Hasinski S, Miller J L, Rose L I
Hahnemann University School of Medicine, Philadelphia, Pennsylvania.
Am Fam Physician. 1992 Nov;46(5):1511-4.
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.
良性前列腺增生的发病机制与5α-二氢睾酮（DHT，睾酮的生理活性形式）的作用有关。睾酮在前列腺组织细胞内由5α-还原酶催化转化为DHT。非那雄胺通过竞争性抑制睾酮与5α-还原酶的结合来阻断5α-还原酶的作用。非那雄胺口服治疗三个月后对减少前列腺体积的作用达到最大。大多数患者的尿流率有所改善，且副作用极小。然而，停药后，血清DHT水平在两周内恢复至基线。
