The shifting interface between IBS and IBD

Recent data developing from the study of postinfectious IBS has challenged the belief that IBS is a purely psychological disorder. Distinct abnormalities of the gut mucosa have been reported including immune activation and increased release of inflammatory mediators with some overlap with IBD. New studies show that genetic factors which predispose to IBD are also associated with IBS. A common feature is impaired gut barrier function which appears to precede the development of IBD while in IBS it may be the result of either a preceding infection or psychosocial stress. Stress can activate mast cells which are a feature in most but not all IBS series. Anti-inflammatory treatments targeting activated mast cells may benefit IBS patients but currently the evidence is weak and larger trials are needed. Changes in the commensal microbiota have been recently described with a “dysbiosis” in CD characterised by reduced diversity. Inconsistent changes have also been described in IBS but studies controlling for antibiotic use and differences in diet and bowel habit are needed before definitive conclusions can be made.

► Impaired gut barrier function is common to both conditions, which correlates well with pain in IBS.
► Commensal microbiota are abnormal in both conditions with reduced diversity in CD.
► Both conditions show evidence of increased reaction to commensal microbes with upregulation of Toll-like receptor 4 and increased fecal β-defensin.
► Stress can cause flares in both conditions possibly by activating mast cells which may cause increased permeability.
► Treatments targeting activated mast cells and increased permeability may benefit IBS patients but larger trials are needed.