The pathophysiology of benign prostatic hyperplasia.

Abstract

The development of human benign prostatic hyperplasia and its related signs and symptoms clearly requires a combination of testicular androgens and aging. Although the role of androgens as a causative factor for human benign prostatic hyperplasia is debated, they undoubtedly play at least a permissive role. The principle prostatic androgen is dihydrotestosterone. Two isoenzymes of 5-alpha reductase have been discovered. Type 2 is dominant in the genital issue. Testosterone is reduced by the 5-a reductase to dihydrotestosterone. Benign prostatic hyperplasia is predominantly due to stromal hyperplasia of the gland and affects more than 70% of men of 70 years or older with or without obstruction. Recent studies identified transforming growth factor-b, fibroblast growth factor and insulin-like growth factor family members as key regulators of cell proliferation and extracellular matrix turnover with interrelated activities. Furthermore, estrogens, andenergic signaling and inflammatory processes have been shown to have an impact. Without a solid understanding of the physiology and pathophysiology of benign prostatic hyperplasia it can be difficult to interpret the results of clinical trials and symptoms.