Abstract
Objective:
To investigate Post-Finasteride Syndrome, a broad range of symptoms reported in case reports and case series among patients who have received finasteride, a five-alpha reductase inhibitor. We evaluate the frequency of these symptoms in the Prostate Cancer Prevention Trial (PCPT), a large-scale randomized, placebo-controlled trial of finasteride.
Methods:
Records of subjects enrolled in the PCPT were linked to Medicare claims data. Medicare claims were queried for a group of 22 conditions potentially attributed to PFS, including sexual and cognitive symptoms. Logistic regression and Cox regression analyses, comparing former finasteride use to matched placebo, were adjusted for age, race, BMI, and family history of prostate cancer.
Results:
Of 18,880 eligible subjects, 15,122 were linked to Medicare; of these 14,239 had one or more years of continuous coverage. Median follow-up from study registration to end of Medicare enrollment was 20 years with 267,983 person-years of follow-up. Of the 22 conditions potentially related to PFS, none had a statistically significant association with treatment arm.
Conclusions:
In the largest placebo-controlled study of the five-alpha reductase inhibitor, finasteride, long-term follow-up does not support the concept of a ‘Post-Finasteride Syndrome’. The anecdotal reports to date are likely related to the ubiquitous nature of these symptoms in an aging population and reporting bias.
Introduction
Registered for the treatment of benign prostatic hyperplasia symptoms in 1992, finasteride is one of the most-studied pharmacologic agents in phase III trials for BPH and thereafter in the 18,880-subject Prostate Cancer Prevention Trial (PCPT), which found a 24.8% reduction in risk of prostate cancer among men randomized to finasteride versus placebo.1 In the initial PCPT report, sexual/endocrine side effects were higher among men receiving finasteride (e.g., erectile dysfunction: 67.4% versus 61.5%; loss of libido: 65.4% versus 59.6%; gynecomastia 4.5% versus 2.8%) while genitourinary effects were less common in men receiving finasteride (benign prostatic hyperplasia 5.2% versus 8.7%; urinary urgency or frequency 12.9% versus 15.6%; urinary retention 4.2% versus 6.3%).1 About a decade later, reports began to emerge of a collection of side effects that were reported to occur in men receiving finasteride and that persisted following drug discontinuation. The first report of Post-Finasteride Syndrome as an entity was in 2016.2 In that year, our group published long-term outcomes of the PCPT using a Medicare linkage.3 In that report, there were no differences in risk of ischemic or thrombotic events, endocrine diagnoses, or, notably, risk of sexual dysfunction among men who had previously taken finasteride. Lower urinary tract symptoms were significantly less common among former finasteride users. While dementia was unaffected by study arm assignment, the risk of depression was greater among men who had taken finasteride (Hazard Ratio 1.10 [95% confidence interval 1.01 to 1.19; p = .04]).
Subsequently, multiple publications have included case reports, reviews, and examination of adverse events reported to the FDA’s Adverse Event Reporting System of a constellation of symptoms that are often referred to as Post-Finasteride Syndrome (PFS). As many of the symptoms reported to be associated with PFS are common among aging patients (e.g., erectile dysfunction, low libido, anxiety and depression, cognitive difficulties), the optimal method of assessing the validity of such a syndrome is in long-term follow-up of a randomized study of finasteride. Herein, we present such an analysis.
Methods
Clinical Trial Details
The design of the PCPT has previously been described1. Briefly, 18,880 men age ≥55 years, with normal digital rectal examination and prostate-specific antigen (PSA) of ≤3.0 ng per milliliter, were randomly assigned between 1993–1997 to receive finasteride or placebo daily for 7 years. Prostate cancer was detected either by “for-cause” biopsies on study, based on annual screenings with abnormal digital rectal exams or elevated PSA, or by end-of-study biopsies, recommended for all men after 7 years on-study. The trial was closed early because of the positive finding of a statistically significant 24.8% overall reduction in prostate cancer in those randomly assigned to finasteride.
Linkage Between PCPT Clinical Records and Medicare Claims
We linked PCPT clinical records to Medicare claims data by common social security number, sex, and date of birth. We required that patients have had at least one year of continuous Medicare Parts A & B coverage at any point after registration to the PCPT to ensure a sufficient minimum amount of coverage to identify potential symptoms of PFS. Also, because Medicare claims for HMO patients are not available for research, we required that patients must simultaneously have had no HMO coverage for one continuous year. Medicare records were used to identify symptoms of PFS based on physician supplier Part B (i.e., carrier), hospital outpatient, and hospital inpatient claims. Events were determined from start of Medicare claims coverage using ICD9 and ICD10 diagnosis codes. We included patients with one or more years of Medicare claims at any time in the follow-up period; thus, patients need not have been age 65 years or older at random assignment but, instead, could have aged into the Medicare claims cohort. The date of death was based on the PCPT clinical record when available and on Medicare records when PCPT data were not available. Demographic factors at study registration (age [<65 years vs ≥65 years], race [Black vs white vs other], body mass index [BMI, <25 kg/m2 vs ≥25 kg/m2], and family history of prostate cancer in a first-degree relative [yes vs no]) were obtained from trial records.
Medicare claims were available starting on January 1, 1999, through December 31, 2019, whereas registrations to PCPT occurred from 1994 to 1997. We were thus unable to use claims data to rule out potential pre-existing events occurring prior to study registration.
Written informed consent for the clinical protocol was previously obtained for all participants. Approval to conduct this research was obtained from the Institutional Review Board of Cancer Research and Biostatistics (Seattle, WA). The PCPT predates the NIH Clinical Trials Registry and is tracked in the Physician Data Query System at https://www.cancer.gov/types/prostate/research/finasteride-reduces-low-grade.
Definition of Long-Term Consequences of Intervention
An event was identified as any hospital claim—or two or more physician or outpatient claims at least 30 days apart—for the following prespecified PFS outcomes: decreased libido, erectile dysfunction, loss of orgasm and decreased semen volume, penile shrinkage, Peyronie’s disease, scrotal shrinkage, gynecomastia, fatigue, muscle pain and muscle weakness, less oily skin and Melasma, localized loss of fat tissue, tinnitus, increased body mass/BMI, decreased body temperature, reduced HDL or raised fasting glucose or raised triglycerides, attempted or completed suicide, memory loss, impaired cognition, flat emotion, insomnia, obstructive sleep apnea, and depression (Supplemental Table 1).
Statistical Methods
Participant characteristics at trial entry are presented for those on the finasteride arm and those on the placebo arm in the current analysis. Additionally, characteristics are compared between those included in the current analysis and those not included, using chi-square tests for categorical variables and t-tests for continuous variables.
To incorporate time until evidence of an event and to account for potential competing risk of death, we analyzed the cumulative incidence of events. The data were left truncated because there was (in all instances) a gap between random assignment and the initiation of Medicare claims coverage. To account for this, we derived cause-specific cumulative incidence rates for left-truncated and right-censored data4. Cox regression was used to examine time to PFS events, adjusting for covariates5. The assumption of proportional hazards was assessed by testing the interaction of intervention with the log of time. Analyses were conducted separately for each event. Patients who died were censored at their date of death; if no death was observed, the date at end of observed Medicare coverage was used. To examine event rates alone (rather than time to event), logistic regression models were used. Logistic regression and Cox regression analyses were adjusted for baseline age, race, BMI, and family history of prostate cancer. Two-sided tests are reported. To balance the need for multiplicity adjustment to limit Type I error (given 22 comparisons) with the aim to identify potentially adverse consequences of finasteride, a P value of less than .01 was considered statistically significant. Table cell counts <11 are suppressed per privacy regulations.
In order to explore a potential dose response, a sensitivity analysis was performed, including only the men who reported taking study drug (finasteride or placebo) for 5 years or more while on PCPT. Also, because finasteride reduces the incidence of prostate cancer6 and of BPH requiring surgery7, either of which can lead to some PFS outcomes, an additional sensitivity analysis was performed that excluded men with a prostate cancer diagnosis or BPH surgery, identified through PCPT records or Medicare claims data.
Results
A total of 18,880 eligible subjects from the PCPT were randomly assigned to finasteride vs placebo. We linked 15,122 of these patients to Medicare claims, and 14,239 (75.4% of total eligible patients) had one or more years of continuous Medicare parts A & B coverage with no HMO participation (7087 on the finasteride arm and 7152 on the placebo arm). This cohort comprised the evaluable patient set for this analysis. Of the 7087 men on the finasteride arm, 2281 (32%) completed PCPT finasteride use prior to the start of Medicare coverage, with a median gap time of 1.7 years (IQR, 0.73, 3.36), and 4806 (68%) were still taking PCPT finasteride at the start of Medicare coverage, with a median overlap time of 2.5 years (IQR, 1.94, 3.20).
Patient Characteristics
The median amount of time from trial registration to the end of Medicare claims was 20.0 years, which was similar between the finasteride and placebo arms (20.0 vs 19.9 years respectively; Table 1). Most participants had a BMI greater than 25 (74.3%) and no family history of prostate cancer (84.6%).
Table 1.
Baseline characteristics of included participants by arm, and compared to participants not included
| Characteristic | Current Medicare Study | PCPT | |||
|---|---|---|---|---|---|
|
| |||||
| Finasteride | Placebo | All | Not linked to Medicare | p-value† | |
|
| |||||
| (n=7087) | (n=7152) | (n=14,239) | (n=4641) | ||
| Age, y | <.0001 | ||||
| Mean (SD) | 63.5 (5.6) | 63.4 (5.6) | 63.5 (5.6) | 64.2 (5.9) | |
| 55–59 | 2300 (32.2%) | 2318 (32.7%) | 4618 (32.4%) | 1290 (27.8%) | |
| 60–64 | 2160 (30.2%) | 2249 (31.7%) | 4409 (31.0%) | 1385 (29.9%) | |
| 65+ | 2692 (37.6%) | 2520 (35.6%) | 5212 (36.6%) | 1963 (42.3%) | |
| BMI, kg/m2 | 0.76 | ||||
| Mean (SD) | 27.7 (4.2) | 27.7 (4.1) | 27.7 (4.1) | 27.8 (4.3) | |
| <25 | 1820 (25.7%) | 1804 (25.7%) | 3624 (25.7%) | 1193 (25.9%) | |
| 25+ | 5252 (74.3%) | 5219 (74.3%) | 10471 (74.3%) | 3406 (74.1%) | |
| Race | 0.15 | ||||
| White | 6764 (94.6%) | 6700 (94.5%) | 13464 (94.6%) | 4354 (93.8%) | |
| Black | 276 (3.9%) | 268 (3.8%) | 544 (3.8%) | 188 (4.1%) | |
| Asian/PI | 71 (1.0%) | 63 (0.9%) | 134 (0.9%) | 53 (1.1%) | |
| Native | 22 (0.3%) | 34 (0.5%) | 56 (0.4%) | 25 (0.5%) | |
| Unknown | 19 (0.3%) | 22 (0.3%) | 41 (0.3%) | 21 (0.5%) | |
| Family history | 0.61 | ||||
| No | 6083 (85.1%) | 5970 (84.2%) | 12053 (84.6%) | 3914 (84.3%) | |
| Yes | 1069 (14.9%) | 1117 (15.8%) | 2186 (15.4%) | 727 (15.7%) | |
| Years of follow-up, median [range] | |||||
| Trial registration to end of Medicare coverage | 20.0 [2.7–25.9] | 19.9 [3.6–25.9] | 20.0 [2.7–25.9] | ||
| Beginning to end of Medicare coverage | 14.0 [0.9–20.9] | 13.9 [0.9–20.9] | 14.0 [0.9–20.9] | ||
PCPT= Prostate Cancer Prevention Trial; y = year; SD = standard deviation; BMI = body mass index; kg = kilogram; m = meter; PI = Pacific Islander
Chi-square tests were conducted to compare characteristics between those included in the current study, and those not linked to Medicare data. Two-sided tests are reported.
Patients with Medicare coverage were 0.7 years younger on average at study registration (P < .001) than patients without Medicare coverage.
Long-term Consequences
Table 2 displays rates of conditions/symptoms in subjects in the two study arms as well as 5-year and 10-year rates of cumulative incidence during a total of 267,983 person-years of follow-up (134,599 on the placebo arm, 133,384 on the finasteride arm). Overall, the most commonly recorded events on the finasteride and placebo arms were reduced HDL (74.9% and 75.2% respectively), fatigue (50.2% and 48.9%), muscle pain or weakness (31.7% and 30.9%), depression (25.2% and 24.3%), and erectile dysfunction (21.8% and 21.7%).
Table 2.
Associations between treatment assignment and symptoms of Post-Finasteride Syndrome
| Overall | Placebo | Finasteride | CumInc | 5-Year CumInc | 10-Yr CumInc | |||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|
|
| ||||||||||||
| Condition/Symptom | N (%) | N (%) | N (%) | OR (95%CI) | p-value | Total | Pla | Fin | Pla | Fin | HR (95%CI) | p-value |
|
| ||||||||||||
| Decreased Libido | 45 (0.3%) | 18 (0.3%) | 27 (0.4%) | 1.65 (0.89–3.07) | 0.11 | 0.3 | 0 | 0 | 0.1 | 0.1 | 1.65 (0.89–3.05) | 0.11 |
| Erectile dysfunction | 3100 (21.8%) | 1552 (21.7%) | 1548 (21.8%) | 0.99 (0.92–1.08) | 0.90 | 34.8 | 13.6 | 13.7 | 25.3 | 25.6 | 0.99 (0.92–1.06) | 0.78 |
| Loss of orgasm, decreased semen volume | NP | 0 | NP | -- | 0 | 0 | 0 | 0 | 0 | -- | ||
| Penile shrinkage | 93 (0.7%) | 47 (0.7%) | 46 (0.6%) | 0.98 (0.65–1.48) | 0.94 | 0.9 | 0.1 | 0.1 | 0.5 | 0.5 | 0.98 (0.65–1.47) | 0.91 |
| Peyronie’s disease | 55 (0.4%) | 36 (0.5%) | 19 (0.3%) | 0.52 (0.30–0.90) | 0.02 | 0.6 | 0 | 0 | 0.1 | 0 | 0.52 (0.30–0.90) | 0.02 |
| Scrotal shrinkage | 13 (0.1%) | NP | NP | NP | p>.01 | NP | NP | NP | NP | NP | NP | p>.01 |
| Gynecomastia | 185 (1.3%) | 98 (1.4%) | 87 (1.2%) | 0.89 (0.67–1.20) | 0.45 | 2.1 | 0.5 | 0.4 | 1 | 0.9 | 0.89 (0.66–1.19) | 0.42 |
| Fatigue | 7058 (49.6%) | 3497 (48.9%) | 3561 (50.2%) | 1.06 (1.00–1.14) | 0.07 | 65.1 | 19.6 | 20.2 | 42.2 | 43.3 | 1.04 (0.99–1.09) | 0.12 |
| Muscle pain, muscle weakness | 4457 (31.3%) | 2208 (30.9%) | 2249 (31.7%) | 1.04 (0.97–1.12) | 0.23 | 41.6 | 3.6 | 3.7 | 8.6 | 8.8 | 1.04 (0.98–1.10) | 0.24 |
| Less oily skin, Melasma | 2685 (18.9%) | 1386 (19.4%) | 1299 (18.3%) | 0.93 (0.85–1.01) | 0.09 | 27.8 | 6.5 | 6.1 | 14.3 | 13.5 | 0.93 (0.86–1.00) | 0.06 |
| Localized loss of fat tissue | NP | NP | NP | NP | p>.01 | NP | NP | NP | NP | NP | NP | p>.01 |
| Tinnitus | 511 (3.6%) | 259 (3.6%) | 252 (3.6%) | 0.98 (0.82–1.18) | 0.86 | 5.3 | 1 | 0.9 | 2.6 | 2.5 | 0.98 (0.82–1.16) | 0.80 |
| Increased body mass/BMI | 2292 (16.1%) | 1140 (15.9%) | 1152 (16.3%) | 1.02 (0.93–1.11) | 0.74 | 22.7 | 3.6 | 3.7 | 8.2 | 8.4 | 1.01 (0.93–1.10) | 0.75 |
| Decreased body temperature | 24 (0.2%) | NP | NP | NP | p>.01 | NP | NP | NP | NP | NP | NP | p>.01 |
| Reduced HDL, raised fasting glucose, raised triglycerides | 10684 (75.0%) | 5377 (75.2%) | 5307 (74.9%) | 0.97 (0.90–1.05) | 0.45 | 91.8 | 53.7 | 53.6 | 77.7 | 77.6 | 0.99 (0.95–1.03) | 0.52 |
| Attempted or completed suicide | 155 (1.1%) | 77 (1.1%) | 78 (1.1%) | 1.09 (0.78–1.51) | 0.62 | 1.4 | 0.2 | 0.2 | 0.4 | 0.4 | 1.08 (0.78–1.50) | 0.63 |
| Memory loss | 1512 (10.6%) | 756 (10.6%) | 756 (10.7%) | 1.00 (0.90–1.12) | 0.96 | 13.3 | 0 | 0 | 0.8 | 0.8 | 1.00 (0.90–1.11) | 1.00 |
| Impaired cognition (impaired thought processes, problem solving) | 1197 (8.4%) | 581 (8.1%) | 616 (8.7%) | 1.07 (0.95–1.21) | 0.25 | 11.6 | 0 | 0 | 0 | 0 | 1.06 (0.95–1.19) | 0.29 |
| Flat emotion | 53 (0.4%) | 25 (0.3%) | 28 (0.4%) | 1.13 (0.66–1.95) | 0.65 | 0.5 | 0.1 | 0.1 | 0.2 | 0.2 | 1.13 (0.66–1.93) | 0.67 |
| Insomnia | 2006 (14.1%) | 1009 (14.1%) | 997 (14.1%) | 0.99 (0.90–1.09) | 0.90 | 19.7 | 2.5 | 2.5 | 6.2 | 6.2 | 0.99 (0.91–1.08) | 0.80 |
| Obstructive sleep apnea | 2307 (16.2%) | 1182 (16.5%) | 1125 (15.9%) | 0.94 (0.86–1.03) | 0.17 | 20.4 | 0 | 0 | 0.3 | 0.3 | 0.95 (0.88–1.03) | 0.22 |
| Depression | 3523 (24.7%) | 1740 (24.3%) | 1783 (25.2%) | 1.06 (0.98–1.14) | 0.17 | 37.2 | 10.9 | 11.4 | 18 | 18.7 | 1.05 (0.98–1.12) | 0.16 |
All models are adjusted for age at registration (<65 vs 65+), race (white vs Black vs other), BMI (<25 vs ≥25 kg/m2), and family history of prostate cancer (yes vs no).
CumInc = cumulative incidence; OR = odds ratio; HR = hazard ratio; CI = confidence interval; NP = not presented due to privacy regulations
In adjusted multivariate Cox regression, there was a lower risk on the finasteride arm than the placebo arm of both Peyronie’s disease (0.3% vs 0.5%, HR=0.52, 95% CI= 0.30–0.90, p=.02) and less oily skin and Melasma (18.3% vs 19.4%, HR=0.93, 95% CI= 0.86–1.00, p=.06), and the risk of decreased libido was higher on the finasteride arm (0.4% vs 0.3%, HR=1.65, 95% CI= 0.89–3.05, p=.11). However, none of these associations was statistically significant at the alpha=.01 level. Plots of cumulative incidence of the individual symptoms of Post-Finasteride Syndrome are shown in Figure 1.
Figure 1.
Cumulative incidence of each individual symptom of Post-Finasteride Syndrome, by treatment arm. Solid lines represent the finasteride treatment arm, dotted lines represent the placebo arm.
In a sensitivity analysis including only the men who reported taking finasteride or placebo for five years or more on PCPT, and a sensitivity analysis excluding men with evidence of a prostate cancer diagnosis or of BPH requiring surgery, the results were similar (Supplemental Tables 2 and 3).
Discussion
Finasteride is widely used for the management of lower urinary tract symptoms in men and alopecia in both men and women. In the Prostate Cancer Prevention Trial, multiple urinary outcomes were improved and subsequent analyses found a 40% reduction of incident clinical BPH with finasteride.8 As finasteride inhibits five-alpha reductase, thereby reducing androgen activity, it was not unexpected that in the initial phase III trial in men with BPH, the treatment group had higher incidence of erectile dysfunction, decreased libido, and ejaculatory disorders.9 The PCPT subsequently confirmed these findings.1
The increasing number of reports of a group of symptoms, collectively referred to as Post-Finasteride Syndrome, that was postulated to be related to the drug and which did not diminish after cessation of drug administration, has been of interest. Several of these reports relied on data in the US Food and Drug Administration’s Adverse Event Reporting System (FAERS) which are generally physician-reported. Of interest, one analysis examined reporting of depression and suicide; no association of finasteride with these conditions was noted between 2006–2011 but an increase was noted in 2013–2018 and in 2019–2023.10 The authors of this analysis speculated that these reports may have been due to increased awareness. Most reports have been case reports or clinical series. To our knowledge, this is the first to examine these putative side effects in the context of a randomized clinical trial.
What is strikingly apparent from this examination from long-term follow-up of men who were randomized to receive finasteride or placebo in the PCPT is that the symptoms and conditions examined were unaffected by finasteride administration, even when results were limited to men confirmed to have taken finasteride for at least five years. While it is not surprising, given experience with the medication in phase III trials, that decreased libido was numerically more common in men receiving finasteride, the increase was not statistically significant. Also surprising was the observation that erectile dysfunction was unaffected by finasteride and that Peyronie’s disease was less common (although not statistically significant) in men receiving finasteride. While impaired cognition and depression were slightly more common with finasteride, the differences were not statistically significant, and memory loss was unaffected.
While the strengths of this study are the large number of patients, long-term follow-up, and, unlike previous reports, a placebo control for subjects who received finasteride, there are a number of limitations. One limitation is that while some outcomes had large numbers of events (e.g., erectile dysfunction) others, such as impaired cognition, had considerably smaller numbers of affected patients, calling into question the precision of the incidence estimates. Because PCPT was a cancer chemoprevention trial conducted in otherwise healthy men, a paramount goal during the study and follow-up was to measure potential side effects of finasteride. While urinary and sexual side effects were rigorously collected, the constellation of effects thought to be associated with PFS were not. It is for this reason that it was necessary to rely on Medicare claims data. Claims data are subject to misclassification, and the accuracy of these claims cannot be fully verified. Additionally, claims data identify conditions sufficiently symptomatic to prompt a health care visit and diagnostic coding, which may focus on more severe symptoms and underreport some conditions (e.g. tinnitus or erectile dysfunction) that may be less likely to be reported to a physician. However, there is no reason to expect that study arm assignment would have affected diagnosis assignment for billing and collection by treating healthcare providers.
The only method to fully understand if the symptoms attributed to PFS are truly causal would be to conduct a randomized, placebo-controlled, prospective trial with rigorous ascertainment of symptoms. As many of the putative symptoms of PFS are ubiquitous among aging men and, as reporting could be due to misattribution, the present study is the best assessment of these symptoms until a large-scale randomized trial is conducted with patient-reported symptom assessments. Symptom misattribution, from information provided to patients (by physicians, in the package insert, on the internet) likely leads to greater reporting of side effects in patients receiving finasteride than among those not receiving it. Clear evidence of such misattribution can be seen in the PCPT. In the original study design, there was a two-step process of study entry. At the first visit, after informed consent to include information related to the randomization and potential side effects of finasteride, subjects were tested for PSA and given a 3-month bottle of study drug. The first 3-month study drug was placebo for all patients (a placebo run-in design). At the subsequent 3-month visit, subjects with a PSA from the first visit of <3.0 ng/mL, who were compliant with daily pill intake, and who had no significant side effects from the first 90 days of study drug, were then randomized to finasteride or placebo. All others were not randomized. Illustrating the potential for misattribution to common conditions of aging, 135 (0.55%) subjects receiving the 90 days of placebo reported the development of sexual side effects. Additionally, in late 1997, in a report to PCPT study sites and participants, study leadership provided information on sexual symptoms in men receiving placebo.11 Among 8,337 men in the placebo group ranging in age from 55 to 86 with an average age of 63, we reported on the change in rates of impotence, loss of libido, and decrease in ejaculate volume between baseline and the two-year mark. Figure 2 shows the rates of these symptoms at these two points. Most notable is that with a two-year exposure to placebo, significant numbers of men who had been informed they may have been taking finasteride developed these three symptoms.
Figure 2.
Percent of participants who reported sexual symptoms at baseline and at two-years of follow-up in 8,337 men in the placebo arm of the Prostate Cancer Prevention Trial. Age range of participants 55 to 86; average age 63.
We have found no evidence that Post-Finasteride Syndrome is a true clinical syndrome. The conditions ascribed to it cannot be attributed to finasteride until an appropriately designed and adequately powered trial is conducted. Until that time, patients should be told that side effects of the drug include those that are adverse (decreased libido, erectile dysfunction, and reduced ejaculate volume) and those that are beneficial (lower risk of BPH, urinary retention, urinary infections, and prostate cancer).
Supplementary Material
Acknowledgments
This research was supported in part by the US National Institutes of Health, National Cancer Institute (grants CA189974 and CA182883); and in part by the Hope Foundation for Cancer Research in support of infrastructure, data analysis, and trial design within the SWOG Cancer Research Network, at the SWOG Statistics and Data Management Center.
Approval to conduct this research was obtained from the Institutional Review Board of Cancer Research and Biostatistics (Seattle, WA). Written informed consent for the clinical protocol was previously obtained for all participants.
Studies in Human
This study was performed in compliance with relevant laws, regulatory frameworks and guidelines where the research took place.
This study was approved by the Institutional Review Board of Cancer Research and Biostatistics. (Approval No. FHIRB0008262)
Footnotes
Ethics declaration
Informed consent and patient details
Written informed consent to take part in the study and to publish the article has been obtained from all participants or their legal representatives. The privacy rights of participants have been observed.
Clinical Trials
The results of this clinical trial and any associated work have been posted in a registry.
This clinical trial was registered with number https://www.cancer.gov/types/prostate/research/finasteride-reduces-low-grade (Physician Data Query System).
Declaration of interests
The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
Joseph M. Unger reports a relationship with AstraZeneca Pharmaceuticals LP that includes: consulting or advisory. Joseph M. Unger reports a relationship with Eli Lilly and Company that includes: consulting or advisory. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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