Objective: The aim of the present study was to investigate the relationship among serum mean platelet volume (MPV) levels, benign prostatic hyperplasia (BPH)/lower urinary tract symptoms (LUTS) and metabolic syndrome (MetS), and study the potential role of serum MPV levels in BPH/LUTS progression in an indirect manner. Methods: Five hundred fifty-one men aged 45 or older with moderate to severe LUTS due to benign prostatic enlargement were recruited into this study by consecutive routine physical examination programs. Urologic evaluation included transrectal ultrasound, International Prostate Symptom Score and maximum urinary flow rate (Qmax). Overnight fasting venous blood specimens were collected and serum levels of prostate-specific antigen, fasting blood glucose, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, total cholesterol, triglyceride and C-reactive protein (CRP) were recorded. In addition, MPV were determined by automated hematology analyzer. We divided subjects into 2 groups according to the presence of MetS. We also took the MPV values as a categorical variable and divided subjects into 2 groups (≥11.8 or <11.8 fl) or 4 groups according to the different levels of MPV (9.3-11.0, 11.1-11.5, 11.6-11.9, 12.0-12.5 and ≥12.5 fl). The clinical characteristics and parameters of BPH/LUTS in different groups were measured and compared to identify their relationships. Results: MetS was diagnosed in 37.0% of the subjects. There were significant interactive correlation among the number of positive MetS components, CRP, MPV and parameters of BPH/LUTS. The ratio of PV ≥31 ml and Qmax <10.6 ml/s were positively correlated with the increased level of MPV. Additionally, the OR in relation to PV ≥31 ml and Qmax <10.6 ml/s significantly rose as the level of MPV increased after adjusting for age, suggesting of a threshold effect at 12.0-12.5 fl for PV ≥31 ml (OR 2.678, 95% CI 1.425-5.035) and at >12.5 fl for Qmax <10.6 ml/s (OR 3.190, 95% CI 1.768-5.755). However, only the value of MPV more than 12.5 fl still showed statistically significant effect on Qmax <10.6 ml/s after adjusting for age and the presence of MetS (OR 2.164, 95% CI 1.162-4.032). Conclusions: Our results add to the evidence that chronic inflammation is a candidate mechanism at the crossroad between MetS and BPH/LUTS, and the presence of elevated MPV may serve as a predictor of MetS-induced inflammation in the progression of BPH/LUTS.

Biologic rationales exist for the associations between metabolic syndrome (MetS) and benign prostatic hyperplasia (BPH). However, epidemiologic studies have yield inconsistent results. The aim of the present study was to prospectively evaluate the associations of MetS with the risk of BPH. The presence of MetS, the number of MetS components, and the individual MetS components were evaluated. After adjusting for potential confounders, MetS was associated with increased risk of BPH (HR: 1.29; 95% CI, 1.08–1.50; p < 0.001). Compared with subjects without any MetS components, the HRs were 0.88 (95% CI, 0.67–1.09; p = 0.86), 1.18 (95% CI, 0.89–1.47; p = 0.29) and 1.37 (95% CI, 1.08–1.66; p = 0.014) for subjects with 1, 2, or ≥3 MetS components, and there was a biologic gradient between the number of MetS components and the risk of BPH (p-trend < 0.001). Central obesity and low high-density lipoprotein cholesterol were the two main divers of the associations between these two conditions, with HRs of 1.93 (95% CI, 1.14–2.72; p = 0.001) for central obesity, and 1.56 (95% CI, 1.08–2.04; p = 0.012) for low HDL-C. Our findings support the notion that MetS may be an important target for BPH prevention and intervention.

The actual lowering effect of MetS on serum PSA levels was partly concealed by the enlarged prostate in men with MetS, and the presence of MetS was independently associated with lower serum PSA levels. Urologists need to be aware of the effect of MetS on serum PSA levels and should discuss this subject with their patients.