| dc.description.abstract | For years, a set of bowel-related symptoms and signs manifesting in diverse combinations, in the absence of a documented "organic" cause, have been collectively described under the term irritable bowel syndrome (IBS). Dating back from initial description of the syndrome, its close proximity to emotional distress and psychological or even psychiatric disorders has led to the conclusion that it represented a repertoire of psychosomatic manifestations. Since then, additional evidence has offered intriguing alternative pathogenetic pathways: visceral dysmotility or hypersensitivity, low-grade intestinal inflammation, presence of increased/altered microbial populations and their metabolites, persistent post-infectious changes in hormones, cytokines and immune cells. The line between the syndrome and more severe inflammatory diseases became thinner due to the observation that IBS could precede or co-exist with inflammatory bowel disease (IBD) and the discovery of common genetic background in IBS, IBD and celiac disease patients. Similarly, the detection of various antibodies ie against microbial components (flagellin), food antigens or "autoantibodies", also involved in the pathogenesis of IBD, celiac disease or endocrine disorders, have made this matter even foggier. In the present chapter, all these important data are presented and critically evaluated while addressing issues associated with grey areas ie those between food intolerance or gluten sensitivity and IBS, and the implication of the brain-gut axis in the onset of the syndrome. Finally, the "pros" and "cons" of different theories about the pathogenesis of IBS are weighed, and hard evidence is used for "drawing lines" between IBS subsets which in turn allow correct stratification of IBS patients thus, allowing a better and more individualized/tailored therapeutic approach. © 2012 by Nova Science Publishers, Inc. All rights reserved. | en |
