J Clin Pharmacol
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First published on June 13, 2007, doi:10.1177/0091270007301623

The Journal of Clinical Pharmacology 2007;47:930.

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©© 2007 American College of Clinical Pharmacology, Inc.
The Journal of Clinical Pharmacology , 10.1177/0091270007301623


Article

The Role of TNF{alpha} in Ulcerative Colitis

Bruce E. Sands 1* and Gilaad G. Kaplan 1

1 Massachusetts General Hospital Crohn's and Colitis Center and Harvard University

* To whom correspondence should be addressed. E-mail: bsands{at}partners.org.


   Abstract
Standard of care for ulcerative colitis involves long-term pharmacotherapy or colectomy. Approximately 20% to 30% of patients eventually require a colectomy because patients either do not respond or cannot tolerate the currently available pharmacotherapies. Advances in our knowledge of the pathophysiology of ulcerative colitis have highlighted the importance of cytokines such as tumor necrosis factor alpha (TNF{alpha}) in the inflammatory process. TNF{alpha} is a proinflammatory mediator that plays an integral role in the pathogenesis of inflammatory bowel disease. In addition, mounting evidence indicates a genetic association between TNF{alpha} and ulcerative colitis. Furthermore, increased TNF{alpha} levels have been demonstrated in studies of patients with ulcerative colitis. TNF{alpha} is likely an important component in the pathophysiology of ulcerative colitis, and thus agents targeting TNF{alpha} in ulcerative colitis have been studied. Recent randomized controlled trials have confirmed that biologic anti-TNF{alpha} therapy is effective in ulcerative colitis. Soluble TNF{alpha} receptors or biologic agents that suppress or inhibit TNF{alpha} production may also show therapeutic promise.
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