Optimizing Targets in Patient Management of Ulcerative Colitis: The Role of Fecal Calprotectin in Guiding Maintenance Therapy

Publication of THE LATEST IN ULCERATIVE COLITIS CARE supplement was made possible by an unrestricted educational grant from Aptalis Pharma

A. Hillary Steinhart, MD,

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Abstract: Although medical therapy for ulcerative colitis is usually effective at inducing clinical remission, numerous studies have shown that patients in clinical remission may have ongoing and varying degrees of mucosal inflammation. It appears that patients who have greater degrees of active mucosal inflammation, despite the absence of clinical symptoms, are at higher risk of developing a symptomatic flare in the near term. In patients with UC, the level of calprotectin in stool correlates not only with the degree of clinical severity but also with the presence or absence of mucosal inflammation. These findings raise the possibility of using fecal calprotectin as a non-invasive means of monitoring patients in clinical remission and adjusting treatment in those who demonstrate a rise in fecal calprotectin, before symptoms recur.

Key Words: ulcerative colitis, fecal calprotectin, flare prediction, mucosal inflammation, non-invasive monitoring.

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Patients who experience a symptomatic flare after having been in clinical remission often have increased mucosal inflammation that predates the flare—sometimes by several months.

With the importance of mucosal healing acknowledged, there has been increasing interest in more frequent assessment of mucosal healing and mucosal inflammation.

This has led to the examination of a number of non-invasive and less expensive means of assessing these parameters.

The presumption is that if such risk factors can be identified, then effective interventions can be applied earlier in the course of disease in order to prevent a clinical flare.

In patients with UC, the level of fecal calprotectin correlates not only with the degree of clinical severity but also with the presence of absence of mucosal inflammation.

These findings raise the possibility of using fecal calprotectin as a non-invasive means of monitoring patients in clinical remission, and adjusting treatment in those who demonstrate a rise in fecal calprotectin, before symptoms recur.

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