Geller J
Department of Medical Education, Mercy Hospital and Medical Center, San Diego, CA 92103-2180.
Cancer. 1992 Jul 1;70(1 Suppl):339-45.
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.
对去势者的流行病学研究有力地支持了睾丸在良性前列腺增生（BPH）发病机制中的关键作用。由于睾丸分泌雄激素和雌激素，这两种激素都与BPH有关。许多数据支持双氢睾酮（DHT）在BPH中的重要作用。现在可以用可靠的新技术量化前列腺大小和功能，并利用雄激素撤除研究来检验DHT理论的有效性。
已证实多种雄激素阻断药物可通过以下方式使前列腺大小减小约30%：阻断循环睾酮和肾上腺雄激素的分泌、抑制5α-还原酶以阻止DHT形成或阻断DHT与雄激素受体的结合。
当使用其中一种药物进行双盲、大型多中心研究时，约50%的患者前列腺大小发生这些变化的同时，前列腺增生的临床症状也有显著改善。尽管这些结果表明雄激素，尤其是双氢睾酮，在BPH发病机制中起非常重要的作用，但由于大量患者并未完全康复，除了雄激素代谢异常外，可能还存在其他异常情况。有强有力的间接证据表明雌激素在BPH发病机制中可能起作用，目前正在进行研究以检验撤除雌激素对前列腺大小和症状的影响。同样，受α肾上腺素能调节的前列腺梗阻动态方面也可能是该疾病的一个组成部分，可用α肾上腺素能阻滞剂进行治疗。
因此，BPH似乎可能是多因素的，需要联合治疗。雄激素对于这种疾病的发病机制肯定似乎是必要的，但可能并不充分。
