Histological prostatitis and its influence on benign prostatic hyperplasia: a systematic review and meta-analysis

Inflammation is considered one of the potential etiological factors in the development and progression of benign prostatic hyperplasia (BPH). However, whether inflammation plays a critical role in the onset or progression of BPH remains controversial. Therefore, we conducted this systematic review and meta-analysis to comprehensively evaluate the impact of histological prostatitis on BPH.

We systematically searched cohort and cross-sectional studies published up to April 2025 in PubMed, the Cochrane Library, Embase, and Web of Science. The quality of the included cohort studies was assessed using the Newcastle-Ottawa Scale (NOS), and cross-sectional studies was evaluated with the Joanna Briggs Institute (JBI) checklist. Data were extracted on prostate volume (PV), International Prostate Symptom Score (IPSS), prostate-specific antigen (PSA), maximum urinary flow rate (Qmax), and residual urine volume (RUV). The effect sizes were pooled using the weighted mean difference (WMD) with corresponding 95% confidence intervals (CIs).

A total of 11 studies were included, comprising 6 cohort studies and 5 cross-sectional studies, with a combined sample of 3,135 patients. In cross-sectional studies, compared with patients with BPH alone, those with BPH combined with histological prostatitis had an increase of 1.50 ng/mL in PSA level (95% CI: 0.09 to 2.91; I²=91%; P<0.05), an increase of 3.92 points in IPSS score (95% CI: 2.20 to 5.64; I²=28%; P<0.00001), and an increase of 13.78 mL in PV (95% CI: 10.00 to 17.56; I²=0%; P<0.00001). Qmax decreased by 1.56 mL/s (95% CI: -3.44 to 0.32; I²=80%; P=0.10), with no statistically significant difference. In cohort studies, compared with patients with BPH alone, those with BPH combined with histological prostatitis showed an increase of 1.19 ng/mL in PSA level (95% CI: 0.37 to 2.02; I²=28%; P<0.05), an increase of 10.24 mL in PV (95% CI: 0.79 to 19.69; I²=89%; P<0.05), and a decrease of 2.42 mL/s in Qmax (95% CI: -3.44 to -1.40; I²=65%; P<0.00001). Changes in IPSS (95% CI: -1.33 to 6.22; I²=97%; P=0.20) and RUV (95% CI: -1.66 to 18.07; I²=39%; P=0.10) were not statistically significant.

Histological prostatitis may play a promoting role in the progression of BPH. Compared to patients with BPH alone, those with coexisting histological prostatitis exhibited higher PSA levels, higher IPSS, larger PV, and lower Qmax. Therefore, the clinical significance of histological prostatitis should not be overlooked, and it ought to be considered as an important factor in the clinical management of urological patients. Future large-scale prospective studies are warranted to clarify its role in the pathogenesis of BPH.