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Researchers find evidence of chronic inflammation in the bladder.

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  • Researchers find evidence of chronic inflammation in the bladder.

    Editor's Commentary - Elevation of serum C-reactive protein in patients with OAB and IC/BPS implies chronic inflammation in the urinary bladder

    Thu, 21 April 2011 | Philip M. Hanno, MD

    BERKELEY, CA (UroToday.com) -
    Evidence For Chronic Inflammation in IC/BPS and Overactive Bladder
    UroToday.com - Chronic inflammation, whether triggered by urinary tract infections or otherwise, has been considered a possible underlying mechanism for overactive bladder (OAB) and interstitial cystitis/bladder pain syndrome. Shiu-Dong Chung and colleagues from Hualien and Tapei sought to determine whether an association exists between serum C reactive protein (CRP), urinary nerve growth factor (NGF), and these two conditions.

    Serum CRP and urinary NGF levels were examined in 22 patients with OAB refractory to antimuscarinic therapy, 48 patients with IC/BPS who had glomerulations or Hunner’s lesions on endoscopy, and 12 patients with overactive bladder in association with chronic medical illness. Serum CRP levels were significantly higher in subjects with overactive bladder or IC/BPS than in a group of 33 controls. There was no difference in CRP between overactive bladder and IC/BPS. Patients with OAB-wet had higher levels than OAB-dry, but this did not reach statistical significance. Urinary NGF/creatinine levels were elevated in OAB and IC/BPS compared to controls with no significant difference between the conditions.

    Although the mean serum CRP level was elevated in patients with OAB and IC/BPS, the levels were not as high as that in acute systemic infection or inflammation. Only 13.6% of OAB and 8.7% of IC/BPS patients had a clinically significant elevated serum CRP level, suggesting the inflammatory process in these chronic bladder disorders is local and mild.

    The population studied was not controlled for age or gender, and no mention is made of other possibly underlying conditions that may have confounded the authors’ results. In addition, it is difficult to interpret the possible effect of the exclusion criteria used, in that all OAB patients were refractory to anticholinergic therapies. Nevertheless, the data is interesting and further studies should shed additional light on the role of inflammation in these disorders.

    Chung SD, Liu HT, Lin H, Kuo HC
    Neurourol Urodyn. 2011 Mar;30(3):417-20
    10.1002/nau.20938
    PubMed Abstract

    REPRINTED WITH PERMISSION
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