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Pathogenesis and medical treatment of benign prostatic hyperplasia

Tissue concentrations of dihydrotestosterone (DHT) and the enzymes that regulate its level, such as 5α‐reductase, appear to play a major role in the pathogenesis of benign prostatic hyperplasia (BPH). This argument is strongly supported by the objective decreases in prostate size and improvement in symptoms of prostatism that occur following androgen withdrawal. A variety of androgen‐withdrawal therapies for BPH have been reported since the early 1900s. Although success in the treatment of BPH has been claimed for all of them, including surgical castration, medical castration with progestational antiandrogens, gonado‐tropin‐releasing hormone (GNRH)‐agonist castration, or androgen‐receptor blockade with pure antiandrogens such as flutamide, very few studies, until recently, have provided convincing objective evidence for therapeutic efficacy in BPH. Recently, magnetic resonance imaging (MRI) scanning and ultrasound have become available to quantify objective changes in prostate volume and have indisputably demonstrated that androgen withdrawal does significantly decrease prostate size. The consequences of this on clinical symptoms of prostatism are currently under study.