Overview of benign prostatic hypertrophy

Abstract

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.