The underlying mechanism of metabolic syndrome on benign prostatic hyperplasia and prostate volume

• Published in: The Prostate Vol. 80; no. 6; pp. 481 - 490
• Main Authors: Xia, Bo‐Wen, Zhao, Si‐Cong, Chen, Zong‐Ping, Chen, Chao, Liu, Tian‐Shu, Yang, Fan, Yan, Yong
• Format: Journal Article
• Language: English
• Published: United States Wiley Subscription Services, Inc 01.05.2020
• Subjects: Adiponectin; Benign; benign prostatic hyperplasia; Globulins; Hyperplasia; Inflammation; Insulin; Leptin; lower urinary tract symptoms; Metabolic syndrome; Prostate; prostate volume; Sex hormones; Testosterone; Tumor necrosis factor; Tumor necrosis factor-TNF; tumor necrosis factor‐α; Urinary tract; metabolic syndrome; prostate volume; lower urinary tract symptoms; tumor necrosis factor-α; benign prostatic hyperplasia
• ISSN: 0270-4137; 1097-0045
• DOI: 10.1002/pros.23962

Objective To investigate the potential mechanism of the effect of metabolic syndrome (MetS) on prostate volume (PV) and the risk of benign prostatic hyperplasia (BPH)/lower urinary tract symptoms (LUTS) and the relationships of MetS and the major pathogenic factors of MetS with the clinical progression of BPH/LUTS in older Chinese men. Subjects and Methods We analyzed clinical data obtained from 506 ostensibly healthy men who underwent routine health check‐ups and recruited 415 subjects from a group of previously studied men after 4 years. We evaluated the associations of major pathological factors of MetS, including insulin resistance, subclinical inflammatory state, and sex hormone changes, with PV, the risk of BPH and the clinical progression of BPH/LUTS by using multiple linear regression and logistic regression. Results After adjustment for age, insulin, HOMA (homeostatic model assessment) index, leptin, resistin, adiponectin, C‐reactive protein, tumor necrosis factor‐α (TNF‐α), sex hormone‐binding globulin, and testosterone levels were significantly associated with PV (all P < .05), and in the age‐adjusted logistic regression model, positive associations of resistin and TNF‐α with BPH/LUTS were found (OR, 1.662, P = .007 and OR, 1.044, P < .001, respectively). Predictors of BPH/LUTS clinical progression were significantly correlated with MetS and TNF‐α. The group with higher TNF‐α levels had a higher rate of newly diagnosed BPH (9.5% vs 19.1%, P = .006) and a greater increase in PV levels (0.61 ± 0.08 vs 1.09 ± 0.35 cm3, P <.001) after 4 years. Conclusions MetS and its pathological factors were associated with an increased PV and an increased risk of BPH/LUTS that is more prone to clinical progression. TNF‐α may serve as an early biological indicator to identify which patients with BPH/LUTS are at higher risk of unfavorable outcomes.