Urology Unit, Magna Graecia University of Catanzaro, Catanzaro, Italy; Doctorate Research Program, Magna Graecia University of Catanzaro, Catanzaro, Italy.
Int J Urol. 2014 Mar;21(3):264-9. doi: 10.1111/iju.12233. Epub 2013 Aug 4.
To investigate the pathological relationship between metabolic syndrome and peri-urethral fibrosis status secondary to chronic prostate inflammation.
Peri-urethral prostate tissue from 80 consecutive patients who underwent retropubic radical prostatectomy for prostate cancer was analyzed. Patients were divided in two groups according to whether or not they had a diagnosis of metabolic syndrome. A 16-peri-urethral core bench biopsy was carried out on each radical prostatectomy specimen to evaluate the extent of peri-urethral inflammatory infiltrate, and collagen and elastin amount. Spearman's correlation analysis was used to test the association between variables. Furthermore, the data were used to define a bivariate logistic regression model in which the presence (>50% collagen amount for each patients) or absence (≤50% collagen amount) of fibrosis was analyzed after adjusting for clinical and pathological variables.
A significant difference was found between the two groups in terms of International Prostatic Symptoms Score (P < 0.05) and urodynamics findings (all P < 0.05). Patients with metabolic syndrome showed a more extended inflammatory infiltrate and higher peri-urethral collagen amount, along with a lower peri-urethral elastin amount (all P < 0.05). A positive correlation was observed between inflammation, International Prostatic Symptoms Score, Bladder Outlet Obstruction Index and collagen amount, whereas inflammation was inversely correlated with elastin amount. On multivariate logistic regression analysis, prostate inflammation and metabolic syndrome were the only independent predictors of peri-urethral fibrosis (OR 1.73, 1.52, respectively).
The present findings suggest that metabolic syndrome might represent an independent risk factor for prostate inflammation and fibrotic changes secondary to inflammation within the peri-urethral prostatic tissue.
探讨代谢综合征与慢性前列腺炎继发的尿道周围纤维化之间的病理关系。
分析了 80 例连续接受耻骨后根治性前列腺切除术治疗前列腺癌的患者的尿道周围前列腺组织。根据是否存在代谢综合征，将患者分为两组。对每个根治性前列腺切除标本进行 16 个尿道周围核心活检，以评估尿道周围炎症浸润、胶原和弹性蛋白的程度。采用 Spearman 相关分析检验变量之间的相关性。此外，使用这些数据定义了一个双变量逻辑回归模型，其中在调整了临床和病理变量后，分析了纤维化的存在（每位患者的胶原量>50%）或不存在（胶原量≤50%）。
两组在国际前列腺症状评分（P<0.05）和尿动力学检查结果方面存在显著差异（均 P<0.05）。代谢综合征患者的炎症浸润程度更广泛，尿道周围胶原量更高，而尿道周围弹性蛋白量更低（均 P<0.05）。炎症、国际前列腺症状评分、膀胱出口梗阻指数与胶原量之间存在正相关，而炎症与弹性蛋白量之间存在负相关。多变量逻辑回归分析显示，前列腺炎症和代谢综合征是尿道周围纤维化的唯一独立预测因子（OR 分别为 1.73、1.52）。
本研究结果表明，代谢综合征可能是前列腺炎症和尿道周围前列腺组织炎症继发纤维化变化的独立危险因素。
