Moving towards disease modification in inflammatory bowel disease therapy

Curr Opin Gastroenterol. 2013 Jul;29(4):397-404. doi: 10.1097/MOG.0b013e3283622914.

Abstract

Purpose of review: The inflammatory bowel diseases (IBDs) are chronic disabling conditions. Despite the benefits of anti-tumor necrosis factor (TNF)-α agents in improving quality of life and reducing the need for surgeries, overall only one-third of patients are in clinical remission at 1 year and loss of response is frequent. It seems clear that treatment must go beyond alleviation of symptoms in IBD. It is important that treatment targets in IBD will ensure mucosal healing and deep remission.

Recent findings: The induction of deep remission might be the best way to alter the natural course of these diseases by preventing disability and bowel damage. New disability indices and the new Crohn's disease damage score have recently been developed and they can be used to evaluate the long-term effect on patients and as new endpoints in trials. Early intervention with disease-modifying anti-IBD drugs (DMAIDs) should be considered in patients with poor prognostic factors.

Summary: New therapeutic targets in IBD patients who failed anti-TNF-α therapy are urgently required, and tofacitinib, vedolizumab and ustekinumab appear to be the most promising drugs. Herein, we review the new and current trends in IBD therapy, with the final aim of changing disease course and patients' lives by both improving quality of life and avoiding disability.

Publication types

  • Review

MeSH terms

  • Algorithms
  • Antibodies, Monoclonal, Humanized / therapeutic use
  • Gastrointestinal Agents / therapeutic use*
  • Humans
  • Inflammatory Bowel Diseases / diagnosis
  • Inflammatory Bowel Diseases / drug therapy*
  • Prognosis
  • Remission Induction / methods
  • Severity of Illness Index
  • Treatment Outcome
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors

Substances

  • Antibodies, Monoclonal, Humanized
  • Gastrointestinal Agents
  • Tumor Necrosis Factor-alpha