Finasteride [5ARI] Induced/Associated Effects

Narasimhalu CR. Randomized Questionnaire Based Case-Control Research Study on Evaluation of Sexual Function in Indian Patients Taking Oral Finasteride for Androgenetic Alopecia. Dermatol Ther (Heidelb). http://link.springer.com/article/10.1007/s13555-015-0084-3

INTRODUCTION: Finasteride is one of the most common drugs used in androgenetic alopecia. The literature discusses the sexual side effects of the drug; however, in practice there is little evidence to support this. The aim of the present study was to investigate the sexual dysfunction in patients taking finasteride 1 mg for androgenetic alopecia.

METHODS: A questionnaire, based on the International Index of Erectile Function, was given to approximately 586 patients with androgenetic alopecia who were being treated with finasteride 1 mg for an average of 16 weeks. These patients were compared to an age-related control group who were attending the Dermatology Out Patients Department for various other skin ailments not related to hair disorders.

RESULTS: Statistical analysis of the results showed no significant difference in the scores between patients taking finasteride and the control group.

CONCLUSION: Analysis showed no significant difference in sex-related problems with that of patients taking finasteride and age matched controls, suggesting that sex-related issues are not a side effect of finasteride.
 
Robinson D, Garmo H, Stattin P, Michaelsson K. Risk of Fractures and Falls during and after 5-alpha Reductase Inhibitor Use: A Nationwide Cohort Study. PLoS One 2015;10(10):e0140598. http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0140598

BACKGROUND: Lower urinary tract symptoms are common among older men and 5-alpha reductase inhibitors (5-ARI) are a group of drugs recommended in treating these symptoms. The effect on prostate volume is mediated by a reduction in dihydrotestosterone; however, this reduction is counterbalanced by a 25% rise in serum testosterone levels.

Therefore, 5-ARI use might have systemic effects and differentially affect bone mineral density, muscular mass and strength, as well as falls, all of which are major determinants of fractures in older men.

METHODS: We conducted a nationwide cohort study of all Swedish men who used 5-ARI by comparing their risk of hip fracture, any type of fracture and of falls with matched control men randomly selected from the population and unexposed to 5-ARI.

RESULTS: During 1 417 673 person-years of follow-up, 10 418 men had a hip fracture, 19 570 any type of fracture and 46 755 a fall requiring hospital care. Compared with unexposed men, current users of 5-ARI had an adjusted hazard ratio (HR) of 0.96 (95% CI 0.91-1.02) for hip fracture, an HR of 0.94 (95% CI 0.90-0.98) for all fracture and an HR of 0.99 (95% CI 0.96-1.02) for falls. Former users had an increased risk of hip fractures (HR 1.10, 95% CI 1.01-1.19).

CONCLUSION: 5-ARI is safe from a bone health perspective with an unaltered risk of fractures and falls during periods of use. After discontinuation of 5-ARI, there is a modest increase in the rate of fractures and falls.
 
Dual 5-Alpha Reductase Inhibition [Dutasteride] Promotes Hepatic Lipid Accumulation


CONTEXT: 5α reductase 1 and 2 (SRD5A1, SRD5A2) inactivate cortisol to 5α-dihydrocortisol in addition to their role in the generation of dihydrotestosterone. Dutasteride (dual SRD5A1 and SRD5A2 inhibitor) and Finasteride (selective SRD5A2 inhibitor) are commonly prescribed, but their potential metabolic effects have only recently been identified.

OBJECTIVE: Our aim was to provide a detailed assessment of the metabolic effects of SRD5A inhibition and in particular the impact upon hepatic lipid metabolism.

DESIGN: We conducted a randomized study in 12 healthy male volunteers with detailed metabolic phenotyping performed before and after 3-weeks treatment with Finasteride (5mg od) or Dutasteride (0.5mg od). Hepatic magnetic resonance spectroscopy (MRS) and 2-step-hyperinsulinemic euglycemic clamps incorporating stable isotopes with concomitant adipose tissue microdialysis were used to evaluate carbohydrate and lipid flux. Analysis of the serum metabolome was performed using ultra high performance liquid chromatography-mass spectrometry.

SETTING: The study was performed in the Wellcome Trust Clinical Research Facility, Queen Elizabeth Hospital, Birmingham, United Kingdom.

MAIN OUTCOME MEASURE: Incorporation of hepatic lipid was measured with MRS.

RESULTS: Dutasteride, not Finasteride, increased hepatic insulin resistance. Intrahepatic lipid increased on MRS after Dutasteride treatment and was associated with increased rates of de novo lipogenesis. Adipose tissue lipid mobilization was decreased by Dutasteride. Analysis of the serum metabolome demonstrated that in the fasted state, Dutasteride had a significant effect on lipid metabolism.

CONCLUSIONS: Dual SRD5A inhibition with Dutasteride is associated with increased intrahepatic lipid accumulation.

Hazlehurst JM, Oprescu AI, Nikolaou N, et al. Dual 5-alpha reductase inhibition promotes hepatic lipid accumulation in man. The Journal of Clinical Endocrinology & Metabolism. http://press.endocrine.org/doi/abs/10.1210/jc.2015-2928
 
Re: Finasteride, Not Tamsulosin, Increases Severity of Erectile Dysfunction and Decreases Testosterone Levels in Men with Benign Prostatic Hyperplasia

Editorial Comment

This study is interesting as it demonstrates the negative effects of finasteride on male erectile function using an objective questionnaire.

In this retrospective registry study a cohort of 470 men 47 to 68 years old (mean ± SD 57.78 ± 4.81) were treated with 5 mg finasteride daily. A second cohort of 230 men 52 to 72 years old (mean ± SD 62.62 ± 4.65) were treated with 0.4 mg tamsulosin.

All men were followed for 45 months. At intervals of 3 months and at each visit plasma testosterone (T) level was measured and the International Index of Erectile Function questionnaire, erectile function domain score was determined.

Long-term treatment with finasteride therapy is associated with worsening of erectile dysfunction (ED), as shown by the significant decrease in the International Index of Erectile Function, erectile function domain scores in men treated with finasteride. No worsening of ED was observed in men treated with tamsulosin.

The increase in ED due to finasteride did not resolve with continued treatment with finasteride. Most importantly long-term finasteride therapy resulted in reduction in total T levels, contributing to a state of hypogonadism. By comparison, no changes in T levels were noted in men treated with tamsulosin.

The negative impact of finasteride on erectile function is noteworthy. The authors did not study ejaculatory function, which may have shown a negative effect using either drug. The data demonstrate that finasteride has a negative impact on male erectile function. Ejaculatory function and libido were not examined.

Seftel AD. Re: Finasteride, Not Tamsulosin, Increases Severity of Erectile Dysfunction and Decreases Testosterone Levels in Men with Benign Prostatic Hyperplasia. J Urol 2016;195(1):139. https://www.sciencedirect.com/science/article/pii/S0022534715050107


Traish AM, Haider KS, Doros G, Haider A. Finasteride, not tamsulosin, increases severity of erectile dysfunction and decreases testosterone levels in men with benign prostatic hyperplasia. Horm Mol Biol Clin Investig. http://www.degruyter.com/view/j/hmbci.ahead-of-print/hmbci-2015-0015/hmbci-2015-0015.xml?format=INT
 
Dr Scally, i dont get it. The study above with 586 patients says this- "CONCLUSION: Analysis showed no significant difference in sex-related problems with that of patients taking finasteride and age matched controls, suggesting that sex-related issues are not a side effect of finasteride.

Then anothet study of 470 men says they did see some sexual side effects ( erection issues).
Which studies are we to believe?
I have a friend who has been on Finasteride for 3 1/2 years and has no sexual side effects. In fact, he takes 1/2 of finasteride per day which is 2 1/2 mgs; much higher than the 1mg standard propecia.
There seems to be a lot of conflicting reports here. Are sexual side effects happening in healthy men who work out and eat healthy ?
 
^^^

That's a legit question and I suppose in many respects the answer is both are correct. (For further details compare and contrast the study designs)

What does that mean?

It means in young healthy patients with otherwise normal TT levels the reduction of either TT or DHT will NOT be significant enough to increase the frequency of ED.

However in those whom already have relatively low TT/DHT levels, as can be the case with many of those over the age of 50, the reduction of TT/DHT induced by Finesteride may be sufficient to increase the occurrence of ED in SOME patients.

Understand this is NOT an all or none phenomena, as only a small minority of patients notice an adverse impact from DHTI on their "sexuality".
 
Ganzer CA, Jacobs AR, Iqbal F. Persistent sexual, emotional, and cognitive impairment post-finasteride: a survey of men reporting symptoms. Am J Mens Health 2015;9(3):222-8. Persistent Sexual, Emotional, and Cognitive Impairment Post-Finasteride

Finasteride is a synthetic 5-alpha reductase inhibitor, which prevents the conversion of testosterone to dihydrotestosterone and has been used for more than 20 years in the treatment of male pattern hair loss. Randomized, controlled trials have associated finasteride with both reversible and persistent adverse effects. In this pilot study, we sought to characterize sexual and nonsexual adverse effects that men reported experiencing at least 3 months after stopping the medication. Based on previous research on persistent side effects of finasteride, we constructed an Internet survey targeting six domains: physical symptoms, sexual libido, ejaculatory disorders, disorders of the penis and testes, cognitive symptoms, and psychological symptoms and was e-mailed to patients who reported experiencing symptoms of side effects of finasteride. Responses from 131 generally healthy men (mean age, 24 years) who had taken finasteride for male pattern hair loss was included in the analysis. The most notable finding was that adverse effects persisted in each of the domains, indicating the possible presence of a "post-finasteride syndrome."
 
Chiriacò G, Cauci S, Mazzon G, Trombetta C. An observational retrospective evaluation of 79 young men with long-term adverse effects after use of finasteride against androgenetic alopecia. Andrology. An observational retrospective evaluation of 79 young men with long-term adverse effects after use of finasteride against androgenetic alopecia - Chiriacò - 2016 - Andrology - Wiley Online Library

Concern regarding adverse effects of finasteride is increasing. We aimed to determine the type and frequency of symptoms in men having long-term sexual and non-sexual side effects after finasteride treatment (a condition recently called post-finasteride syndrome, PFS) against androgenetic alopecia (AGA).

Subjects were recruited at the Urology Unit of the Trieste University-Hospital, and from a dedicated website. Out of 79 participants, 34% were white Italians, mean age was 33.4 ± 7.60 years, mean duration of finasteride use was 27.3 ± 33.21 months; mean time from finasteride discontinuation was 44.1 ± 34.20 months. Symptoms were investigated by an ad hoc 100 questions' questionnaire, and by validated Arizona Sexual Experience Scale (ASEX) and Aging Male Symptom Scale (AMS) questionnaires.

By ASEX questionnaire, 40.5% of participants declared getting and keeping erection very difficult, and 3.8% never achieved; reaching orgasm was declared very difficult by 16.5%, and never achieved by 2.5%.

By the ad hoc questionnaire, the most frequent sexual symptoms referred were loss of penis sensitivity (87.3%), decreased ejaculatory force (82.3%), and low penile temperature (78.5%). The most frequent non-sexual symptoms were reduced feeling of life pleasure or emotions (anhedonia) (75.9%); lack of mental concentration (72.2%), and loss of muscle tone/mass (51.9%).

We contributed to inform about symptoms of PFS patients; unexpectedly loss of penis sensitivity was more frequent than severe erectile dysfunction and loss of muscle tone/mass was affecting half of the subjects. Further studies are necessary to investigate the pathophysiological and biochemical pathways leading to the post-finasteride syndrome.
 
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It seems as though " loss of penis sensitivity" is the true issue here. We all know we are chock full of dht receptors in the penis so perhaps there is real reaon for concern.
However, i dont understand how it continues indefinitely after cessation of the drug.
Arimadex is to extrogen as finasteride is to dht correct? Think about Arinadex preventing conversion. Why does estrogen come back after discontinuing arimadex. Does finasteride actually KILL receptors? Why wouldnt Finasteride keep working on hair loss after discontinuation??
I just dont unferstand that.
 
It seems as though " loss of penis sensitivity" is the true issue here. We all know we are chock full of dht receptors in the penis so perhaps there is real reaon for concern.
However, i dont understand how it continues indefinitely after cessation of the drug.
Arimadex is to extrogen as finasteride is to dht correct? Think about Arinadex preventing conversion. Why does estrogen come back after discontinuing arimadex. Does finasteride actually KILL receptors? Why wouldnt Finasteride keep working on hair loss after discontinuation??
I just dont unferstand that.

Potentially, something epigenetic. Or, something like when a girl takes testosterone for a long period. Certain effects of T will be irreversible because they've triggered changes in the body. A lack of DHT might cause some kind of signaling pathway to atrophy.
 
[QUOTE="Raven101, post: 1495190, member: 77213"

1) " loss of penis sensitivity" is the true issue here

2) Why wouldnt Finasteride keep working on hair loss after discontinuation??
I just dont unferstand that.[/QUOTE]

1) There are two potential mechanism that would alter penile sensitivity and they would include the nervous and vascular supply.

So unless you have an undiagnosed metabolic disorder such as DM, or a spinal cord tumor, the penile sensitivity issues you have mentioned are in your head fella.

2) Come on think! Finesteride looses its effectiveness, as a drug for alopecia bc ITS EXCRETED like every other medication. Moreover hormonal receptors are NOT static immobile structures but rather REGENERATE and relocate elsewhere within the cell membrane.

None of this should be a surprise bc essentially every physiologic process has a finite "life span" which requires regeneration to varying degrees

Good luck
 
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So Dr Jim, are you saying the effects of finasteride should be reversible?
Because dht receptors arent being activated and remain dormant for long periods of time, they can die off but eventually regenerate?
I do know ejaculation issues are a direct result of FIn because the prostate shrinks ( a good thing). If FIN had long lasting effects after stopping, the prostate would remain small and that would be a miracle drug, however, that doesnt happen. How can it only be happening with only the unwanted sexual effects?
 
Is there anyone that is in a law suit with the manufacturer of Propecia? I found some law form online wanting to take my case.

Now we know "the rest of the story" but will filling the pockets of attorneys remedy what you seem convinced is a PHYSIOLOGIC PROBLEM, NOT !

You think I jest? You should spend a lot more time investigating class action settlements in which the individual payouts were well below a grand!

The latter is typical when the litigants failed to demonstrate a cause and effect relationship exists bt the drug and the "injuries" sustained on behalf of their clients. I mean good luck attempting to convince anyone outside of a law firms office, 5ARIs "caused" your constipation, prostatitis, ED or "brain fog" to worsen.

The plaintiff attorneys and the defendant Big Pharma will joust thru some less than transparent discovery process and after YEARS of "negotiations" these 5ARIs cases will reach an "out of court settlement". The legal firms will get their $500/ hour billing pls expenses and the "patients" having been unable to prove causation will receive a few hundred dollars EACH! And after years of anxiously waiting, how do you think your psyche will handle that news!

My suggestion, cease using 5ARI's if you believe they are causing either physiologic or psychologic harm, since that's what any "reasonable person" would do!
 
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Now we know "the rest of the story" but will filling the pockets of attorneys remedy what you seem convinced is a PHYSIOLOGIC PROBLEM, NOT !

You think I jest? You should spend a lot more time investigating class action settlements in which the individual payouts were well below a grand!

The latter is typical when the litigants failed to demonstrate a cause and effect relationship exists bt the drug and the "injuries" sustained on behalf of their clients. I mean good luck attempting to convince anyone outside of a law firms office, 5ARIs "caused" your constipation, prostatitis, ED or "brain fog" to worsen.

The plaintiff attorneys and the defendant Big Pharma will joust thru some less than transparent discovery process and after YEARS of "negotiations" these 5ARIs cases will reach an "out of court settlement". The legal firms will get their $500/ hour billing pls expenses and the "patients" having been unable to prove causation will receive a few hundred dollars EACH! And after years of anxiously waiting, how do you think your psyche will handle that news!

My suggestion, cease using 5ARI's if you believe they are causing either physiologic or psychologic harm, since that's what any "reasonable person" would do!

I agree somewhat, but there is a compelling magazine story about a married SWAT team member who took Propecia, suffered ED and chronic malaise - completely new experiences for him, and so discontinued the drug. The problem: the side effects never went away. His wife left him. He tried to date, but it was useless with ED. He attempted suicide. He is now suing the manufacturer. He'd never heard of any of the online communities that make similar claims. He only ever used his computer for email. With a story so cut and dry, it's hard to place blame elsewhere. You'd just have to write off his story as a very weird and dramatic lie.
 
I agree somewhat, but there is a compelling magazine story about a married SWAT team member who took Propecia, suffered ED and chronic malaise - completely new experiences for him, and so discontinued the drug. The problem: the side effects never went away. His wife left him. He tried to date, but it was useless with ED. He attempted suicide. He is now suing the manufacturer. He'd never heard of any of the online communities that make similar claims. He only ever used his computer for email. With a story so cut and dry, it's hard to place blame elsewhere. You'd just have to write off his story as a very weird and dramatic lie.

A SWAT TEAM MEMBER? One can only begin to understand what those in his profession have to confront on a daily basis OR in years past as many have a relatively extensive military background and also suffer from varying degrees of PTSD.

Every case is different but the common denominator seems to be a functional disorder that predated 5ARI use in EVERY INSTANCE in my practice. That being said, while Ive no doubt some outliers exist, they are the exception rather than the rule especially when individual PFS cases are scrutinized on a purely objective basis.

How else does one explain the fact 5ARIs are indeed "well tolerated" by more than 95% of patients, including MYSELF!

The latter is one hell of a hurdle for plaintiff attorneys to overcome especially when the signs and symptoms of those afflicted are so vague and nonspecific and do NOT exceed that of the general population!
 
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It's prophetic how the media frenzy has changed my practice as I currently only prescribe 5ARI's to those patients with a "emotional disorder" after they have signed a wavier and attested to reading select anecdotal excerpts of Meso posts and TWO of the evidence based citations listed by Dr Scally! (THX @Michael Scally MD

I insist on a 72 waiting period in these cases yet for some the "risk" is worth it bc the only other option is "surgery" as in TURP. The latter is certainly not wo risk of ED either however

Perhaps there IS a yet identified biochemical foundation for the complaints of PFS patients that is only manifested when the putative neuro-chemical abberations are combined with 5ARIs, IDK
 
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Characterization of 5alpha-Reductase Activity and Isoenzymes in Human Abdominal Adipose Tissues

Highlights
· The SRD5A3 isoenzyme is the most highly expressed 5α-reductase in human abdominal adipose tissue.
· Little influence of adipocyte differentiation is seen on SRD5A1 and SRD5A3 mRNA expression.
· 4-dione is the main local source for DHT formation in human preadipocyte cultures.

Fouad-Mansour M, Pelletier M, Tchernof A. Characterization of 5alpha-reductase activity and isoenzymes in human abdominal adipose tissues. J Steroid Biochem Mol Biol. Characterization of 5α-reductase activity and isoenzymes in human abdominal adipose tissues

INTRODUCTION: The substrate for the generation of 5alpha-dihydrotestosterone (DHT) is either androstenedione (4-dione) which is first converted to androstanedione and then to DHT through 17-oxoreductase activity, or testosterone, which is directly converted to DHT. Three 5alpha-reductase isoenzymes have been characterized and designated as types 1, 2 and 3 (SRD5A1, 2 and 3).

OBJECTIVE: To define the predominant source of local DHT production in human adipose tissues, identify 5alpha-reductase isoenzymes and test their impact on preadipocyte differentiation.

METHODS: Cultures of omental (OM) and subcutaneous (SC) preadipocytes were treated for 0, 6 or 24h with 30nM 14C-4-dione or 14C-testosterone, with and without 500nM 5alpha-reductase inhibitors 17-N,N-diethylcarbamoyl-4-methyl-4-aza-5-androstan-3-one (4-MA) or finasteride. Protein level and mRNA abundance of 5alpha-reductase isoenzymes/transcripts were examined in whole SC and OM adipose tissue. HEK-293 cells stably transfected with 5alpha-reductase type 1, 2 or 3 were used to test 5alpha-reductase inhibitors. We also assessed the impact of 5alpha-reductase inhibitors on preadipocyte differentiation.

RESULTS: Over 24h, DHT formation from 4-dione increased gradually (p<0.05) and was significantly higher compared to that generated from testosterone (p<0.001). DHT formation from both 4-dione and testosterone was blocked by both 5alpha-reductase inhibitors. In whole adipose tissue from both fat compartments, SRD5A3 was the most highly expressed isoenzyme followed by SRD5A1 (p<0.001). SRD5A2 was not expressed.

In HEK-293 cells, 4-MA and finasteride inhibited activity of 5alpha-reductases types 2 and 3 but not type 1. In preadipocyte cultures where differentiation was inhibited by 4-dione (p<0.05, n=7) or testosterone (p<0.05, n=5), the inhibitors 4-MA and finasteride abolished these effects.

CONCLUSION: Although 4-dione is the main source of DHT in human preadipocytes, 5alpha-reductase-mediated DHT production mediates the inhibitory effect of both 4-dione and testosterone on preadipocyte differentiation.
 
Ganzer CA, Jacobs AR. Emotional Consequences of Finasteride: Fool's Gold. Am J Mens Health. Emotional Consequences of Finasteride

Androgenetic alopecia, the gradual, progressive loss of hair frequently results in psychological despair, in part related to changes in self-image. Current androgenetic alopecia treatments are limited to hair transplantation and medications that inhibit dihydrotestosterone, a potent androgen associated with follicular micronization.

Users of finasteride, which prevents dihydrotestosterone production, report serious physical and emotional adverse effects, collectively known as post-finasteride syndrome. Psychiatric illnesses and personality traits, specifically neuroticism influence emotional well-being. Limited research exists exploring the psychological corollaries of post-finasteride syndrome and preexisting Axis I and Axis II mental health conditions.

The aim of this study was to explore how having a preexisting personal and/or familial history of a psychiatric diagnosis and certain personality traits may influence anxiety and depression among finasteride users. Participants in this online survey completed the Beck Depression Inventory, the Beck Anxiety Inventory, and Ten-Item Personality Inventory.

An important finding in this study was that almost 57% (n = 97) of men reported a psychiatric diagnosis and 28% (n = 27) had a first-degree relative with a mental health disorder, of this group 17 only had a family history. Nearly 50% of the men surveyed reported clinically significant depression as evidenced by Beck Depression Inventory score and 34% experienced anxiety on the Beck Anxiety Inventory. There were no statistically significant trends in personality traits reported.

Results provide evidence on the need to screen for psychiatric history and counseling patients about the potential psychological consequences of finasteride. Prescribing clinicians should carefully weigh the risk/benefit ratio with these patients.
 
Morales EE, Grill S, Svatek RS, Kaushik D, Thompson IM, Jr., et al. Finasteride Reduces Risk of Bladder Cancer in a Large Prospective Screening Study. Eur Urol. http://www.europeanurology.com/article/S0302-2838%2815%2900772-1/abstract/finasteride-reduces-risk-of-bladder-cancer-in-a-large-prospective-screening-study (http://www.europeanurology.com/article/S0302-2838(15)00772-1/abstract/finasteride-reduces-risk-of-bladder-cancer-in-a-large-prospective-screening-study)

The androgen receptor has been implicated in the development and progression of bladder cancer (BCa), largely based on studies of animal models.

We investigated whether finasteride was associated with a reduced incidence of BCa as observed by self-report in the Prostate, Lung, Colorectal, and Ovarian cancer screening trial. Cox proportional hazard regression analysis was performed to determine the association of finasteride use with time to diagnosis of BCa, controlling for age and tobacco use.

Of the 72 370 male participants who met inclusion criteria, 6069 (8.4%) had reported the use of finasteride. BCa was diagnosed in 1.07% (65 of 6069) of those who reported finasteride compared with 1.46% (966 of 66 301) of those who reported no use during the trial.

In a multiple Cox regression analysis, self-reported use of finasteride was associated with a decreased risk of development of BCa (hazard ratio: 0.634; 95% confidence interval, 0.493-0.816; p=0.0004), controlling for age and smoking.

Limitations of this study include that it is observational and not randomized, that many of the confounding variables for BCa, such as alcohol use, were not available for use in the analysis, and that finasteride use was by annual self-report, which is subject to missing values and error.

PATIENT SUMMARY: Finasteride is a common medication used to reduce the size of the prostate and to promote hair growth by manipulating testosterone in men. Men are more likely than women to develop bladder cancer (BCa), but our study noted that men using finasteride were less likely to have a BCa diagnosis.

Re: Finasteride Reduces the Risk of Bladder Cancer in a Large Prospective Screening Study
http://www.europeanurology.com/article/S0302-2838(15)01231-2/fulltext/re-finasteride-reduces-the-risk-of-bladder-cancer-in-a-large-prospective-screening-study (Re: Finasteride Reduces the Risk of Bladder Cancer in a Large Prospective Screening Study - European Urology)


Expert's comments:

Despite the large population examined in the PLCO study, it failed to demonstrate that organized cancer screening was superior to opportunistic screening in PCa. The trial was considered to be underpowered with respect to addressing organized screening. Recent reports have suggested that there is a subtype of reversible PCa http://www.europeanurology.com/article/S0302-2838(15)01231-2/fulltext/re-finasteride-reduces-the-risk-of-bladder-cancer-in-a-large-prospective-screening-study#bib0030 ([1]) and http://www.europeanurology.com/article/S0302-2838(15)01231-2/fulltext/re-finasteride-reduces-the-risk-of-bladder-cancer-in-a-large-prospective-screening-study#bib0035 ([2]). Cancer chemoprevention is the use of natural, synthetic, or biologic substances to reverse, suppress, or prevent the development of cancer. The REDEEM trial explored the role of partial androgen modulation by 5α-reductase inhibitors and had positive results http://www.europeanurology.com/article/S0302-2838(15)01231-2/fulltext/re-finasteride-reduces-the-risk-of-bladder-cancer-in-a-large-prospective-screening-study#bib0030 ([1]).

In the current study, the authors extracted data from the large population of men enrolled in the PLCO trial and focused on BCa. The title makes a strong assessment of the potential impact of the intake of finasteride for chemoprevention of BCa. The possibility of using finasteride is undeniably intriguing for both physicians and scientists in the field of BCa. Nevertheless, I would suggest using caution when interpreting the conclusions.

First, the primary objective of the PLCO study was to examine PCa, not BCa. Several past examples of debates or ongoing controversies were raised by statistical conclusions that were not hypothesized by clinicians or basic researchers http://www.europeanurology.com/article/S0302-2838(15)01231-2/fulltext/re-finasteride-reduces-the-risk-of-bladder-cancer-in-a-large-prospective-screening-study#bib0040 ([3]) and http://www.europeanurology.com/article/S0302-2838(15)01231-2/fulltext/re-finasteride-reduces-the-risk-of-bladder-cancer-in-a-large-prospective-screening-study#bib0045 ([4]). In addition, it is also important to emphasize that these conclusions were based on observational data from a large sample of men but the data were not randomized. Second, no women were considered in the analysis. This limitation is a major concern because the incidence of BCa is increasing in women in the Western world.

Finally, the scientific rationale behind the conclusion (ie, finasteride and chemoprevention of BCa) is weak http://www.europeanurology.com/article/S0302-2838(15)01231-2/fulltext/re-finasteride-reduces-the-risk-of-bladder-cancer-in-a-large-prospective-screening-study#bib0050 ([5]). In their article, the authors mentioned that the androgen receptor has been implicated in the development BCa; however, no robust data from the laboratory support this association. Consequently, I would strongly discourage using finasteride for the chemoprevention of BCa until additional convincing data are released from experts on urothelial carcinomas.

 
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