Nonsurgical treatment of prostatic hyperplasia

Abstract

Epidemiologic studies in castrates strongly support the key role of the testis in the pathogenesis of benign prostatic hyperplasia (BPH). Since the testis secretes both androgen and estrogen, both of these hormones have been implicated in BPH. Many data support the important role of dihydrotestosterone (DHT) in BPH. It is now possible to quantify prostate size and function with reliable new techniques and to utilize androgen withdrawal studies to test the validity of the DHT theory. A variety of androgen-blocking drugs have been demonstrated to decrease prostate size by approximately 30% by either blocking secretion of circulating testosterone and adrenal androgen, inhibiting 5 alpha-reductase to prevent DHT formation, or blocking DHT binding to androgen receptors. Accompanying these changes in size have been significant improvement in clinical symptoms of prostatism in approximately 50% of patients when double-blind, large multicenter studies were conducted with one of these drugs. Although these results suggest a very important role for androgen, particularly dihydrotestosterone, in the pathogenesis of BPH, other abnormalities besides those of androgen metabolism may coexist since significant numbers of patients do not show a total reversal of disease. There is strong indirect evidence for a possible role for estrogen in the pathogenesis of BPH and studies are under way to test the effects of estrogen withdrawal on prostate size and symptoms. Similarly, dynamic aspects of prostatic obstruction, which are under alpha adrenergic regulation, may also be a component of this disease and amenable to therapy with alpha-adrenergic blockers. Therefore it would seem that BPH may be multifactorial and require combined therapy. Androgen would certainly appear to be necessary, but perhaps not sufficient, for the pathogenesis of this disorder.