BERKELEY, CA (UroToday.com) - To date, many studies have reported a significant correlation between metabolic syndrome (MetS) and lower urinary tract symptoms (LUTS)/benign prostate hyperplasia (BPH).[1, 2] Several pathophysiological mechanisms have been suggested in this setting, i.e., insulin resistance, hormone changes, pelvic atherosclerosis, and, last but not least, chronic prostate inflammation.[3]
In our study,[4]we showed the significant role of metabolic syndrome ( MetS), interpreted as a low-grade chronic inflammation state, in promoting prostate inflammation, and consequently the formation of peri-urethral fibrosis secondary to inflammation, which could have a negative impact on urinary status. For instance, it can be speculated that peri-urethral fibrosis secondary to MetS-related prostate chronic inflammation may cause LUTS through a decreased urethral flexibility; this would eventually compromise the ability of the prostatic urethra to enlarge itself and to adequately accommodate urinary flow during micturition. This hypothesis has been supported by our urodynamic findings that showed a more common obstructive condition in patients with inflammatory status than in men without inflammation. In addition, at multivariate analysis, prostate inflammation and MetS were the only independent risk factors for inflammation-related peri-urethral fibrosis and subsequent LUTS. Unfortunately we did not evaluate the correlation between each component of MetS, prostate inflammation, and inflammation-dependent peri-urethral fibrotic changes, but we hypothesize that visceral obesity, with an increased production of pro-inflammatory adipokines, might play an important role in the development and progression of prostate inflammation and fibrotic changes.
I would like to emphasize that our study is not without limitations, such as the absence of a special microtome to obtain complete prostate macro-sections (on radical prostatectomy specimens), where prostate areas could be comprehensively studied (not only the peri-urethral area) or a digital histological scanner with a dedicated imaging program to overcome the intra-observatory (pathologist) variability. However, the experimental findings of the present study suggest that BPH-related LUTS observed in patients with MetS could be improved by anti-inflammatory therapy and /or treatment targeting MetS itself.
References:
- Gacci M, Vignozzi L, Sebastianelli A et al. Metabolic syndrome and lower urinary tract symptoms: the role of inflammation. Prostate Cancer Prostatic Dis 2013; 16: 100-5.
- Moul S, McVary KT. Lower urinary tract symptoms, obesity and the metabolic syndrome. Curr Opin Urol 2010; 20:7-12.
- De Nunzio C, Aronson W, Freedland SJ et al. The correlation between metabolic syndrome and prostatic diseases. Eur Urol 2012; 61:560-70.
- Cantiello F, Cicione A, Salonia A et al. Metabolic syndrome correlates with peri-urethral fibrosis secondary to chronic prostate inflammation: evidence of a link in a cohort of patients undergoing radical prostatectomy. Int J Urol 2013, doi: 10.1111/iju.12233.
Written by:
Francesco Cantiello, MD, PhD as part of Beyond the Abstract on UroToday.com. This initiative offers a method of publishing for the professional urology community. Authors are given an opportunity to expand on the circumstances, limitations etc... of their research by referencing the published abstract.
Researcher in Urology, Urology Unit, Magna Graecia University of Catanzaro, Italy
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