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The relationship between cystic fibrosis (CF) and the risk of developing inflammatory bowel disease (IBD) is not clear. CFTR mutations can influence dysbiosis and increased intestinal permeability, which are two key elements in the pathophysiology of IBD. These patients have increased intestinal inflammation, as demonstrated by increase pro-inflammatory gene expression in the bowel, specific fecal markers (fecal calprotectin), gross lesions (capsule endoscopy) and histological lesions on examination of surgical specimens.

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