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Abdominal pain is one of the most difficult to treat symptoms in patients suffering from IBS. Recent evidence shows that abnormal perception of visceral stimuli, or visceral hypersensitivity, represents an important underlying mechanism. Of interest, similar mechanisms may be involved in abdominal pain reported by UC and Crohn's disease patients in remission. Although the underlying mechanisms are not fully understood, it becomes increasingly clear that intestinal inflammation may provide an initial stimulus for a persistent state of visceral hypersensitivity. Most insight in the role of inflammation in chronic abdominal pain comes from studies evaluating patients with postinfectious (PI)-IBS. Colonic biopsies of patients with PI-IBS reveal no signs of overt inflammation but show persistent minor increases in epithelial T lymphocytes and mast cells,1 suggesting that long-term inflammatory changes may be responsible for colonic hypersensitivity. To date, mast cells are considered to play a key role in this process. Supernatant of mucosal biopsies of visceral hypersensitive patients with IBS indeed contains more mast cell mediators such as serotonin, histamine and proteases, which are able to activate visceral afferent nerve fibres.2 Moreover, abdominal pain in patients with IBS was reported to be correlated with …
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