The Current State of Care for Black and Hispanic Inflammatory Bowel Disease Patients

Julia J Liu; Bincy P Abraham; Paula Adamson; Edward L Barnes; Kelly A Brister; Oriana M Damas; Sarah C Glover; Kimberly Hooks; Ana Ingram; Gilaad G Kaplan; Edward V Loftus, Jr; Dermot P B McGovern; Melodie Narain-Blackwell; Florence-Damilola Odufalu; Sandra Quezada; Vonda Reeves; Bo Shen; Thaddeus S Stappenbeck; Latonia Ward

doi:10.1093/ibd/izac124

. 2022 Jul 11;29(2):297–307. doi: 10.1093/ibd/izac124

The Current State of Care for Black and Hispanic Inflammatory Bowel Disease Patients

Julia J Liu ^1,^✉, Bincy P Abraham ², Paula Adamson ³, Edward L Barnes ⁴, Kelly A Brister ⁵, Oriana M Damas ⁶, Sarah C Glover ⁷, Kimberly Hooks ⁸, Ana Ingram ⁹, Gilaad G Kaplan ¹⁰, Edward V Loftus Jr ¹¹, Dermot P B McGovern ¹², Melodie Narain-Blackwell ¹³, Florence-Damilola Odufalu ¹⁴, Sandra Quezada ¹⁵, Vonda Reeves ¹⁶, Bo Shen ¹⁷, Thaddeus S Stappenbeck ¹⁸, Latonia Ward ¹⁹

¹ Division of Gastroenterology, Morehouse School of Medicine, Atlanta, GA, USA

² Division of Gastroenterology and Hepatology, Houston Methodist Academic Institute, Houston, TX, USA

³ Division of Gastroenterology, Morehouse School of Medicine, Atlanta, GA, USA

⁴ Division of Gastroenterology and Hepatology, UNC School of Medicine, Chapel Hill, NC, USA

⁵ Department of Surgery, University of Mississippi Medical Center, Jackson, MS, USA

⁶ Division of Gastroenterology and Hepatology, Department of Medicine, University of Miami Miller School of Medicine, Miami, FL, USA

⁷ Division of Gastroenterology and Hepatology, University of Mississippi Medical Center, Jackson, MS, USA

⁸ Color of Crohn’s and Chronic Illness, Glenarden, MD, USA

⁹ Color of Crohn’s and Chronic Illness, Glenarden, MD, USA

¹⁰ Division of Gastroenterology and Hepatology, Department of Medicine and Community Health Sciences, University of Calgary, Calgary, AB, Canada

¹¹ Division of Gastroenterology and Hepatology, Mayo Clinic College of Medicine and Science, Rochester, MN, USA

¹² F. Widjaja Foundation Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA

¹³ Color of Crohn’s and Chronic Illness, Glenarden, MD, USA

¹⁴ Division of Gastroenterology and Liver Diseases, Keck School of Medicine of the University of Southern California, Los Angeles, CA, USA

¹⁵ Division of Gastroenterology and Hepatology, University of Maryland, College Park, College Park, MD, USA

¹⁶ GI Associates and Endoscopy Center, Jackson, MS, USA

¹⁷ Inflammatory Bowel Disease Center, NewYork-Presbyterian Hospital/Columbia University Irving Medical Center, New York, NY, USA

¹⁸ Department of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA

¹⁹ Color of Crohn’s and Chronic Illness, Glenarden, MD, USA

^✉

Address correspondence to: Julia J. Liu, MD, Division of Gastroenterology, Morehouse School of Medicine, 720 Westview Dr SW, Atlanta, GA 30310, USA (jjliu@msm.edu).

PMCID: PMC10210746 PMID: 35816130

Abstract

Research on the care of inflammatory bowel disease (IBD) patients has been primarily in populations of European ancestry. However, the incidence of IBD, which comprises Crohn’s disease and ulcerative colitis, is increasing in different populations around the world. In this comprehensive review, we examine the epidemiology, clinical presentations, disease phenotypes, treatment outcomes, social determinants of health, and genetic and environmental factors in the pathogenesis of IBD in Black and Hispanic patients in the United States. To improve health equity of underserved minorities with IBD, we identified the following priority areas: access to care, accurate assessment of treatment outcomes, incorporation of Black and Hispanic patients in therapeutic clinical trials, and investigation of environmental factors that lead to the increase in disease incidence.

Keywords: disparity, outcomes, pathogenesis

On December 12, 2021, in Atlanta, Georgia, Morehouse School of Medicine, in collaboration with a patient advocacy group, Color of Crohn’s and Chronic Illness, held a multistakeholder consensus conference on the care of minorities with inflammatory bowel disease (IBD). This review article is the summary of the conference proceedings.

Epidemiological Trends of IBD

Since Sir Walter Wilks added “ulcerative colitis” to the medical vernacular in 1875, IBD has transitioned from a rare disease of the Western world to a global illness afflicting millions of people in the 21st century.¹ During the 20th century, the incidence of IBD climbed steadily in North America, Europe, and Oceania.² At the turn of the 21st century, however, the incidence of IBD is stabilizing in these regions.³ The prevalence of IBD now exceeds 0.7% of the population in North America and Europe^4,5 and is expected to rise over the next decade due to compounding prevalence.⁶ Its high prevalence will challenge the ability of healthcare providers in the Western world to provide high-quality and affordable care to patients with IBD.⁷ Moreover, as newly industrialized countries in Asia, Africa, and Latin America transition toward a Westernized society, IBD is increasingly being diagnosed and its incidence is escalating rapidly.^8,9 We have yet to observe a peak in the incidence of IBD in these newly industrialized nations.⁶ With IBD becoming a global disease,¹⁰ understanding the fundamental etiologies of IBD will be crucial to implementing effective preventative strategies for IBD.¹¹

The population demographics of the United States are shifting. Current estimates indicate that the United States will become a majority-minority nation in 2044.¹² However, most of the studies on the epidemiology of IBD in the United States were performed in predominantly White populations.¹³ One of the best-studied epidemiologic cohorts is in Olmsted County, Minnesota, USA. From 2000 through 2010, the adjusted annual incidence rates for Crohn’s disease (CD) and ulcerative colitis (UC) in Olmsted County were 10.7 and 12.2 cases per 100 000 person-years, respectively.¹⁴ In the same analysis, the adjusted prevalence of CD and UC were found to be 246.7 and 286.3 cases per 100 000 persons, respectively, as of January 1, 2011.¹⁴ If these prevalence rates are extrapolated to an estimated U.S. population of 324 million currently, an estimated 1.6 to 1.7 million Americans are currently living with IBD. However, a more recent but preliminary analysis for Olmsted County in 2010 to 2019 indicated that on December 31, 2019, the incidence had stabilized at 7.8 per 100 000 person-years for CD and at 11.5 per 100 000 for UC and that the prevalence was 284 and 250 per 100 000 for CD and UC, respectively.¹⁵ Thus, over 0.63% of the population of Olmsted County had IBD at the end of 2019. These updated prevalence rates suggest that approximately 2.2 million Americans will be living with IBD in 2025.

In addition to the work from Olmsted County, other large data sources have also contributed to our understanding of the epidemiology and natural history of IBD in the United States. An earlier evaluation of U.S. administrative claims data estimated the prevalence of UC and CD as 238 and 201 per 100 000 persons respectively.¹⁶ The Centers for Disease Control and Prevention estimated from the National Health Interview Survey that in 2015 as many as 3.1 million persons in the United States (1.3%) had IBD; however, this result should be interpreted with caution, as the estimates were based on self-reporting.¹⁷ In prospectively collected data from the Nurses’ Health Study I and Nurses’ Health Study II, Khalili et al¹⁸ demonstrated variations in the incidence of CD and UC according to geographical location. When compared with women 30 years of age residing in northern latitudes at 30 years of age, the multivariate-adjusted hazard ratio for similar women residing in southern latitudes was 0.48 for CD and 0.62 for UC (ie, the southern women were at significantly decreased risk for developing CD and UC). This north-south gradient in which the incidence of CD and UC increased significantly with increasing latitude was similar to that found in earlier reports from Europe. The Nurses’ Health Studies have also contributed many other findings to our understanding of the epidemiology of IBD, particularly with respect to the underlying environmental risk factors that potentially influence the development of CD and UC.^19-21

Recent studies indicate a potential shift in the epidemiology of IBD in the United States, with significantly greater increases in incidence rates noted in non-White patients.^22,23 In a recent analysis of Medicare fee-for-service beneficiaries 67 years of age and older, the crude prevalence rates of CD and UC were 0.4% and 0.6%, respectively.²² However, examinations of changes in prevalence over time by race and ethnicity in the same population show that the greatest increase in prevalence was among non-Hispanic Black patients, with an annual percentage increase of 5.0% for CD and 3.5% for UC between 2001 and 2018.²² In a separate evaluation of the Rochester Epidemiology Project and of the residents of Olmsted County, Minnesota, USA, the greatest increases in age-adjusted incidence rates over time were noted among non-White populations.²³ When coupled with recent work demonstrating the potential impacts of immigration on the prevalence of IBD,²⁴ it is clear that an improved understanding of the burden of IBD among all groups in the United States is necessary.

These findings should prompt close re-examinations of the challenges and factors that affect the epidemiology of IBD in non-White populations, including access to care issues and financial barriers.²⁵ Prior studies have indicated that Black patients with IBD are less likely to receive care from gastroenterologists and IBD specialists when compared with similar White patients, and the former are also more likely to report concerns about the cost of care.²⁶ This difference may contribute to delays in diagnosis and in the initiation of appropriate treatment for IBD. Additionally, decreased access to care or decreased willingness to seek care from gastroenterologists may affect the accuracy of estimates of IBD by race and ethnicity when researchers use large administrative studies of electronic medical records or similar sources to determine the incidence and prevalence of IBD in minority groups. Proper access to care is important not only for accurate assessments of the true incidence and prevalence of IBD among non-White populations, but also in resolving or reducing many previously demonstrated disparities in their care.²⁷

These factors have limited much previous work in studying the incidence and prevalence of IBD by race and ethnicity in the United States. An ideal traditional data source for the estimation of the incidence and prevalence of IBD in the United States by race and ethnicity may not exist, given that data from single health systems or hospital discharge data may not be representative and that administrative claims data often do not contain data regarding race and ethnicity. However, recognizing the limitations of prior studies may allow new study designs using novel data sources²⁸ to provide more complete and accurate estimates of the incidence and prevalence of IBD among non-White populations.

Presentation of IBD in Black and Hispanic Patients

The age of onset and the duration of IBD presentation may differ by ethnicity in Western countries. Furthermore, the age of IBD diagnosis is influenced by country of birth. In one retrospective study of 325 patients with IBD, the age of diagnosis was older in foreign-born Hispanics when compared with U.S.-born Hispanics and non-Hispanic Whites.²⁹ Similar studies identified an older age of IBD presentation among Hispanics who were born and lived in Latin America compared with those who were born and lived in the United States.³⁰ Other studies in U.S. Hispanics that examined the age of IBD presentation provided conflicting results, although they did not distinguish by country of nativity.^31,32 On the other hand, most studies that examined the age of presentation of IBD in Black patients did not identify differences in age compared with that of non-Hispanic White counterparts.^33-35 In one multicenter study, however, Black children were found more likely to get diagnosed a full 12 years after the presentation of symptoms, raising concerns that long delays in diagnosis were due to a low index of suspicion for IBD in minority children.³⁶ Therefore, taking it all together it is important to recognize that while age of presentation may be a phenotypic difference among minority populations, particularly in Latin American–born Hispanics, it will be important to identify and distinguish age of diagnosis from age of symptom onset and consider access to care barriers when examining diagnosis age in future studies.

In addition to age of presentation, significant differences in disease phenotypes of CD (particularly in Black patients) have been reported by the U.S. National Institute of Diabetes and Digestive and Kidney Diseases genetics consortium and others; notably, the 2 most severe forms of CD, perianal and fistulizing disease, are more common in Black patients.^13,33,37-40 A multicenter retrospective cohort study of disease phenotypes found that Black patients had a lower frequency of ileal disease and a higher frequency of upper gastrointestinal and colonic CD involvement.³⁹ However, Hispanic patients had a greater prevalence of perianal CD than other groups.³⁹ In another study examining the disease location in UC patients, pancolitis was the most common disease location in Black and Hispanic patients.²⁹ The observed heterogeneity in these results may be due to reasons such as differences in access to care that may then result in delayed diagnoses and progression to more severe phenotypes. Alternatively, the inconsistent results could result from studying different subpopulation cohorts. We know that the term Hispanic comprises a large Latin American population originating from various countries. For instance, studies performed in California and Texas may include primarily Mexican American Hispanics, while studies performed in south Florida may include a population with more Cuban and South American origins.

Studies of racial and ethnic differences in extraintestinal manifestations among non-White populations have conflicting results. A multicenter analysis found that Black IBD patients compared with Whites had a >5-fold increased risk of uveitis⁴¹ and were more likely to have a diagnosis of sacroiliitis.⁴¹ In addition, one study from the pediatric literature reported that higher prevalence of dermatologic manifestations in Black patients.⁴² However, studies examining prevalence of extraintestinal manifestations in Hispanics do not identify any differences compared with non-Hispanic Whites, although a few studies report a slightly increased risk of joint involvement and erythema nodosum.^39,43,44 Therefore, these studies suggest that Black patients may have a greater prevalence of eye and joint manifestations and that Hispanics have a greater prevalence of joint and dermatologic manifestations. That said, results are heterogeneous, thereby limiting any final conclusions.

Lastly, several studies indicate that Black IBD patients have a greater frequency of emergency room visits, IBD-related hospitalizations, and even IBD-related mortality when compared with non-Hispanic Whites and Hispanics in the United States.⁴¹ Some of these studies identify that race and socioeconomic status can influence differences in IBD outcomes, including in-hospital mortality rates and health-related quality of life.⁴⁵ Other studies indicate a higher frequency of operative rates among Black patients with CD compared with non-Hispanic Whites.⁴⁶ However, not all studies indicate that income and education are factors, suggesting that healthcare disparities may stem from reasons beyond financial insecurity.

Treatment Outcomes

Medical Treatments

Existing evidence suggests that IBD phenotypes maybe severe and aggressive in Black patients.⁴⁷ Biologics, which are monoclonal antibodies that target specific cellular inflammatory pathways, are the most effective therapies for treating the more aggressive forms of CD.^48-52 However, the clinical responses and remission rates for all existing biological agents and small molecules for IBD were assessed in clinical trials consisting of primarily White patients, with <3% of patients in these trials were Black.^40,48,49 Moreover, postmarketing reports on the treatment outcomes in non-White IBD patients are limited in scope because the preferences of the payers in the U.S. healthcare system drive the choices of agents for IBD patients in clinical practice.^27,47 Additionally, Black patients accounted for only 1% of 200 outcome-based IBD studies,¹³ so the treatment guidelines for all IBD patients are based on data from primarily White patients: no prospective data are available on whether Black patients can achieve similar responses to treatment using similar approaches. Retrospective cohort studies suggest that Black, Asian, or Hispanic patients are less likely to receive biologic therapies.^26,35 However, no clear differences in the clinical outcomes between Black and White patients were reported.⁴⁷ The current American Gastroenterological Association guidelines are written in support of the physician’s choice in managing patients with IBD across race and ethnicity.⁵³

Endoscopic Treatments

Endoscopic therapy has emerged in the evolving field of interventional IBD as a valid treatment option for IBD or complications associated with IBD surgery. In candidate patients with conditions such as strictures, interventional IBD provides treatment that is more effective than medical therapy and less invasive than surgical therapy. Currently, the main applications of interventional IBD are (1) strictures, (2) fistulas and abscesses, (3) lumen-blocking structures (such as bezoars, foreign bodies, and inflammatory polyps), (4) surgical complications (such as acute or chronic anastomotic leaks and bleeding), and (5) colitis-associated neoplasia. Commonly used endoscopic treatment modalities are endoscopic balloon dilation, stricturotomy, strictureplasty, fistulotomy, sinusotomy, incision and drainage, polypectomy, endoscopic mucosal resection, and endoscopic submucosal dissection.^54,55

It appears that disease behaviors and courses in Black patients with IBD are different from other ethnic groups. Black children with CD were more likely to develop stricturing or penetrating diseases.⁴² All Black patients were found to have a higher risk for clinical recurrence (but not endoscopic recurrence) after ileal, colonic, or ileocolonic resection in CD.⁵⁶ An initial small study (N = 12) showed no significant differences between Black and White patients in the frequency of chronic pouchitis, CD of the pouch, or pouch failure.⁵⁷ A subsequent study showed that both Black (n = 26) and White patients had a higher risk than Hispanic and Asian-Indian American patients for the development of CD of the pouch.⁴³

While endoscopic therapy of IBD is practiced across all ethnic groups, limited published data are available on the differences in outcomes. In the currently available historical cohort studies that compare either endoscopic balloon dilation, endoscopic stricturotomy, surgical resection, and surgical strictureplasty of primary or anastomotic strictures in patients with CD^58-60 or ileal pouch-anal anastomosis in UC,^61,62 ethnicity (including that of Black and Hispanic) was not found to be a factor affecting treatment outcomes.

Diagnostic and therapeutic endoscopy bears risks for procedure-associated complications, including perforation, bleeding, and gas retention. Although Black patients displayed a lower risk for inpatient diagnostic or therapeutic colonoscopy–associated complications in a National (Nationwide) Inpatient Sample study,⁶³ the actual risks for procedure-associated complications for endoscopic therapy in Black and Hispanic American patients with IBD are not clear. Interestingly, more extensive use of systemic corticosteroids than controls was found in Hispanic Americans⁶⁴ but not in Black patients,²⁶ but Black patients with IBD are more likely to have comorbidities such as hypertension and asthma⁶⁵; steroid use and comorbidities can affect the outcomes of endoscopic therapy in IBD.⁵⁴ Prospective studies are needed to further define the preparations, roles, and outcomes of endoscopic therapy in Black, Hispanic, and other ethnic group patients.

Surgical Treatments

Surgical intervention is indicated in 20% to 30% of UC patients, with restorative total proctocolectomy with ileal pouch–anal anastomosis in 1 stage, 2 stages, or 3 stages and total proctocolectomy with end ileostomy vs continent ileostomy as surgical options.^66,67 Total abdominal colectomy with ileorectal anastomosis is an option for patients with rectal-sparing disease. A retrospective cohort study of patients undergoing surgery for IBD using the American College of Surgeons National Surgical Quality Improvement Program database compared outcomes in non-White and White patients and showed a higher length of stay in minority patients and Hispanic patients having the highest odds of readmission.⁶⁷ Black patients had a higher odds of sepsis, bleeding requiring transfusion, and renal dysfunction.⁶⁷ Moreover, a retrospective review showed no differences in the frequency of pouch failure, CD of the pouch, or chronic pouchitis, although Black patients did have a shorter duration of disease and more left-sided colitis (compared with pancolitis) at the time of colectomy.⁵⁷

For the treatment of CD, the goals of surgical intervention are to induce remission to control symptoms, decrease complications and recurrence, and preserve small bowel length.⁶⁶ Abdominal surgical options include balloon dilatation, internal bypass, external bypass with ostomy creation, strictureplasty, and bowel resection. A comparison of abdominal surgeries in Black and White patients showed no differences in surgical outcomes.⁶⁸ In a comparison of postoperative recurrence in Black and White patients who had undergone CD surgeries, clinical recurrence was significantly higher in Black patients but endoscopic remissions did not differ.⁵⁶

Perianal CD is more common in Black and Hispanic patients, but surgical outcome data in these patients are limited.³⁹ For anorectal fistulas, most patients undergo drainage procedures such as seton placement and are less likely to undergo definitive surgical intervention.⁶⁹

As the incidence of CD and UC are rising in Black, Asian, and Hispanic patients, future studies are needed to better identify the effects of race on surgical outcomes and disease prognosis.⁷⁰ In addition, disparities in healthcare access and their impacts on surgical outcomes should be more closely examined.

Clinical Trials in IBD

A wide variety of novel therapeutic agents are in development for CD and UC, as shown in Figure 1. We anticipate that several additional products will become clinically available in the next few years. The mechanisms of action include anticytokine therapies (specifically anti-interleukin [IL]-23 inhibitors); downstream signaling blockage with JAK-STAT pathway inhibitors; and anti-lymphocyte trafficking agents, including anti-integrins and S1p (sphingosine-1-phosphate) receptor modulators.

Clinical efficacy over placebos and good consistent safety profiles have been seen in all of the anti-IL-23 inhibitors in clinical trials (mirikizumab, brazikumab, guselkumab)^71-73 or awaiting U.S. Food and Drug Administration (FDA) approval (risankizumab).⁷⁴ Unfortunately, limited data are available on their effects on fistulizing disease, which typically affects Black patients. However, the clinical benefits of JAK-STAT inhibitors, including updacitinib⁷⁵ and filgotinib,⁷⁶ have been shown in both CD (phase II) and UC (phase II and III) trials. Both of these latter agents are approved for treatment of rheumatoid arthritis and psoriatic arthritis and are waiting for FDA approval. We still have limited data on the safety of JAK-STAT inhibitors in pregnancy and on their efficacy in Black and Hispanic patients. More information will also be needed on their effects on thromboembolic disease, major adverse cardiovascular events, and malignancy.

For anti-integrins, etrolizumab (the leading gut-selective α1βE/α1β7 antagonist candidate)⁷⁷ had mixed results in patients with UC or CD. However, ozanimod⁷⁸ has already been approved for UC treatment, and phase II and III studies for treatment of CD are ongoing. A new mechanism of action being studied is the TLR-9 (Toll-like receptor 9) agonist cobitolimod,⁷⁹ which activates TLR-9 on intestinal T and B lymphocytes and antigen-presenting cells to prevent the development of mucosal inflammation and promote healing. Cobitolimod has shown benefits over placebos when used with standard-of-care medications and could be used as an adjunct therapy to mesalamines based on the results from phase II studies.

In all completed or ongoing clinical trials of IBD, the participation of non-White people has been inadequate to reflect the demographics of the U.S. population. In the 2020 census report, non-Hispanic White Americans accounted for 60% of the population, while Black and Hispanic people accounted for nearly 32% of the population.⁸⁰ In clinical trials, however, almost 90% of study participants in all fields of medicine were White.⁸¹ In IBD therapeutic trials, and despite the increase in the incidence of IBD in non-White patient populations, 2 recent systematic reviews of IBD clinical trials^82,83 showed that the representation of non-White populations within IBD clinical trials was limited. In 55 phase II and III IBD trials from 2000 to 2010, only about 60% included race demographics: 40% did not report these demographics.

To improve diversity in clinical trials, barriers to participation by Black and Hispanic communities need to be assessed and addressed. Factors that may limit trial participation include lack of access, investigator bias regarding the willingness of patients to participate, and the compliance of patients. From the standpoint of patients, potential barriers may include mistrust owing to historical exploitation, transportation problems, lack of ability to take time off from work, and lack of access to the required technologies. As new therapeutic drugs continue to be introduced and numerous new trials are undertaken, we hope that concerted efforts will be made to ensure the adequate representation of all racial and ethnic patient populations.

Social Determinants of Health in the Disparities of IBD Care

The concept of social determinants of health contributing to healthcare outcomes is based on the recognition that social and economic factors are linked to health of individuals. Rising disease and poverty were closely intertwined in the Industrial Revolution, but the phrase was first coined by British physician Thomas McKeown in the 1970s.⁸⁴ The World Health Organization established the Commission on Macroeconomics and Health in the early 2000s, and the U.S. Office of Disease Prevention and Health Promotion has released a Healthy People document each decade since 1980 that defines these social determinants and sets goals to mitigate their impacts on disease outcomes. In their most recent document, Healthy People 2030, the social determinants of health are defined as “the conditions in the environments in which people are born, live, learn, work, play, worship, and age that affect a wide range of health, functioning, and quality-of-life outcomes and risks.”⁸⁵ The specific categories and examples may differ slightly across nations, but significant overlap is present and consensus exists that this topic must be included in medical education curriculae.⁸⁶

The dual pandemics of 2020—the unyielding COVID-19 (coronavirus disease 2019) pandemic and blatant displays of systemic racism and health inequities—have resulted in disparate rates of infection and death in minority low-income communities and have once again brought the discussion of social determinants of health to the forefront. The clear impact of historical racist policies such as redlining (ie, refusing a loan or insurance to someone because they live in an area deemed to be a poor financial risk) that continue to generate ongoing unequal distributions of resources and access have demonstrated that we have omitted racism as a social determinant of health and that racism has been a driver of health disparities. Importantly, the persistent and unscientific narrative of race as a biological construct has often suggested that genetics are the underlying explanation and has delayed progress in addressing the social determinants of health as a modifiable risk factor for disease. Race is not genetically or biologically defined. Indeed, as social constructs, racial health disparities only highlight the underlying embedded social and systemic inequities that generate these different outcomes.

Racial and ethnic disparities in IBD outcomes have certainly been identified, but in most scenarios the underlying explanations for these differences have not been explored—often suggesting that potentially social or biological factors or some combination of these can explain the disparities.^26,27 Disparate IBD outcomes across socioeconomic strata have also been identified in studies in which race is often omitted from the discussion.^87,88 Some studies have examined the intersection of these variables and have suggested that the social variables are the strongest drivers of disparities, although each of the drivers is independently significant in generating unequal outcomes.⁸⁹

Despite this extensive historical perspective and not only our understanding of the critical impact of socioeconomic variables on disease outcomes in general, but also the growing appreciation that this interplay also affects patients with IBD, few efforts have been made that directly incorporate and implement social determinants of health awareness into clinical practice. Similarly, few studies have measured the utility and impacts on IBD health outcomes of social determinants of health awareness and related clinical practice tool implementation.⁹⁰

Pathogenesis of IBD Across Race and Ethnicity

Genetic Factors

Genetic studies in general have hugely underrepresented Black and other populations of non–Northern European ancestry, and IBD is no different. Genome-wide association studies, and increasingly whole-exome and whole-genome sequencing studies, have identified over 250 susceptibility loci for IBD with most of these advances in populations with Northern European ancestry.⁹¹ In other diseases, improving our understanding of the genetic susceptibly in individuals of African ancestry has led to improved treatment strategies for individuals across ancestries. For example, variations in the gene for PCSK9 (proprotein convertase subtilisin/kexin type 9) was found to be associated with individuals of African ancestry who have low levels of low-density lipoprotein, and this discovery led directly to the development of anti-PCSK9 antibodies for the treatment of hyperlipidemia.⁹²

An additional challenge is the genetically admixed nature of the Black population (generally 80% West African and ~20% European ancestry, but this admixture can vary widely). However, several studies have tested for IBD susceptibility loci in Black patients. The most significant associations found in an Immunochip-based study of Black patients with IBD (1088 with CD, 361 with UC, and 1797 control subjects) were at HLA, chromosome 5p, and KAT2A. Associations were also seen at African-specific single nucleotide polymorphism in STAT5A and STAT3. Further analyses implicated the JAK-STAT, cytokine, and chemokine signaling pathways as well as measles pathogenesis. Interestingly, CD-associated NOD2 allele frequency is lower in Black patients with CD than in subjects of European ancestry with CD (3.5% vs 23.5%). In a subsequent genome-wide association study of Black patients with IBD (1646 with CD, 583 with UC, 116 with unclassified IBD, and 5002 without IBD), associations were identified at HLA-DRB1 and with African-specific single nucleotide polymorphism at ZNF649 and LSAMP (UC) and USP25 (IBD). No novel genome-wide signals were detected for CD.³⁷ Nine loci previously identified in European ancestry showed associations in Black patients after accounting for multiple testing, including ADCY3, CXCR6, IL12B, PTGER4, and NOD2. In addition, TNC, CXCR6, and alleles at HLA demonstrated unique patterns with African-specific alleles. LSAMP deletions have been associated with prostate cancer risk in African American men.⁹³ More recently, a whole-genome sequencing approach in over 1700 Black IBD patients and over 1600 control subjects identified a rare variant in the calcium-binding neuroimmunomodulator (CALB2). A highly significant overlap was also found for the known common IBD risk variants between African American and European ancestry individuals.⁹⁴ This last study summarized both the current knowledge in African American IBD genetics as well as the challenges in performing these studies. The studies, to date, have shown that the genetic architecture of African American and European IBD has significant overlaps, although some genes that show differential effect sizes (eg, IL23R and NOD2) demonstrate higher genotype-relative risks in individuals of European ancestry with IBD, while PTGER3, LACC1, and FCGR2A do so in African Americans with IBD. At other loci, African-specific signals may exist (eg, STAT3, STAT5A, TNC) and the associations at CALB2 and LSAMP suggest the possibility of African-specific “genes.” However, this whole-genome sequencing study in African Americans has approximately 1/50th of the sample size of the latest European-ancestry IBD genetics study, which highlights that significant and sustained efforts are needed to address this disparity.

IBD genetics in East Asians also varies from that seen in patients of European ancestry. Specifically, susceptibility loci for NOD2, IL23R, and ATG16L1 have not been found in East Asians.⁹⁵ Instead, TNFSF15 is the dominant susceptibility gene in East Asians, and the effect size dwarfs those of other loci.⁹⁶ While IBD genetic studies in East Asians have been larger than those in African Americans, they are still much smaller than those in European-ancestry populations. Hispanic populations have substantial (~50%) Native American admixtures, and this provides a unique opportunity to identify rare variants with larger effects, as bottleneck populations can result in hundreds of thousands of genetic variants at uniquely high frequency.⁹⁷ Genetic studies in Hispanics currently lag far behind those in other populations, but significant efforts are in progress to remedy this.

More recently, the potential utility of the polygenic risk score (PRS) has been studied, and the benefit of transethnic strategies in the development of the PRS is now clear—as is the limitation of applying PRS values derived from people with European ancestries to other populations.⁹⁸ In addition to the PRS (and the PCSK9 example described previously), another clear example of transethnic approaches showing benefits is in pharmacogenomics. A common missense variant in NUDT15 confers susceptibility to thiopurine-induced leukopenia in individuals of East Asian ancestry, and this gene has also more recently been implicated in thiopurine toxicity in Europeans.^99,100 Other pharmacogenomic studies with significant clinical implications have implicated the HLA in the risk of immunogenicity to anti-tumor necrosis factor therapies in European populations, but the relevance of this finding in other ancestries remains unknown.¹⁰¹ The social, clinical, and scientific reasons to ensure that future genetic studies—including those in IBD—are more inclusive are overwhelming, and the IBD community must work hard to ensure these advances are available for all segments of society.

Environmental Factors

IBD pathogenesis is driven in large part by genetic predisposition (G) in combination with environmental triggers (E).¹⁰² Specific combinations of these G+E factors show a pattern of association with IBD that can be tested in the laboratory using in vivo model systems containing corresponding IBD susceptibility mutations and exposure to environmental factors associated with IBD. Once established in experimental systems, G+E factors found within patient samples can be examined and evaluated using a combination of DNA sequencing and biomarker-based methods capable of capturing the environmental components. These G+E–associated biomarkers will also be useful in the subclassification of IBD. For example, the T300A variant of the CD susceptibility gene ATG16L1, which when paired with an appropriate environmental trigger (ie, infection, smoking, or diet) can lead to cellular phenotypes in mice similar to those observed in CD patients.¹⁰³ Paneth cell defects also occur under these G+E circumstances: the hallmark signals of these defects are the lack of delivery of amphipathic antimicrobial peptides to the intestinal lumen, which can alter the composition of the microbiome and lead to dysbiosis.¹⁰⁴ Indeed, smoking in adults is a significant environmental trigger for CD in an ATG16L1 T300A genetic background, and a key feature of IBD shown in these patients is abnormal Paneth cells.¹⁰⁵ In addition, NOD2 and LRRK2 are 2 other genes found in association with abnormal Paneth cells in CD.¹⁰⁶ Once any of these phenotypic Paneth cells have been identified in IBD patients, they may be useful in subclassifying IBD in the affected patients,¹⁰⁶ as shown in Figure 2.

Figure 2. — Genetic and environmental factors in the pathogenesis of inflammatory bowel disease.

We propose to analyze cellular defects in IBD such as Paneth cell abnormalities to expand our concept of G+E in IBD across race and ethnicity. This idea will allow us to associate specific environmental factors with a variety of host cellular processes, including absorption, barrier function, metabolism, and endoplasmic reticulum stress. In specific racial and ethnic populations (in studies of mostly White IBD patients), many variables are known to act as potential triggers of IBD—such as diet, smoking, stress, exercise, sleep, drugs (nonsteroidal anti-inflammatory drugs) geography, pollution, and infections. However, the specific features and prevalence of these trigger categories need to be addressed in patients in a wider variety of racial and ethnic groups, particularly in Black IBD patients.

A few examples include flavored cigarettes (ie, menthol) that are especially popular in some Black communities, as these flavorings encourage increased smoking. The FDA has recently announced a proposal to ban menthol flavoring in cigarettes and all added flavorings in cigars.¹⁰⁷ The effects of flavored cigars, cigarettes, and now e-cigarettes have not been explored in the context of IBD genetic susceptibility. Additionally, a higher prevalence of physiologic stress is known to occur more generally in Black people than in other racial and ethnic groups, and this in turn may lead to systemic effects such as hypertension and inflammation.¹⁰⁸ The amount of sleep per night is also lower in Black people compared with other ethnic groups,¹⁰⁹ and lack of sleep may worsen IBD as gut inflammation can lead to additional sleep disturbances.¹¹⁰ The Black population in the United States also has a greater incidence of obesity¹¹¹ and greater exposure to pollution,¹¹² which can affect inflammatory phenotypes. Drugs such as proton pump inhibitors are associated with increased infections such as severe acute respiratory syndrome coronavirus 2 in Black patients, highlighting the importance of drug response studies in ethnic and racial groups.¹¹³ Other environmental triggers that may require further investigation include Debaryomyces hansenii, a yeast that was found to be preferentially localized in nonhealing ulcers of CD patients.¹¹⁴ This fungus may represent another environmental trigger of CD that warrants evaluation across disparate populations with IBD. Interestingly, anti–Saccharomyces cerevisiae antibodies have been associated with more severe forms of CD in both European and African ancestries.^115,116 All of these factors can potentially exacerbate inflammation occurring in IBD patients, and further studies in these areas are indeed essential to evaluate these environmental effects in the context of genetics in racial and ethnic groups.

Patient Perspectives

Representatives of patients with UC and CD at our meeting described their diagnosis and treatment journeys. They expressed the following concerns after vivid accounts of their experiences and encounters with the U.S. healthcare system. In particular, they were told that their race is not appropriate for the disease that they have and that IBD is a disease of Jewish or White people and not of Black people.

Importantly, we lack clinical disease indices that capture variables and outcomes important to Black and Hispanic patients, such as symptoms of perianal and fistulizing disease and proctitis. In addition, aspects brought up by patients included the scarcity of data on the clinical effectiveness of treatment options for minority patients, the of lack family and community support, and the lack of education on how to manage their disease.

Recommendations made by the patient members of our conference included (1) creating disease activity indices that capture symptoms important to Black and Hispanic IBD patients, (2) encouraging more studies of these patients, and (3) initiating more education and research engagement efforts for these patients.

Summary and Future Directions

There have been some efforts made in our understanding of the unique challenges present in the care of Black and Hispanic IBD patients, this comprehensive review at our consensus conference demonstrated that significant gaps remain. Literature on medical, endoscopic, and surgical outcomes in Black and Hispanic IBD patients are sparse, and their participation in clinical trials remain low. Future short- and long-term efforts should focus on improving access to care among minority patients with IBD, which will allow timely diagnosis and treatment. Additionally, the recognition that social determinants of health are a modifiable risk factor for disparities will be critical in examining outcomes among Black and Hispanic patients with IBD, and these considerations should be paired with those research efforts examining other constructs such as genetic and environmental factors. The 2 top priorities identified for further research at this meeting are (1) treatment outcomes and (2) environmental factors in the pathogenesis of the disease.

Acknowledgments

The authors thank other participants of our consensus conference who contributed to the lively discussions: Dr Ramona Burress, Mr. Chad Cassie, Mrs. Donna Cryer, Mr. Richard Standifer, Mr. Michael Williams, and Dr London Wills. They also express gratitude to Mr. Stan J. Backs for his editorial assistance.

Contributor Information

Julia J Liu, Division of Gastroenterology, Morehouse School of Medicine, Atlanta, GA, USA.

Bincy P Abraham, Division of Gastroenterology and Hepatology, Houston Methodist Academic Institute, Houston, TX, USA.

Paula Adamson, Division of Gastroenterology, Morehouse School of Medicine, Atlanta, GA, USA.

Edward L Barnes, Division of Gastroenterology and Hepatology, UNC School of Medicine, Chapel Hill, NC, USA.

Kelly A Brister, Department of Surgery, University of Mississippi Medical Center, Jackson, MS, USA.

Oriana M Damas, Division of Gastroenterology and Hepatology, Department of Medicine, University of Miami Miller School of Medicine, Miami, FL, USA.

Sarah C Glover, Division of Gastroenterology and Hepatology, University of Mississippi Medical Center, Jackson, MS, USA.

Kimberly Hooks, Color of Crohn’s and Chronic Illness, Glenarden, MD, USA.

Ana Ingram, Color of Crohn’s and Chronic Illness, Glenarden, MD, USA.

Gilaad G Kaplan, Division of Gastroenterology and Hepatology, Department of Medicine and Community Health Sciences, University of Calgary, Calgary, AB, Canada.

Edward V Loftus, Jr., Division of Gastroenterology and Hepatology, Mayo Clinic College of Medicine and Science, Rochester, MN, USA.

Dermot P B McGovern, F. Widjaja Foundation Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA.

Melodie Narain-Blackwell, Color of Crohn’s and Chronic Illness, Glenarden, MD, USA.

Florence-Damilola Odufalu, Division of Gastroenterology and Liver Diseases, Keck School of Medicine of the University of Southern California, Los Angeles, CA, USA.

Sandra Quezada, Division of Gastroenterology and Hepatology, University of Maryland, College Park, College Park, MD, USA.

Vonda Reeves, GI Associates and Endoscopy Center, Jackson, MS, USA.

Bo Shen, Inflammatory Bowel Disease Center, NewYork-Presbyterian Hospital/Columbia University Irving Medical Center, New York, NY, USA.

Thaddeus S Stappenbeck, Department of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.

Latonia Ward, Color of Crohn’s and Chronic Illness, Glenarden, MD, USA.

Funding

The conference that provided the material for this review was supported by Janssen, Takeda, AbbVie, and Bristol Myers Squibb.

Conflicts of Interest

J.J.L. has served as a consultant for Lilly and Janssen. B.P.A. has served as a consultant for AbbVie, Janssen, Bristol Myers Squibb, Pfizer, Takeda, and Lilly. E.L.B. has served as a consultant for AbbVie, Lilly, and Target RWE. G.G.K. has served as a speaker for AbbVie, Janssen, Pfizer, Amgen, Sandoz, Pendophram, and Takeda; has received research support from Ferring, Janssen, AbbVie, GlaxoSmithKline, Merck, and Shire; has served as consultant for Gilead; and shares ownership of a patent (Treatment of inflammatory disorders, autoimmune disease, and PBC. UTI Limited Partnership, assignee. Patent WO2019046959A1. PCT/CA2018/051098. 7 September 2018). B.S. has served as a consultant for AbbVie, Janssen, and Takeda. E.V.L. has consulted for AbbVie, Amgen, Arena, Boehringer Ingelheim, Bristol-Myers Squibb, CALIBR, Celgene, Eli Lilly, Fresenius Kabi, Genentech, Gilead, Gossamer Bio, Iterative Scopes, Janssen, Morphic, Ono Pharma, Pfizer, Protagonist, Scipher Medicine, Sun Pharma, Surrozen, Takeda, and UCB; and has received research support from AbbVie, Bristol-Myers Squibb, Celgene/Receptos, Genentech, Gilead, Gossamer Bio, Janssen, Pfizer, Robarts Clinical Trials, Takeda, Theravance, and UCB.

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PERMALINK

The Current State of Care for Black and Hispanic Inflammatory Bowel Disease Patients

Julia J Liu, MD, MSc

Bincy P Abraham, MD, MS

Paula Adamson, MD

Edward L Barnes, MD, MPH

Kelly A Brister, MD

Oriana M Damas, MD

Sarah C Glover, DO

Kimberly Hooks, BA

Ana Ingram, MA

Gilaad G Kaplan, MD, MPH

Edward V Loftus Jr, MD

Dermot P B McGovern, MD, PhD

Melodie Narain-Blackwell, BA

Florence-Damilola Odufalu, MD

Sandra Quezada, MD, MS

Vonda Reeves, MD

Bo Shen, MD

Thaddeus S Stappenbeck, MD, PhD

Latonia Ward, MM

Abstract

Epidemiological Trends of IBD

Presentation of IBD in Black and Hispanic Patients

Treatment Outcomes

Medical Treatments

Endoscopic Treatments

Surgical Treatments

Clinical Trials in IBD

Figure 1.

Social Determinants of Health in the Disparities of IBD Care

Pathogenesis of IBD Across Race and Ethnicity

Genetic Factors

Environmental Factors

Figure 2.

Patient Perspectives

Summary and Future Directions

Acknowledgments

Contributor Information

Funding

Conflicts of Interest

References

ACTIONS

PERMALINK

RESOURCES

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