Background and Aim: The diagnostic and prognostic values of fecal calprotectin (FC) levels in patients with inflammatory bowel diseases have been proven. However, little is known about the usefulness of FC measurement in predicting intestinal involvement of Behçet's disease (BD). Methods: Forty-four consecutive patients with systemic BD who underwent colonoscopy for the evaluation of gastrointestinal symptoms were prospectively enrolled between November 2012 and March 2014 in a single tertiary medical center. Fecal specimens from the patients were obtained the day before bowel cleansing and 3 months after colonoscopy. Results: Twenty-five patients showed intestinal ulcerations on colonoscopy (12 [48.0%] typical and 13 [52.0%] atypical ulcerations). The median FC level in the intestinal BD group was significantly higher than that in the non-diagnostic group (112.53 [6.86–1604.39] vs 31.64 [5.46–347.60] µg/g, respectively, P = 0.003). Moreover, the typical ulceration group showed a significantly higher median FC level than the atypical ulceration group in patients with intestinal BD (435.995 [75.65–1604.39] vs 71.42 [6.86–476.94] µg/g, respectively, P = 0.033). Multivariate analysis revealed higher FC as an independent predictor of intestinal BD (OR = 38.776; 95% CI = 2.306–652.021; P = 0.011). The cut-off level of FC for predicting intestinal BD was 68.89 µg/g (76% sensitivity and 79% specificity). The absolute changes between fecal calprotectin levels and the disease activity index of intestinal BD from initial diagnosis of intestinal BD to 3 months after diagnosis were significantly correlated (Pearson's correlation coefficient = 0.470, P = 0.027). Conclusion: The FC level might serve as a non-invasive surrogate marker of intestinal involvement of BD.
|Number of pages||7|
|Journal||Journal of Gastroenterology and Hepatology (Australia)|
|Publication status||Published - 2017 Mar 1|
Bibliographical noteFunding Information:
This research was financially supported by the Korean Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health and Welfare, Republic of Korea (Grant Number A120176, HI13C1345) and by the Basic Science Research Program through the National Research Foundation of Korea funded by the Ministry of Science, ICT & Future Planning (NRF-2013R1A2A2A01067123). This work was also supported by the Brain Korea 21 Project for Medical Science, Yonsei University.
© 2016 Journal of Gastroenterology and Hepatology Foundation and John Wiley & Sons Australia, Ltd
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