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Anti- Saccharomyces cerevisiae antibody Crohn’s disease Death domain receptor 3 Extracellular matrix Epithelial-to-mesenchymal transition Inflammatory bowel disease Interferon Interleukin Matrix metalloproteinase Nucleotide-binding oligomerization domain-containing protein 2/caspase recruitment domain-containing protein 15 Soluble latent membrane-type 1 Transforming growth factor Tissue inhibitors of metalloproteinases TNF-like ligand 1A Trinitrobenzenesulfonic acid Tumor necrosis factor Ulcerative colitis Vacuole membrane protein-1 ASCA
CD
DR3
ECM
EMT
IBD
IFN
IL
MMP
NOD2/CARD15
SMIT1
TGF
TIMPs
TL1A
TNBS
TNF
UC
VMP1
Stricture formation is a significant complication of inflammatory bowel disease (IBD) often requiring endoscopic or surgical intervention. Up to 30% of Crohn's disease (CD) patients and 5% of ulcerative colitis (UC) patients develop stricturing disease. Strictures are thought to be formed through a combination of inflammatory and fibrotic processes. Although strictures can arise anywhere in the gastrointestinal tract, the most commonly affected locations are the terminal ileum and ileocecal valve because of the fact that the majority of strictures are found in CD patients. Although less common, colonic strictures in UC are typically asymptomatic, benign, and related to degree of inflammation and fibrosis; however, given their location, malignancy must be evaluated for, and factors related to increased likelihood of malignancy include longstanding disease (over 20 years), location proximal to the splenic flexure, and symptomatic bowel obstruction. Because the wealth of information on stricture formation in IBD derives from CD models and studies, the remainder of this chapter will mainly focus on strictures in the context of CD pathophysiology.
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