5 alpha-metabolism in finasteride-treated subjects and male pseudohermaphrodites with inherited 5 alpha-reductase deficiency. A review.
Male pseudohermaphrodites (MPHs) with inherited 5 alpha-reductase deficiency and decreased dihydrotestosterone production have a global defect in 5 alpha-metabolism affecting both C19 androgen metabolism and C21 steroid metabolism. However, the decreased 5 alpha-reduction of testosterone to dihydrotestosterone is the only impaired steroid conversion to have clinical consequences, e.g., ambiguous genitalia, impaired prostate differentiation and development, and decreased facial and body hair. The 5 alpha-steroid metabolite profile in the MPHs was compared with that of men with benign prostatic hyperplasia who were administered varying doses of the 5 alpha-reductase inhibitor finasteride. Finasteride was found to be a potent inhibitor of both C19 androgen and C21 5 alpha-steroid metabolism affecting both hepatic and peripheral 5 alpha-metabolism. The 5 alpha-steroid metabolite profile was strikingly similar to that of MPHs with inherited 5 alpha-reductase deficiency. The data suggest that a 5 alpha-reductase gene codes for an enzyme with affinity for multiple steroid substrates.
Imperato-McGinley
J
J
Department of Medicine, Cornell University Medical College, New York, NY.
D013741:3-Oxo-5-alpha-Steroid 4-Dehydrogenase / Q000172:deficiency* / Q000378:metabolism; D058891:5-alpha Reductase Inhibitors; D000368:Aged; D000736:Androstenes / Q000627:therapeutic use*; D001378:Azasteroids / Q000627:therapeutic use*; D013196:Dihydrotestosterone / Q000378:metabolism; D012734:Disorders of Sex Development / Q000188:drug therapy* / Q000201:enzymology; D004311:Double-Blind Method; D018120:Finasteride; D006801:Humans; D008297:Male; D008875:Middle Aged; D011470:Prostatic Hyperplasia / Q000188:drug therapy
D058891:5-alpha Reductase Inhibitors; D000736:Androstenes; D001378:Azasteroids; D013196:Dihydrotestosterone; D018120:Finasteride; D013741:3-Oxo-5-alpha-Steroid 4-Dehydrogenase