Abstract

Oral administration of finasteride, a 5α-reductase inhibitor, affects intraprostatic androgens by suppressing dihydrotestosterone and increasing testosterone. This study was designed to determine the correlation of these effects of finasteride with changes in serum dihydrotestosterone, testosterone and androstanediol glucuronide. In a double blind, placebo-controlled study, 27 men with symptomatic benign prostatic hyperplasia were treated with placebo or 1 or 5mg. per day finasteride for 6 to 8 weeks before transurethral resection of the prostate. There was no significant change in serum testosterone in any group, or in serum dihydrotestosterone or androstanediol glucuronide in the placebo group. There was a decrease in serum dihydrotestosterone by 66 ± 4% and 70 ± 8% (p = 0.32), and of serum androstanediol glucuronide by 78 ± 3% and 86 ± 3% (p = 0.012) in the 1 and 5mg. finasteride groups, respectively. Intraprostatic dihydrotestosterone in the placebo group decreased from 18.6 ± 1.4nmol./kg. to 3.8 ± 1.0nmol./kg. and 1.7 ± 0.7nmol./kg. with 1mg. and 5mg. finasteride, respectively (p = 0.049 between 1mg. and 5mg. finasteride). Intraprostatic testosterone in the placebo group increased from 1.1 ± 0.2nmol./kg. to 7.6 ± 1.0nmol./kg. and 8.3 ± 0.7nmol./kg. with 1mg. and 5mg. finasteride, respectively (no significant difference between 1mg. and 5mg. finasteride). Serum and intraprostatic dihydrotestosterone correlated (p = 0.002). There was no correlation between intraprostatic dihydrotestosterone and serum androstanediol glucuronide. We conclude that 5mg. of finasteride cause greater inhibition of intraprostatic 5α-reductase than 1mg. and that serum dihydrotestosterone is a better marker of intraprostatic dihydrotestosterone than androstanediol glucuronide.

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