Abstract
Ulcerative colitis (UC) and Crohn’s disease (CD) comprise a group of inflammatory disorders of the gastrointestinal tract that are collectively termed inflammatory bowel disease (IBD). Both UC and CD are chronic disorders often characterized by exacerbations interposed between variable periods of remission, and are associated with different clinical presentations and histopathological features. Ulcerative colitis is limited to the mucosa of large bowel, whereas Crohn’s diseases is transmural and may affect any portion of the gastrointestinal tract. Although the precise etiology of IBD remains unknown, extensive research in the past decade has led to a greater understanding regarding the pathogenesis of IBD. Application of this knowledge has led to new advances in the treatment of this chronic debilitating condition. In the normal state, the intestinal tract exists in a quiescent inflammatory state presumably to protect the organism from the highly toxic substances and bacteria found in the lumen of the intestinal tract. It is currently believed that inflammatory bowel disease (IBD) constitutes a heterogeneous group of diseases with a common final manifestation of mucosal inflammation resulting from a failure to down-regulate this normal, controlled inflammation that occurs in the gut [1,2].
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Flanigan, A. et al. (2002). PParγ Ligands and Intestinal Inflammation. In: Fruchart, JC., Gotto, A.M., Paoletti, R., Staels, B., Catapano, A.L. (eds) Peroxisome Proliferator Activated Receptors: From Basic Science to Clinical Applications. Medical Science Symposia Series, vol 18. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1171-7_22
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DOI: https://doi.org/10.1007/978-1-4615-1171-7_22
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