Overlap between irritable bowel syndrome and inflammatory bowel disease.

While recent studies have indicated that the colonic mucosa in irritable bowel syndrome (IBS) shows an increase in inflammatory cells, this 'inflammation' is quantitatively less than in inflammatory bowel disease (IBD) and of a different nature with a predominance of mast cells, particularly in female patients. Inflammation can arise via numerous pathways including infection, stress, food allergy and changes in gut microbiota. Low-grade mucosal inflammation throughout the colon and including the terminal ileum can be seen for many months after an attack of acute gastroenteritis and is a feature of post-infective IBS. Measurements of gut permeability also show a prolonged increase in both the small and large bowel in both post-infective IBS and IBS with diarrhoea predominance. This has been linked to visceral hypersensitivity, but whether this is causal or an epiphenomenon remains uncertain. Studying the risk factors for post-infective IBS has shown the importance of both local and microbiological factors, as well as psychological factors, including adverse life events, anxiety and depression. Stress in both animals and humans can activate mast cells, which (by increasing gut permeability) may allow activation of the systemic immune system. Demonstration of the importance of the low-grade inflammation observed awaits definitive large scale trials of agents designed to specifically reverse these changes.