Finasteride for benign prostatic hyperplasia.
The pathogenesis of benign prostatic hyperplasia is related to the action of 5 alpha-dihydrotestosterone (DHT), the physiologically active form of testosterone. The conversion of testosterone to DHT is catalyzed intracellularly in prostatic tissue by the enzyme 5 alpha-reductase. Finasteride blocks the action of 5 alpha-reductase by competitively inhibiting the binding of testosterone to 5 alpha-reductase. The maximum effect of finasteride on reducing prostatic volume occurs after three months of oral therapy. Most patients experience improvement in urine flow rates, and side effects are minimal. However, following discontinuation of treatment, serum DHT levels return to baseline within two weeks.
D058891:5-alpha Reductase Inhibitors; D000284:Administration, Oral; D000736:Androstenes / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D001378:Azasteroids / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D013196:Dihydrotestosterone / Q000378:metabolism / Q000494:pharmacology; D018120:Finasteride; D006801:Humans; D008297:Male; D011470:Prostatic Hyperplasia / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism
D058891:5-alpha Reductase Inhibitors; D000736:Androstenes; D001378:Azasteroids; D013196:Dihydrotestosterone; D018120:Finasteride