Metabolic syndrome correlates with peri-urethral fibrosis secondary to chronic prostate inflammation: evidence of a link in a cohort of patients undergoing radical prostatectomy.

OBJECTIVES

To investigate the pathological relationship between metabolic syndrome and peri-urethral fibrosis status secondary to chronic prostate inflammation.

METHODS

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.

RESULTS

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).

CONCLUSIONS

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.