Abstract
The treatment of patients with ulcerative colitis and Crohn's disease is a huge challenge to the clinician mainly because the etiology of IBD is still completely unknown. Pathogenetic mechanisms, in constrast, have partly been elucidated thanks to immunohistochemical investigation of the tissue in IBD and the study of experimental animal models of gut inflammation. There is extensive evidence that at least in Crohn's disease tolerance for commensal bacteria is lost which leads to uncontrolled inflammation mediated by a T-helper 1 response and to tissue destruction of the gut epithelium with inadequate repair. Genetic factors are probably responsible for increased susceptibility and may define disease phenotypes. These insights have led to a dramatic improvement of our therapeutic means with the development of the chimeric monoclonal antibody to TNF. The pathogenetic mechanisms are less clear in UC. The hypothesis is that UC is a T-helper 2 mediated disease. We have a very attractive way to study the early onset of Crohn's disease in the postoperative Crohn's situation. Newer therapeutic approaches should aim at preventing recurrence of Crohn's lesions in the normal postoperative bowel. Such model is also available for UC since there is increasing evidence that pouchitis is recurrent ulcerative colitis in the small bowel. Cooperation between clinicians and basic scientists is the best way to achieve fast progress in understanding IBD.