMPA = depot medroxyprogesterone acetate; DRSP = drospirenone; DVT = deep venous thrombosis; hCG = human chorionic gonadotropin; HDL = high-density lipoprotein; IUD = intrauterine device; LDL = low-density lipoprotein; LNG-IUD = levonorgestrel intrauterine device; NA = not applicable; PE = pulmonary embolism; PID = pelvic inflammatory disease; POP = progestin-only pill; PrEP = pre-exposure prophylaxis; STI = sexually transmitted infection; VTE = venous thromboembolism.
* Consult the appendix for this contraceptive method for a clarification to this classification.
References
- 1.Workowski KA, Bachmann LH, Chan PA, et al. Sexually transmitted infections treatment guidelines, 2021. MMWR Recomm Rep 2021;70(No. RR-4):1–187. 10.15585/mmwr.rr7004a1 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2.CDC. US Public Health Service preexposure prophylaxis for the prevention of HIV infection in the United States—2021 update: a clinical practice guideline. Atlanta, GA: US Department of Health and Human Services, CDC; 2021. https://www.cdc.gov/hiv/pdf/risk/prep/cdc-hiv-prep-guidelines-2021.pdf
- 3.The Criteria Committee of the New York Heart Association. Nomenclature and criteria for diagnosis of diseases of the heart and great vessels. 9th ed. Boston, MA: Little, Brown and Co; 1994. [Google Scholar]
- 4.Panel on Treatment of HIV During Pregnancy and Prevention of Perinatal Transmission. Recommendations for the use of antiretroviral drugs during pregnancy and interventions to reduce perinatal HIV transmission in the United States. Washington, DC: US Department of Health and Human Services; 2023. https://clinicalinfo.hiv.gov/en/guidelines/perinatal/recommendations-arv-drugs-pregnancy-overview [Google Scholar]
- 5.Panel on Antiretroviral Guidelines for Adults and Adolescents. Guidelines for the use of antiretroviral agents in adults and adolescents with HIV. Washington, DC: US Department of Health and Human Services; 2023. https://clinicalinfo.hiv.gov/sites/default/files/guidelines/documents/adult-adolescent-arv/guidelines-adult-adolescent-arv.pdf
Conflicts of Interest: All authors have completed and submitted the International Committee of Medical Journal Editors form for disclosure of potential conflicts of interest. No potential conflicts of interest were disclosed. To promote transparency, all meeting participants were asked to disclose potential conflicts of interest to CDC before the expert meeting and to report potential conflicts of interest during the introductory portion of the expert meeting. All potential conflicts of interest disclosed by meeting participants are listed. No participants were excluded from discussion based on potential conflicts of interest. CDC staff members who ultimately decided and developed these recommendations have no financial interests or other relationships with the manufacturers of commercial products, suppliers of commercial services, or commercial supporters relevant to these recommendations.
Contributor Information
Courtney Baker, University of Texas Southwestern Medical Center, Dallas, Texas.
Divya Dethier, University of Hawaii, Honolulu, Hawaii.
Sophia Garbarino, Emory University, Atlanta, Georgia.
Heather Gold, Emory University, Atlanta, Georgia.
Emma Halper, Emory University, Atlanta, Georgia.
Nathalie Kapp, International Planned Parenthood Federation, London, England.
Gopika Krishna, Columbia University, New York, New York.
Marielle Meurice, University of California-San Diego, San Diego, California.
Stephanie Ramer, CDC, Atlanta, Georgia.
Jessica Rodenhizer, CDC, Atlanta, Georgia.
Nisha Verma, Emory University, Atlanta, Georgia.
Steffanie Wright, Harvard University, Boston, Massachusetts.
References
- 1.Curtis KM, Nguyen AT, Tepper NK, et al. U.S. selected practice recommendations for contraceptive use, 2024. MMWR Recomm Rep 2024;73(No. RR-3):1.–. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2.Curtis KM, Jatlaoui TC, Tepper NK, et al. U.S. selected practice recommendations for contraceptive use, 2016. MMWR Recomm Rep 2016;65(No. RR-4):1–66. 10.15585/mmwr.rr6504a1 [DOI] [PubMed] [Google Scholar]
- 3.World Health Organization. Medical eligibility criteria for contraceptive use. Geneva, Switzerland: World Health Organization; 2015. https://www.who.int/publications/i/item/9789241549158
- 4.World Health Organization. Selected practice recommendations for contraceptive use. Geneva, Switzerland: World Health Organization; 2016. https://www.who.int/publications/i/item/9789241565400
- 5.CDC. U.S. medical eligibility criteria for contraceptive use, 2010. MMWR Recomm Rep 2010;59(No. RR-4):1–86. [PubMed] [Google Scholar]
- 6.Curtis KM, Tepper NK, Jatlaoui TC, et al. U.S. medical eligibility criteria for contraceptive use, 2016. MMWR Recomm Rep 2016;65(No. RR-3):1–103. 10.15585/mmwr.rr6503a1 [DOI] [PubMed] [Google Scholar]
- 7.Gavin L, Moskosky S, Carter M, et al. ; CDC. Providing quality family planning services: recommendations of CDC and the U.S. Office of Population Affairs. MMWR Recomm Rep 2014;63(No. RR-4):1–54. [PubMed] [Google Scholar]
- 8.Gavin L, Pazol K. Update: providing quality family planning services—recommendations from CDC and the U.S. Office of Population Affairs, 2015. MMWR Morb Mortal Wkly Rep 2016;65:231–4. 10.15585/mmwr.mm6509a3 [DOI] [PubMed] [Google Scholar]
- 9.Gavin L, Pazol K, Ahrens K. Update: providing quality family planning services—recommendations from CDC and the U.S. Office of Population Affairs. MMWR Morb Mortal Wkly Rep 2017;66:1383–5. 10.15585/mmwr.mm6650a4 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 10.American College of Obstetricians and Gynecologists’ Committee on Health Care for Underserved Women, Contraceptive Equity Expert Work Group, and Committee on Ethics. Patient-centered contraceptive counseling: ACOG committee statement number 1. Obstet Gynecol 2022;139:350–3. 10.1097/AOG.0000000000004659 [DOI] [PubMed] [Google Scholar]
- 11.American Public Health Association. Opposing coercion in contraceptive access and care to promote reproductive health equity. Washington, DC: American Public Health Association; 2021. https://www.apha.org/Policies-and-Advocacy/Public-Health-Policy-Statements/Policy-Database/2022/01/07/Contraceptive-Access
- 12.Holt K, Reed R, Crear-Perry J, Scott C, Wulf S, Dehlendorf C. Beyond same-day long-acting reversible contraceptive access: a person-centered framework for advancing high-quality, equitable contraceptive care. Am J Obstet Gynecol 2020;222(4S):S878.e1–e6. 10.1016/j.ajog.2019.11.1279 [DOI] [PubMed] [Google Scholar]
- 13.United Nations Population Fund. Programme of Action of the International Conference on Population and Development. Cairo, Egypt: United Nations; 1995. https://unfpa.org/sites/default/files/pub-pdf/programme_of_action_Web%20ENGLISH.pdf
- 14.World Health Organization. Framework for ensuring human rights in the provision of contraceptive information and services. Geneva, Switzerland: World Health Organization; 2014. https://www.who.int/publications/i/item/9789241507745 [PubMed]
- 15.Tepper NK, Curtis KM, Cox S, Whiteman MK. Update to U.S. medical eligibility criteria for contraceptive use, 2016: updated recommendations for the use of contraception among women at high risk for HIV infection. MMWR Morb Mortal Wkly Rep 2020;69:405–10. 10.15585/mmwr.mm6914a3 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 16.Mohllajee AP, Curtis KM, Flanagan RG, Rinehart W, Gaffield ML, Peterson HB. Keeping up with evidence a new system for WHO’s evidence-based family planning guidance. Am J Prev Med 2005;28:483–90. 10.1016/j.amepre.2005.02.008 [DOI] [PubMed] [Google Scholar]
- 17.CDC. Updating CDC’s contraception guidance documents: U.S. medical eligibility criteria for contraceptive use and U.S. selected practice recommendations for contraceptive use. Atlanta, GA: US Department of Health and Human Services, CDC; 2021. https://www.govinfo.gov/content/pkg/FR-2021-08-31/pdf/2021-18769.pdf
- 18.Page MJ, McKenzie JE, Bossuyt PM, et al. The PRISMA 2020 statement: an updated guideline for reporting systematic reviews. BMJ 2021;372:n71. 10.1136/bmj.n71 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 19.Guyatt G, Oxman AD, Akl EA, et al. GRADE guidelines: 1. Introduction-GRADE evidence profiles and summary of findings tables. J Clin Epidemiol 2011;64:383–94. 10.1016/j.jclinepi.2010.04.026 [DOI] [PubMed] [Google Scholar]
- 20.Guyatt GH, Oxman AD, Vist GE, et al. ; GRADE Working Group. GRADE: an emerging consensus on rating quality of evidence and strength of recommendations. BMJ 2008;336:924–6. 10.1136/bmj.39489.470347.AD [DOI] [PMC free article] [PubMed] [Google Scholar]
- 21.Armstrong MJ, Rueda JD, Gronseth GS, Mullins CD. Framework for enhancing clinical practice guidelines through continuous patient engagement. Health Expect 2017;20:3–10. 10.1111/hex.12467 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 22.Institute of Medicine Committee on Standards for Developing Trustworthy Clinical Practice Guidelines. Clinical practice guidelines we can trust. In: Graham R, Mancher M, Miller Wolman D, Greenfield S, Steinberg E, eds. Clinical practice guidelines we can trust. Washington, DC: National Academies Press; 2011. [PubMed] [Google Scholar]
- 23.Institute of Medicine. Crossing the quality chasm: a new health system for the 21st century. Washington, DC: National Academies Press; 2001. [PubMed] [Google Scholar]
- 24.Bradley SEK, Polis CB, Micks EA, Steiner MJ. Effectiveness, safety, and comparative side effects. In: Cason P, Cwiak C, Edelman A, Kowal D, Marrazzo JM, Nelson AL, et al., editors. Contracept Technol. 22nd ed. Burlington, MA: Jones-Bartlett Learning; 2023. [Google Scholar]
- 25.Potter JE, Stevenson AJ, Coleman-Minahan K, et al. Challenging unintended pregnancy as an indicator of reproductive autonomy. Contraception 2019;100:1–4. 10.1016/j.contraception.2019.02.005 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 26.Reproductive Health National Training Center. Contraceptive counseling and education eLearning. Washington, DC: US Department of Health and Human Services, Office of the Assistant Secretary for Health, Office of Population Affairs, Office on Women’s Health; 2022. https://rhntc.org/resources/contraceptive-counseling-and-education-elearning
- 27.Workowski KA, Bachmann LH, Chan PA, et al. Sexually transmitted infections treatment guidelines, 2021. MMWR Recomm Rep 2021;70:1–187. 10.15585/mmwr.rr7004a1 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 28.CDC. US Public Health Service preexposure prophylaxis for the prevention of HIV infection in the United States—2021 update: a clinical practice guideline. Atlanta, GA: US Department of Health and Human Services, CDC; 2021. https://www.cdc.gov/hiv/pdf/risk/prep/cdc-hiv-prep-guidelines-2021.pdf
- 29.Blackwell S, Louis JM, Norton ME, et al. Reproductive services for women at high risk for maternal mortality: a report of the workshop of the Society for Maternal-Fetal Medicine, the American College of Obstetricians and Gynecologists, the Fellowship in Family Planning, and the Society of Family Planning. Am J Obstet Gynecol 2020;222:B2–18. 10.1016/j.ajog.2019.12.008 [DOI] [PubMed] [Google Scholar]