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New blood tests in inflammatory bowel disease
Idiopathic inflammatory bowel disease (IBD) collectively describes ulcerative colitis (UC) and Crohn’s disease (CD). UC is characterised by inflammation limited to the colonic mucosa and collagen deposition only in the submucosa,1 whereas CD is characterised by transmural, granulomatous inflammation and thickening of the bowel wall as a result of thickening of the muscularis layers and transmural fibrosis. CD can affect any part of the gastrointestinal tract but most commonly affects the distal small intestine and proximal colon. In diseased bowel in CD there is excessive deposition of collagen, especially collagen types V, III, and I, throughout the mucosa, submucosa, and serosa. The resultant bowel strictures may require surgical resection.1–2
It has been suggested that fragments of collagen arising during its synthesis and breakdown and released into blood may be markers of tissue fibrosis and response to non-surgical treatment in CD.3 Disease activity is usually assessed from a combination of symptoms, endoscopy, radiology, isotope scanning, and laboratory findings, including C reactive protein (CRP) and albumin. Increasing interest is being shown in the extracellular matrix (ECM) and the gut epithelial basement membrane, which is a specialised form of ECM, in IBD, but there are so far only sparse data relating the serum concentrations of basement membrane components or other ECM serum markers to IBD. This is partially addressed in last month’s issue by Koutroubakis et al.4
THE EXTRACELLULAR MATRIX IN IBD
In IBD, intestinal inflammation leads to mucosal ulceration and subsequent tissue repair with smooth muscle cell (SMC) proliferation and remodelling of the ECM. A major component of ECM is collagen, which, when present in excess, leads to tissue fibrosis. ECM undergoes constant turnover, with a balance between synthesis and breakdown of its components. The matrix metalloproteinase (MMP) enzymes, of which there are at …