Urinary Inflammatory and Oxidative Stress Biomarkers as Indicators for the Clinical Management of Benign Prostatic Hyperplasia

Oxidative stress and hypoxia-induced inflammation contribute to benign prostatic hyperplasia (BPH) progression. This study investigated the roles of urinary inflammatory and oxidative stress biomarkers in BPH patients. This prospective study enrolled 62 clinical BPH patients (33 treated medically, 29 surgically) and 20 controls. Symptom scores, uroflowmetry, and urinary biomarker levels were assessed at baseline and three months post-treatment. Before treatment, BPH patients exhibited elevated urinary levels of total antioxidant capacity (TAC), PGE2, IL-1 beta, and IL-6. Post-treatment, successful outcomes were reported in 63.6% of the medical treatment group and 86.2% of the surgical treatment group, with improvements in symptom scores and urinary flow rate, along with reductions in urinary 8-isoprostane, TAC, and IL-1 beta. Prior to treatment, voiding efficiency (VE) was negatively correlated with urinary IL-1 beta, IL-6, and IL-8 levels, while bladder wall thickness was positively correlated with TAC. After treatment, changes in VE were negatively correlated with changes in IL-1 beta, and changes in post-void residual urine were positively correlated with changes in IL-1 beta, IL-6, IL-8, and TNF-alpha. Urinary inflammatory and oxidative stress biomarkers may serve as non-invasive indicators of disease severity and treatment response in clinical BPH. Their significant correlations with clinical improvements underscore their potential utility in monitoring treatment efficacy.