Introduction Calprotectin is a protein released by neutrophils in response to the presence of inflammation in the bowel.1 Faecal calprotectin (FC) has been shown to be useful in the diagnosis of inflammatory bowel disease (IBD) as it correlates with mucosal disease activity and can help to predict response to treatment or relapse.1–3 Data from small, selected case series have observed FC correlates better with colonic rather than ileal Crohn’s disease (CD)4 and median FC concentrations are higher in extensive or left-sided ulcerative colitis (UC) disease than in proctitis.5 We report the association of FC concentration with extent and distribution of inflammation in consecutively performed tests at our centre.
Methods All FC tests performed between 01/07/12 and 31/12/12 were systematically collected and associations with activity and distribution using endoscopic, histological and radiological data explored. Proximal disease was defined as inflammation affecting the terminal ileum and ascending colon; left-sided disease as inflammation limited to the colorectum distal to the splenic flexure and pan-colitis with inflammation extending proximal to the splenic flexure.
Results 203 (n = 160 CD; n = 43 UC) patients with IBD had FC tests performed of whom 96 (47.3%) had endoscopic, histological or radiological evidence of active disease. The mean age of IBD patients was 44.7 (SD 17.0) years and 58% were female. The mean FC concentration was significantly higher in patients with active pan-colitis (1038.1 iu (SD 1104.1)) than in active left-sided disease (mean 820.2 iu (SD 1535.1)); p = 0.01. The mean FC concentration was significantly higher in active pan-colitis than in active proximal disease (mean difference -669.3 iu (95% CI-1046.3, -292.4)); p = <0.001. There was no significant difference in the mean FC concentration between active proximal or left-sided disease (mean difference –451.5 (95% CI -965.9, 62.9) or between CD and UC (mean difference 148.5 (95% CI-369.1–666.1).
Conclusion Mean FC concentrations are significantly higher in active pan-colitis than in active left-sided or proximal disease, perhaps reflective of the greater extent of inflammation. Further work is required to explore why FC concentrations are lower in proximal disease despite presence of active inflammation.
World J Gastroenterol 2012;18(46):6782–6789
Inflammatory Bowel Diseases 2013;19(2):332–341
Am J Gastroenterol 2010:105:162–169
Scandinavian Journal of Gastroenterology 2011:46:1081–1091
Disclosure of Interest None Declared.
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