Abstract

Clinical remission at a single point in time provides surprisingly little predictive value for future inflammatory bowel disease (IBD) activity owing to the waxing and waning nature of the disease course. Furthermore, patients often present with complications of IBD despite apparent clinical remission, suggesting that undetected subclinical inflammation is driving these complications. This has led to research on a variety of surrogate markers of biologically significant asymptomatic inflammatory disease activity, including endoscopic healing, histologic normalization and biomarkers of inflammation in the blood and stool. If these have strong predictive value, they could be used to risk-stratify patients and justify the early use of immunomodulators and anti-TNF agents. Mucosal healing has been associated with positive outcomes in IBD, but the supporting data are largely retrospective and subject to channeling bias, and it is not clear whether complete mucosal healing produces better outcomes than partial healing. Stool and blood biomarkers correlate well with mucosal inflammation, but are imperfect surrogates for mucosal healing. Before using surrogate markers of intestinal inflammation to justify long-term, potentially toxic and costly therapy, prospective longitudinal studies are needed to identify surrogate end points with cut points that justify changes in therapy, and which therapies provide cost-effective benefits for mild, moderate or severe inflammation.

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