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Journal ArticleDOI

Finasteride, an inhibitor of 5 alpha-reductase, suppresses prostatic dihydrotestosterone in men with benign prostatic hyperplasia.

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TLDR
It is concluded that finasteride causes profound decrease in prostatic dihydrotestosterone levels in the prostates of men with benign prostatic hyperplasia.
Abstract
The oral administration of finasteride, a 4-aza-steroid inhibitor of 5 alpha-reductase, decreases serum dihydrotestosterone levels, but has little effect on serum testosterone. The current study was designed to assess the effect of finasteride on dihydrotestosterone levels in the prostates of men with benign prostatic hyperplasia. In a double blind, placebo-controlled study, 69 men with symptomatic prostatic hyperplasia were treated with placebo or 1, 5, 10, 50, or 100 mg/day finasteride for 7 days before transurethral resection of the prostate. In the placebo group the mean concentration of prostatic dihydrotestosterone was 10.3 +/- 0.6 nmol/kg (+/- SE), and the mean concentration of testosterone was 0.7 +/- 0.1 nmol/kg. After 7 days of treatment with all doses of finasteride, prostatic dihydrotestosterone declined to 15% or less of control levels, and the testosterone concentration increased in a reciprocal fashion. Compared to the placebo group, there was no significant difference in the mean prostatic dihydrotestosterone level achieved in any of the finasteride-treated groups. However, prostatic dihydrotestosterone levels were lower in the groups receiving higher doses of the drug. In two additional patients, finasteride treatment for 2 days also caused a decrease in prostatic dihydrotestosterone levels. No significant adverse experiences occurred during the study. We conclude that finasteride causes profound decrease in prostatic dihydrotestosterone.

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Journal ArticleDOI

Efficacy and safety of a dual inhibitor of 5-alpha-reductase types 1 and 2 (dutasteride) in men with benign prostatic hyperplasia

TL;DR: Dutasteride is a potent inhibitor of dihydrotestosterone production that is safe and effective in terms of the reduction of prostate volume and symptoms, flow rate improvement, and the reduction the risk of acute urinary retention and surgery during a 24-month study period.
Journal ArticleDOI

Marked Suppression of Dihydrotestosterone in Men with Benign Prostatic Hyperplasia by Dutasteride, a Dual 5α-Reductase Inhibitor

TL;DR: Dutasteride appeared to be well tolerated with an adverse event profile similar to placebo and reduction in its level with 5alpha-reductase inhibitors improves the symptoms associated with BPH and reduces the risk of acute urinary retention and prostate surgery.
Journal ArticleDOI

Dihydrotestosterone synthesis bypasses testosterone to drive castration-resistant prostate cancer

TL;DR: It is shown that the dominant route of DHT synthesis in CRPC bypasses testosterone, and instead requires 5α-reduction of androstenedione by SRD5A1 to 5 α-androstanedione, which is then converted to DHT.
References
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The metabolic basis of inherited disease

TL;DR: The metabolic basis of inherited disease, the metabolic basis for inherited disease as mentioned in this paper, The metabolic basis in inherited disease and inherited diseases, and inherited disease diagnosis and management, in the context of inherited diseases
Journal ArticleDOI

Dihydrotestosterone in prostatic hypertrophy: I. The formation and content of dihydrotestosterone in the hypertrophic prostate of man

TL;DR: It is possible that the local accumulation of dihydrotestosterone may be involved in the pathogenesis of prostatic hypertrophy in man.
Journal ArticleDOI

The pathogenesis of benign prostatic hyperplasia

TL;DR: It is possible to provide a working hypothesis as to the pathogenesis of prostatic hyperplasia and several potential medical treatments may be feasible that do not involve a chemical castration.
Journal ArticleDOI

Effects of Finasteride (MK-906), a 5α-Reductase Inhibitor, on Circulating Androgens in Male Volunteers*

TL;DR: Finasteride is well tolerated by normal volunteers and results in significant suppression of serum DHT at all doses tested, and the T/DHT ratio increased with all doses and returned to baseline when drug was discontinued.
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