Geller J
Department of Medicine, Mercy Hospital San Diego, California.
Urology. 1989 Oct;34(4 Suppl):57-63; discussion 87-96. doi: 10.1016/0090-4295(89)90235-5.
Pathogenesis and therapy of benign prostatic hypertrophy (BPH) are reviewed. Elevated prostate dihydrotestosterone concentrations, increased 5 alpha-reductase activity in the hypertrophic prostate, and prostate atrophy following castration all suggest a significant role for dihydrotestosterone in the pathogenesis of BPH. An increasing plasma estrogen/testosterone ratio with age, and the presence of estrogen receptors in the prostatic stroma, indicate that estrogen also may be involved in the development of BPH. Symptomatic improvement of BPH with androgen withdrawal therapy (including castration, antiandrogens, GnRH agonists, and 5 alpha-reductase inhibitors), as well as effective estrogen withdrawal with tamoxifen, strongly supports the endocrine pathogenesis of BPH.
本文综述了良性前列腺增生（BPH）的发病机制和治疗方法。前列腺二氢睾酮浓度升高、增生前列腺中5α-还原酶活性增加以及去势后前列腺萎缩均提示二氢睾酮在BPH发病机制中起重要作用。随着年龄增长血浆雌激素/睾酮比值升高以及前列腺基质中存在雌激素受体，表明雌激素也可能参与BPH的发生发展。雄激素撤退疗法（包括去势、抗雄激素药物、GnRH激动剂和5α-还原酶抑制剂）可使BPH症状改善，以及他莫昔芬有效撤退雌激素，有力地支持了BPH的内分泌发病机制。
