, Volume 66, Issue 16, pp 2059–2065 | Cite as

Anti-Tumour Necrosis Factor Therapy for Ulcerative Colitis

Evidence to Date
  • Chandrashekhar Thukral
  • Adam Cheifetz
  • Mark A. Peppercorn
Leading Article


Infliximab, the chimeric monoclonal antibody directed against tumour necrosis factor (TNF)-α, has profoundly changed therapy for Crohn’s disease (CD). However, for ulcerative colitis (UC), before the publication of ACT 1 and ACT 2 (Active Ulcerative Colitis Trials 1 and 2), there were only a few open-label and controlled trials that evaluated the role of infliximab in the treatment of UC. Results from these earlier studies were equivocal and ambiguous. However, the ACT 1 and ACT 2 trials were large, randomised and placebo-controlled, and have shown that infliximab is significantly more efficacious than placebo in treating both corticosteroid-responsive and -refractory moderate to severe UC. Data from these two studies showed that in patients with moderate to severe UC, treatment with infliximab (5 and 10 mg/kg), compared with placebo, led to significantly higher rates of clinical response, clinical remission and mucosal healing. However, a significant proportion of patients who were receiving oral corticosteroids at the start of the trials, remained on corticosteroids despite infliximab therapy. Additionally, the safety profile of the drug was found to be similar to what has been reported in clinical studies of infliximab in patients with CD.

On the basis of currently available data, we use infliximab as a remission-inducing agent in patients who have moderate to severe UC and are either refractory to or intolerant of mesalazine (5-ASA) products and immunomodulators. Moreover, infliximab seems to be a reasonable therapeutic modality for remission maintenance in those patients with UC in whom mesalazine products and immunomodulators have failed. Although data are limited, infliximab may be considered as a remission-inducing agent in patients with moderate to severe UC which is refractory to oral corticosteroids. However, the role of infliximab in the treatment of UC patients who are dependent on oral corticosteroids is still unclear and, therefore, should be considered only in patients who cannot be successfully transitioned to or are intolerant of oral immunomodulators. Furthermore, infliximab may be an alternative to ciclosporin (cyclosporin) in hospitalised patients with severe to moderately severe but not fulminant UC who do not respond to intravenous corticosteroids. At present, there is insufficient evidence to advocate using infliximab as a first-line agent for UC patients with mild or moderate to severe disease. Future randomised, controlled trials with clearly defined patient populations should further help to clarify the definitive role of infliximab in the therapeutic scheme for UC.



Dr Peppercorn is on the speakers’ bureau for Procter & Gamble, TAP and Solvay. Dr Cheifetz is on the speakers’ bureau for Centocor, Procter & Gamble and Salix. Dr Thukral has no conflicts of interest directly relevant to the contents of this review. No sources of funding were used to assist in the preparation of this review.


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Copyright information

© Adis Data Information BV 2006

Authors and Affiliations

  • Chandrashekhar Thukral
    • 1
  • Adam Cheifetz
    • 1
  • Mark A. Peppercorn
    • 1
  1. 1.Division of Gastroenterology, Center for Inflammatory Bowel Disease, Beth Israel Deaconess Medical CenterHarvard Medical SchoolBostonUSA

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