Genetic polymorphism and pathogenesis of benign prostatic hyperplasia.

摘要

BPH is the most frequent urological problem of ageing men, manifested as severe obstruction in urinary flow with discomfort and pain. The principal hypothesis for the hypertrophic reaction of prostate tissue is steroid-mediated cellular proliferation and inflammatory response to local infection (Fig. 1). In addition, inefficiency of the apoptotic machinery and aberrant stromal-epithelial interactions probably contribute to the abnormal growth of the prostate . BPH is traditionally-managed with minimal prostate surgery, primarily with TURP, but now there are additional options for patient with moderate to severe symptomatic BPH, which include administration of a-adrenoceptor blockers (e.g. alfuzosin, tamsulosin) and 5a-reductase inhibitors (e.g. finasteride, dutasteride).BPH is still an enigmatic problem for biologists, as the understanding of its pathogenesis is very vague and there is no well-established biochemical or genetic marker for early detection. PSA is the most useful marker for monitoring prostate cancer and is a strong predictor of prostate volume in BPH . However, the level of this kallikrein-related serine protease increases at advanced stages of disease and thus is more helpful for monitoring at later stages for clinical management .