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In the meantime, you can enjoy access to all the latest news, events and resources for different therapy areas on our website.Metabolic syndrome, inflammation and lower urinary tract symptoms: possible translational links
He Q, Wang Z, Liu G, Daneshgari F, MacLennan GT, Gupta S. Prostate Cancer Prostatic Dis 2016; 19(1): 7–13
Metabolic syndrome, inflammation and LUTS: possible translational links
Lower urinary tract symptoms (LUTS) are associated with benign prostatic hyperplasia (BPH) in men. However, a simple causal relationship has been debated and LUTS are currently defined as a global term including all urinary symptoms that impact significantly on patients’ quality of life, without being sex or organ specific.1
A considerable body of epidemiological data suggests a link between metabolic syndrome (MetS) and LUTS.1 MetS can be described as a systemic inflammatory state with tissue remodelling driven by chronic inflammation. Chronic inflammation has been hypothesised to be the linking mechanism between MetS and BPH/LUTS.1
In this systematic literature review, He et al investigated the role of inflammation induced by MetS in LUTS pathogenesis and progression.1 A search for relevant literature published between 2000 and January 2015, including animal studies, observational, prospective and retrospective studies and case-control trials, yielded a total of 52 articles.1
MetS-induced inflammation associated with BPH/bladder outlet obstruction
MetS was associated with biomarkers of inflammation, including C-reactive protein and pro-inflammatory cytokines interleukin (IL)-1, IL-6 and tumour necrosis factor-α.1
Animal studies showed that a high fat diet was associated with inflammation and oxidative stress in the prostate.1 Obesity induced the enlargement of adipose cells, resulting in pro-inflammatory chemokine release, macrophage infiltration and inflammation of adipose tissue.1
The pro-inflammatory chemokine IL-8 was shown to be involved in inflammation associated with BPH.1 IL-8 may stimulate prostate growth and seminal IL-8 was the most predictive and reliable cytokine/chemokine biomarker for prostatitis.1
Other CXC-type chemokines promoted fibrotic changes in prostate tissue (myofibroblast phenotype conversion), which are related to development and progression of lower urinary tract dysfunction.1 Most observational clinical studies support a link between inflammation and development of BPH/LUTS.1
MetS-induced inflammation was associated with overactive bladder and urinary incontinence
A major clinical symptom of LUTS is overactive bladder, with an increased frequency and urge to urinate.1 Strong evidence for a potential link between MetS and overactive bladder/urinary incontinence was lacking. However, the onset of overactive bladder was associated with obesity, and this association was particularly prominent in women.1
Meta-analysis revealed a statistically significant increase in LUTS risk of 2.5% with a 10 cm increase in waist circumference overall. The increase in LUTS risk was 2.8% in females and 1.8% in males.1
Inflammation, infection and their association with LUTS
Urinary tract infections and bacterial prostatitis may induce inflammation and damage to the lower urinary tract.1 Combined analysis of data from five studies (10,617 men in total) showed a considerably increased risk of developing BPH, LUTS and prostate cancer in men with a history of prostatitis.1
Another study in 208 patients with bacteriuria showed significantly higher rates of LUTS (dysuria, frequency and urgency of urination) for the 54% of patients with urinary tract infections.1
Conclusions
Evidence suggests that MetS and inflammation contribute to LUTS and the development of BPH in men. However, the role of these processes in other urinary tract disorders including overactive bladder and urinary incontinence remains to be determined.1 Improving our understanding of the inflammatory pathways in MetS may contribute to the development of new treatments for LUTS-associated disorders.1
Report on: Metabolic syndrome, inflammation and lower urinary tract symptoms: possible translational links. He Q, Wang Z, Liu G, Daneshgari F, MacLennan GT, Gupta S. Prostate Cancer Prostatic Dis 2016; 19(1): 7–13.
