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Canadian Journal of Gastroenterology
Volume 8 (1994), Issue 6, Pages 383-387
IBD – Therapeutics

Immunosppressive Agents in Inflammatory Bowel Disease: Current Status and Future Prospects

Fergus Shanahan, Gerald C O'’Sullivan, and J Kevin Collins

Department of Medicine, Clinical and Molecular Research Group, University College Cork, Cork, Ireland

Copyright © 1994 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Inflammatory bowel disease involves an interaction between genetic susceptibility factors and environmental triggers, and the intestinal injury is mediated by the host immunoinflammatory response. Identification of the mechanisms and mediators that contribute to the tissue injury has provided a sound rationale for the therapeutic use of immunosuppressive and immunomodulatory agents. The efficacy of traditional immunosuppressive drugs, such as the purine analogues in both Crohn’s disease and ulcerative colitis, is well established. The major limitation of the use of these drugs is the delayed clinical response associated with their use. This has prompted an evaluation of other immunosuppressivcs, such as cyclosporine and related drugs, that have a more rapid onset of action. Convincing data indicate a distinct role for cyclosporine in certain patients with acute severe ulcerative colitis. However, despite early promising results with cyclosporine in Crohn’s disease, recent results have been less encouraging. There is also uncertainty about the exact clinical role of cyclosporine because of concerns regarding long term toxicity. At present, many investigators regard cyclosporine as an interim measure for acutely ill patients. The challenge that remains is the development of novel immunomodulatory strategies that are specific for the mucosal immune system and that are based on recent advances in our understanding of the pathogenesis of mucosal inflammation.