Vascular and cellular stress in inflammatory bowel disease: revisiting the role of homocysteine.
Fiche publication
Date publication
mai 2007
Auteurs
Membres identifiés du Cancéropôle Est :
Pr BRONOWICKI Jean-Pierre, Pr GUEANT Jean-Louis, Pr PEYRIN-BIROULET Laurent
Tous les auteurs :
Peyrin-Biroulet L, Rodriguez-Gueant RM, Chamaillard M, Desreumaux P, Xia B, Bronowicki JP, Bigard MA, Gueant JL
Lien Pubmed
Résumé
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 B(12) 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 B(12) 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.
Référence
Am J Gastroenterol. 2007 May;102(5):1108-15