Intestinal fibrosis is a common complication of several enteropathies, with inflammatory bowel disease (IBD) being the major cause. Intestinal fibrosis affects both ulcerative colitis and Crohn's disease, and no specific antifibrotic therapy exists. This review highlights recent developments in this area.
The pathophysiology of intestinal stricture formation includes inflammation-dependent and inflammation-independent mechanisms. A better understanding of the mechanisms of intestinal fibrogenesis and the availability of compounds for other nonintestinal fibrotic diseases bring clincial trials in stricturing Crohn's disease within reach.
Improved understanding of its mechanisms and ongoing development of clinical trial endpoints for intestinal fibrosis will allow the testing of novel antifibrotic compounds in IBD.
aGastroenterology Unit, Department of Life, Health and Environmental Sciences, University of L’Aquila, L’Aquila, Italy
bDepartment of Gastroenterology, Hepatology and Nutrition, Digestive Disease and Surgery Institute
cDepartment of Pathobiology, The Cleveland Clinic Foundation Lerner Research Institute, Cleveland, Ohio, USA
Correspondence to Florian Rieder, MD, Department of Pathobiology, The Cleveland Clinic Foundation Lerner Research Institute, NC221 9500 Euclid Avenue, Cleveland, OH 44195, USA. Tel: +1 216 445 4916; fax: +1 216 636 0104; e-mail: email@example.com