Side effects of finasteride enhanced through SE knowledge

[medmax84]

In med school, we're currently learning about the Reproductive Genitourinary System. In class, I began doing Pubmed searches and came up with this as one of many. I also was researching 5AR effects on muscle anabolism... the study on that demonstrated ZERO effect on skeletal muscle growth on DHT inhibition. The study I've included, however, discusses finasteride's incidence of side effects and how it may be effected via patient counseling. It is a marked effect! I've BOLDED some KEY FINDINGS.

Mondaini N, Gontero P, Giubilei G, Lombardi G, Cai T, Gavazzi A, Bartoletti R.

UO Urology, S Maria Annunziata Hospital, University of Florence, Florence, Italy. nicola.mondaini@unifi.it

INTRODUCTION: Sexual adverse experiences such as erectile dysfunction (ED), loss of libido, and ejaculation disorders have been consistent side effects of finasteride in a maximum percentage of 15% after 1 year of therapy. Such data could be seen as far from reality, if compared to a higher percentage that may be found in any common clinical practice. AIM: This study aims to explain the dichotomy between literature's data and clinical practice data. METHODS: One hundred twenty patients with a clinical diagnosis of benign prostatic hyperplasia (BPH), sexually active and with an International Index of Erectile Function-erectile function (IIEF-EF) domain >/=25 were randomized to receive finasteride 5 mg concealed as an "X compound of proven efficacy for the treatment of BPH" for 1 year with (group 2) or without (group 1) counseling on the drug sexual side effect. The phrase used to inform group 2 patients was ". . . it may cause erectile dysfunction, decreased libido, problems of ejaculation but these are uncommon". MAIN OUTCOME MEASURES: The estimation of side effect was conducted at 6 and 12 months using the male sexual function-4 (MSF-4 item) questionnaire and a self-administered questionnaire. RESULTS: One hundred seven patients completed the study. Group 2 patients (N = 55) reported a significant higher proportion of one or more sexual side effects as compared to group 1 (N = 52) (43.6% vs. 15.3%) (P = 0.03). The incidence of ED, decreased libido, and ejaculation disorders were 9.6, 7.7, and 5.7% for group 1, and 30.9, 23.6, and 16.3% for group 2, respectively (P = 0.02, P = 0.04, and P = 0.06). CONCLUSION: In the current study, blinded administration of finasteride was associated with a significantly higher proportion of sexual dysfunction in patients informed on sexual side effects (group 2) as compared to those in which the same information was omitted (group 1) (P = 0.03). A scenario similar to group 2 of the current study is likely to occur in clinical practice, where the patient is counseled by the physician and has access to the drug information sheet. The burden of this nocebo effect (an adverse side effect that is not a direct result of the specific pharmacological action of the drug) has to be taken into account when managing finasteride sexual side effects.

Note that this was at 5mg dose and in an older population. This explains the 15% incidence which is higher than 2% at least in part.

 

[Bryan]

Hahah! Just shortly after you posted that, I happened to mention that study in another thread! In any event, I'm glad you mentioned it again (I first cited it about a month or so ago). I've always been somewhat skeptical myself of these claims of "side effects" from finasteride.

 

[Mew]

I've always been somewhat skeptical myself of these claims of "side effects" from finasteride.

Bryan, if that's the case, why don't you try it yourself? You obviously have some aversion to taking a hormone altering drug despite such claims, no?

As you know, according to Merck only 2% of men get side effects and they are supposedly "fully reversible" after discontinuing the medication... so why wouldn't you give it a shot if you are skeptical of such side effects? After all, you've got nothing to lose by trying, right?

 

[medmax84]

I am pretty sure he DOES take finasteride. And even though I posted this article, I can attest to the fact that my SEs were real and I'm sure there are many individuals with real ADRs out there.

This just demonstrates a psychosomatic aspect and introduces it into discussion. This thread does not mean that EVERY PERSON EXPERIENCING SIDE EFFECTS is somehow imagining it. That's not my point.

 

[Mew]

I am pretty sure he DOES take finasteride

I'm pretty sure he doesn't as he's mentioned it numerous times in the past he does not, both here and on hairlosshelp.com.

He obviously has his reasons for avoiding the drug, so would be interested to know what they are... despite his skepticism of side effects, real or not.

PS: in my opinion -- don't knock those making such claims unless you've tried it yourself (not recommended of course), regardless of the above study... because those in glass houses shouldn't throw stones.

 

[medmax84]

Here's a superb meta-analysis of the sexual ADRs of finasteride. I've only included the conclusion. If you visit the site, it reviews several studies individually.

This is my last contribution to this topic as I feel my SEs have come back as a result of reading this sh!t. Just goes to show you the power of the mind.

http://www.andrologyjournal.org/cgi/content/full/29/5/514

Conclusions

Finasteride and dutasteride are approved for use in the treatment of men with symptomatic BPH and androgenic alopecia and are also under study in ongoing prostate cancer prevention trials. It was shown that treatment with 5ARIs results in a reduction in median serum DHT levels by 60%–93% after 2 years (Imperato-McGinley et al, 1974; Uygur et al, 1998; Andriole and Kirby, 2003; Clark et al, 2004; Marberger et al, 2006). According to 13 randomized studies in which finasteride was used alone, erectile problems occurred in 3% of the men studied long term (AUA Practice Guidelines Committee, 2003). This percentage of ED would seem minimal, and it is also noteworthy that this adverse event diminished by half over time in men taking finasteride (Stoner, 1994; Roehrborn et al, 2004; Moinpour et al, 2007). Randomized controlled studies report the rates of erectile dysfunction to be between 0.8%–15.8% (Table). The placebo effect demonstrated by Mondaini and associates (Mondaini et al, 2007) has to be taken into account when relating the effects of 5ARIs to ED. On the other hand, ejaculation disorders (premature or retarded) related to the use of these inhibitors has not been reported in detail. This outcome should be better described in further studies.

Although there are controversial studies, as a best example we should look for 5 {alpha}-reductase–deficient men whose mean plasma DHT levels are significantly lower when compared with those in normal subjects. More remarkably, the subjects have normal erections directed towards females, although they have low DHT levels (Imperato-McGinley et al, 1974).

Previous studies have shown that there does not seem to be a strong cause-and-effect relationship between serum androgen concentrations and erectile function; even in severely hypogonadal men, the erectile response is not always lost, and T treatment of hypogonadal men with ED does not necessarily restore lost erectile function (Mills and Lewis, 1999). Studies also verified that MENT, which is resistant to 5 {alpha}-reductase, is able to provide physiological and behavioral androgen replacement in hypogonadal men and may provide indirect evidence that 5 {alpha}-reduction is not required for mediation of the influence of T on these behaviors in men (Andersson, 2001).

T and DHT perform vital functions in various organs in different ratios. DHT is more active in prostate than T. This may be due to the fact that DHT is largely a paracrine hormone and exerts effects in tissues of its origin. On the other hand, T is more relevant than DHT in erectile function, which requires central and peripheral androgenic activity. T exerts both humoral endocrine and local paracrine effects.

In this review, we summarized the effect of 5ARIs with respect to erectile function. It is likely that androgens are vital for the development, maintenance and function of penile tissue and regulation of erectile physiology. However, the critical androgenic substance for these effects is most likely T rather than DHT.