Clinical Review
The American Journal of Gastroenterology (2007) 102, 1108–1115; doi:10.1111/j.1572-0241.2007.01170.x
Vascular and Cellular Stress in Inflammatory Bowel Disease: Revisiting the Role of Homocysteine
Laurent Peyrin-Biroulet MD, PhD1,2, Rosa-Maria Rodriguez-Guéant MD, PhD1, Mathias Chamaillard PhD3, Pierre Desreumaux MD, PhD3, Bing Xia MD4, Jean-Pierre Bronowicki MD, PhD1,2, Marc-André Bigard MD1,2 and Jean-Louis Guéant MD, DSc1,2
- 1Inserm, U724, Laboratory of Cellular and Molecular Pathology in Nutrition, Faculty of Medicine, Nancy-Universitè Vandoeuvre-les-Nancy, F-54511, France
- 2Department of Hepato-Gastroenterology, University Hospital of Nancy, Vandoeuvre-les-Nancy, F-54511, France
- 3Inserm, U795, Physiopathology of Inflammatory Bowel Disease, Lille, F-59037, France; Univ Lille 2, F-59037, France
- 4Department of Internal Medicine and Geriatrics, Zhongnan Hospital and Research Center of Digestive Diseases, Wuhan University Medical School, Wuhan, RP China
Correspondence: Prof Jean-Louis Guéant, MD, DSc, Inserm, U724, University Henri Poincaré and CHU of Nancy, Allée du Morvan, 54511 Vandoeuvre-les-Nancy Cedex, France.
Received 21 September 2006; Accepted 9 January 2007.
Abstract
Moderate hyperhomocysteinemia is a complex trait commonly associated with inflammatory bowel disease (IBD). Nutritional deficiencies and genetic determinants have been identified as risk factors for moderate hyperhomocysteinemia, such as folate and vitamin B12 deprivation and polymorphisms in the 5,10 methylenetetrahydrofolate reductase (MTHFR) encoding gene, respectively. Homocysteine has a crucial role in cellular stress, epigenetic events, inflammatory processes, and host-microbial interactions. Hyperhomocysteinemia might therefore influence the clinical history of IBD, including disease severity, susceptibility to particular enteric infections, and the risk for the development of colorectal cancer. In contrast, homocysteine metabolism does not seem to contribute to the greater risk of thrombosis in IBD subjects. Herein, we review the evidence linking homocysteine metabolism to the pathophysiology of IBD. Furthermore, we discuss the relevance of screening and treating folate and vitamin B12 deficiencies in IBD subjects. Given the peculiar frequency of such deficiencies in IBD, normalizing vitamin levels should be an integral part of the management of these patients, especially those with active disease, history of intestinal resection, and/or treated with methotrexate.
