Abdominal obesity and intra-abdominal pressure: a new paradigm for the pathogenesis of the hypogonadal-obesity-BPH-LUTS connection.

Abstract

Abstract The pathogenesis of benign prostatic hyperplasia-lower urinary tract symptoms (BPH-LUTS) is complicated, multifactorial, and incompletely understood. A number of recent observations have provided for new insights and offer a better appreciation for, and the understanding of, the pathophysiological and hormonal contributions for the development and progression of prostatic enlargement. A major paradox has been the progressive increase in the prostate size at a time when the peripheral blood testosterone levels are decreasing as men age. This has been associated with the findings of increasing obesity-related states and the manifestation of BPH-LUTS. Several converging and new findings combine the mechanisms that result in an integration of the hypogonadal-obesity-increased intra-abdominal pressure (IAP)-BPH-LUTS connection. The net positive caloric balance results increased the IAP and damaged the one-way valves of the internal spermatic veins. This results in an increased venous back pressure that leads to the reflux of the high testicular testosterone concentrations and venous pressures that are transmitted to the communicating prostatic venous system. Simultaneously, increasing obesity results in an increased aromatase activity, which leads to a reduction of the testosterone levels. Consequently, there is also an increased estradiol production, which inhibits gonadotropin secretion and the production of testosterone. This hypogonadal obesity cycle eventually results in a progressive hypogonadal state, while the prostate continues to enlarge and produce increasing LUTS.