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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 deficiencyand 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 5alpha-steroid metabolism affecting both hepatic and peripheral 5 alpha-metabolism. The 5alpha-steroid metabolite profile was strikingly similar to that of MPHs with inherited 5alpha-reductase deficiency. The data suggest that a 5 alpha-reductase gene codes for an enzyme with affinity for multiple steroid substrates.



Imperato-McGinley J;



Eur Urol, 1991;20-1:78-81.


Department of Medicine, Cornell University Medical College, New York, NY.




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