FINASTERIDE FOR BENIGN PROSTATIC HYPERPLASIA

The pathogenesis of benign prostatic hyperplasia is related to the action of 5alpha-dihydrotestosterone (DHT), the physiologically active form of testosterone. The conversion of testosterone to DHT is catalyzed intracellularly in prostatic tissue by the enzyme 5alpha-reductase. Finasteride blocks the action of 5alpha-reductase by competitively inhibiting the binding of testosterone to 5alpha-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.