The Pathophysiology of Irritable Bowel SyndromeCME - Medscape

The Pathophysiology of Irritable Bowel Syndrome CMESlide 11.Just as there is a mucosal barrier in the small intestine, there is also a low permeability in the normal state in the colon. [4] Thebarrier in the colon may be broken, however, when malabsorption of either carbohydrates or fat results in the production ofSCFAs, when there is bile acid malabsorption or immune activation, in the presence of genetic predisposition to inflammation orimmune activation or bile acid synthesis. Typically, this is going to be associated with IBS-D, increased fluid secretion andactivation of sensory mechanisms.Research has documented an increased intestinal permeability in IBS [9] ; this is relevant because 1 of the agents used in thetreatment of IBS, lubiprostone, has been shown in a porcine ischemia model to restore tight junction function and normalizepermeability of the intestine. [10] This may be advantageous if permeability is indeed a significant mechanism causing the patient’sdiarrhea.The cumulative excretion of a sugar molecule such as mannitol has been shown to be a fairly good noninvasive marker ofpermeability, as has been demonstrated in patients who have IBS-D. [9] Although the increase in permeability is lower than thatwhich is observed in patients with inactive or microscopic or ulcerative colitis, changes in permeability and tight junctionproteins appear to be quite relevant in IBS. There is a relationship among duration of disease, body mass index, and, importantly,the expression of the tight junction protein occludin and pain in IBS.Pg.12