Benign prostatic hyperplasia - what do we know?

Objectives To present historical and contemporary hypotheses on the pathogenesis of benign prostatic hyperplasia (BPH), and the potential implications for current medical therapies. Methods The literature on BPH was reviewed. BPH is a prevalent disease with significant health and economic impacts on patients and health organisations across the world, whilst the cause/initiation of the disease process has still not been fully determined. Results In BPH, pathways involving androgens, oestrogens, insulin, inflammation, proliferative reawakening, stem cells and telomerase have been hypothesised in the pathogenesis of the disease. A number of pathways first described >40 years ago have been first rebuked and then have come back into favour. A system of an inflammatory process within the prostate, which leads to growth factor production, stem cell activation, and cellular proliferation encompassing a number of pathways, is currently in vogue. This review also highlights the physiology of the prostate cell subpopulations and how this may account for the delay/failure in treatment response for certain medical therapies. Conclusion BPH is an important disease, and as the pathogenesis is not fully understood it impacts the effectiveness of medical therapies. This impacts patients, with further research potentially highlighting novel therapeutic avenues.

Automated summary

The pathogenesis of benign prostatic hyperplasia (BPH) involves pathways related to androgens, estrogens, insulin, inflammation, proliferative reawakening, stem cells, and telomerase. Some pathways described over 40 years ago have been reevaluated and are now considered important in the development of BPH. Current research focuses on inflammatory processes within the prostate leading to growth factor production, stem cell activation, and cellular proliferation as key mechanisms in BPH.