Finasteride, a 5 alpha-reductase inhibitor, does not bind to the andro
gen receptor and has no other known hormonal activity. To determine wh
at effect, if any, it has on adrenal steroidogenesis, 10 healthy men r
eceived 5 mg finasteride daily for 28 days. Adrenocorticotropic hormon
e (ACTH) stimulation tests were performed before and after 4 weeks of
finasteride administration (5 mg daily). Serum levers of 17-hydroxypre
gnenotone, 17-hydroxyprogesterone, deoxycorticosterone, corticosterone
, aldosterone, cortisol, dehydroepiandrosterone, and androstenedione w
ere measured before and 60 minutes after i.v. ACTH. Finasteride decrea
sed serum dihydrotestosterone levels from 31 +/- 5 to 4.4 +/- 1.2 ng/d
l (P < 0.001). There were no significant changes in basal or ACTH-stim
ulated serum levels of adrenal steroids. There was also no significant
decrease in the product to precursor ratio for the seven adrenal enzy
mes tested. Finasteride increased mean serum androstenedione levels by
17% (P = 0.10) and significantly increased the androstenedione to 17-
hydroxyprogesterone ratio (P = 0.02 before ACTH and 0.05 after ACTH).
These changes are most likely due to inhibition of androstenedione met
abolism by 5 alpha-reductase. In conclusion, finasteride has no detect
able effect on adrenal steroidogenesis, other than that which can be e
xplained by inhibition of the 5 alpha-reductase enzyme.