Oral administration of finasteride, a 5alpha-reductase inhibitor, affe
cts intraprostatic androgens by suppressing dihydrotestosterone and in
creasing testosterone. This study was designed to determine the correl
ation of these effects of finasteride with changes in serum dihydrotes
tosterone, testosterone and androstanediol glucuronide. In a double bl
ind, placebo-controlled study, 27 men with symptomatic benign prostati
c hyperplasia were treated with placebo or 1 or 5 mg. per day finaster
ide for 6 to 8 weeks before transurethral resection of the prostate. T
here was no significant change in serum testosterone in any group, or
in serum dihydrotestosterone or androstanediol glucuronide in the plac
ebo 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 5 mg. finasteride
groups, respectively. Intraprostatic dihydrotestosterone in the placeb
o group decreased from 18.6 +/- 1.4 nmol./kg. to 3.8 +/- 1.0 nmol./kg.
and 1.7 +/- 0.7 nmol./kg. with 1 mg. and 5 mg. finasteride, respectiv
ely (p = 0.049 between 1 mg. and 5 mg. finasteride). Intraprostatic te
stosterone in the placebo group increased from 1.1 +/- 0.2 nmol./kg. t
o 7.6 +/- 1.0 nmol./kg. and 8.3 +/- 0.7 nmol./kg. with 1 mg. and 5 mg.
finasteride, respectively (no significant difference between 1 mg. an
d 5 mg. finasteride). Serum and intraprostatic dihydrotestosterone cor
related (p = 0.002). There was no correlation between intraprostatic d
ihydrotestosterone and serum androstanediol glucuronide. We conclude t
hat 5 mg. of finasteride cause greater inhibition of intraprostatic 5a
lpha-reductase than 1 mg. and that serum dihydrotestosterone is a bett
er marker of intraprostatic dihydrotestosterone than androstanediol gl
ucuronide.