Association between Prostatic Inflammation and Detrusor Overactivity in men with Benign Prostatic Hyperplasia and Bladder Outlet Obstruction: A prospective urodynamic and histological study

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Abstract

Background Benign prostatic hyperplasia (BPH) frequently leads to bladder outlet obstruction (BOO) and lower urinary tract symptoms (LUTS) in aging men. Detrusor overactivity (DO) is a common functional consequence of BOO, often persisting even after surgical intervention. Prostatic inflammation (PI) has been implicated in BPH pathogenesis, but its relationship with DO remains unclear. This study aimed to evaluate the association between histologically confirmed PI and DO in men undergoing transurethral resection of the prostate (TURP) for BPH-related BOO. Methods We conducted a prospective, observational study involving 125 men aged ≥ 50 years with BPH, BOO confirmed by pressure-flow studies, and moderate-to-severe LUTS (IPSS ≥ 7). All patients had received standard medical therapy and were candidates for TURP. Urodynamic testing was performed before and three months after surgery. Based on baseline urodynamic findings, patients were categorized into two groups: those with DO (Group A) and those without (Group B). Resected prostate tissue was examined histologically, and PI was graded using the Irani score. Statistical analysis was performed using SPSS v26, with odds ratios (OR) and 95% confidence intervals (CI) reported. Results Prostatic inflammation was identified in 78.4% of patients overall and was significantly more prevalent in those with DO (84.9% vs. 69.2%; OR = 2.47, 95% CI: 1.11–5.49, p = 0.02). Inflammation was also more severe in Group A. DO resolved postoperatively in 75.3% of patients, while persistent DO was associated exclusively with moderate-to-severe PI. The odds of persistent DO following TURP were significantly higher in this subgroup (OR = 4.00, 95% CI: 1.33–12.05). Conclusions Prostatic inflammation is more frequent and severe in men with DO and is associated with its persistence after TURP. These findings suggest that PI contributes to both the pathogenesis and postoperative course of DO, supporting its role as a therapeutic target in BPH-related LUTS management.

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