The aim of this study was to investigate markers of inflammation and oxidative stress in the corpus cavernosum (CC) and to compare levels of inflammatory markers recorded in CC to venous blood from the arm to examine the potential impact of inflammatory parameters on erectile function and endothelial dysfunction in vitro. Ninety-seven patients with no complaint of erectile dysfunction (ED) at inclusion were prospectively included and completed the Erectile Function domain of the IIEF questionnaire. Several parameters, including lipids, MPO-dependent oxidised LDL (Mox-LDL), IL-8, IL-18, were measured. After RNA extraction, the expression of eNOS was analysed. A paired t-test was used for comparisons between arm and CC blood results. A two-way ANOVA was used to estimate the effects of IL-18 and IL-8 on the IIEF score. Mean patient age was 59 ± 14.5 years. IL-18, Mox-LDL, and Mox-LDL/ApoB levels were significantly increased in CC compared to arm blood. The IIEF score was correlated with IL-18 levels in the venous blood (R = -0.31, p = .003) and in the CC (R = -0.37, p = .004) and with IL-8 (R = -0.31, p = .009 and R = -0.28, respectively, p = .02). There was a significant effect with the IL-18 on IIEF potentiated by high serum IL-8 concentrations. IL-18 and Mox-LDL significantly decreased eNOS mRNA expression in human aortic endothelial cell line (HAEC). These preliminary results address the importance of inflammation in the CC and highlight a difference in marker concentrations between venous and CC blood. However, they do not show any difference in terms of clinical erectile score predictivity. Involvement of inflammatory cytokines isolated in CC in the genesis of ED requires further studies.

Epidemiological studies document a positive and independent association between metabolic syndrome (MetS) and lower urinary tract symptoms (LUTS). In the male, the pathogenesis of MetS-related LUTS involves a complex interplay among pathophysiological mechanisms mainly affecting the prostate and the bladder. Recently, hypogonadism has been recognized as a key factor bridging MetS and LUTS. Preclinical data have evidenced that MetS-induced hypogonadism is associated with alterations not only of the prostate but also of the bladder, and testosterone supplementation can counteract both. Interestingly, testosterone also shows a marked effect on the bladder, preventing the MetS-related RhoA/ROCK hyperactivation, which drives the pathogenesis of bladder overactivity and LUTS. The precise mechanisms through which testosterone exerts its protective action on the LUT remains to be fully elucidated; however, indirect (through improved cardiometabolic status) and direct (through local androgen receptor-mediated pathways) actions are both likely to play a role.

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