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Inflammatory Bowel Disease

Introduction . IBD characterized by a tendency for chronic or relapsing immune activation and inflammation within the GIT.Crohn's disease (CD) and ulcerative colitis (UC) are the 2 major forms of idiopathic IBD.. Less common entities are: . Microscopic colitis (collagenous and lynphocytic)OthersD

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Inflammatory Bowel Disease

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    1. Inflammatory Bowel Disease A Aljebreen FRCPC

    2. Introduction IBD characterized by a tendency for chronic or relapsing immune activation and inflammation within the GIT. Crohns disease (CD) and ulcerative colitis (UC) are the 2 major forms of idiopathic IBD.

    3. Less common entities are: Microscopic colitis (collagenous and lynphocytic) Others Diversion colitis Radiation colitis Drug induced colitis Infectious colitis Ischemic colitis

    4. Introduction CD is a condition of chronic inflammation potentially involving any location of the GIT from mouth to anus. UC is an inflammatory disorder that affects the rectum and extends proximally to affect variable extent of the colon.

    5. Epidemiology CD: 1st peak 15-30 years of age, 2nd peak around 60 y UC: High incidence areas: US, UK, northern Europe Young adults, commoner in females

    6. Genetics Studies suggested that 1st degree relatives of an affected patient have a risk of IBD that is 4-20 times higher than that of general population. The best replicated linkage region, IBD1, on chromosome 16q contains the CD susceptibility gene, NOD2/CARD15. Having one copy of the risk alleles confers a 24-fold risk for developing CD, whereas double-dose carriage increases the risk 2040-fold.

    7. Etiology Mutations within the NOD2/ CARD15 gene contribute to CD susceptibility. Functional studies suggest that inappropriate responses to bacterial components may alter signaling pathways of the innate immune system, leading to the development and persistence of intestinal inflammation. Initiating pathogen? Infectious? ? Possibly non-pathogenic commensal enteric flora

    8. Pathogenesis The mucosa of CD patients is dominated by Th1 (T helper), which produce interferon-? and IL-2. In contrast, UC dominated by Th2 phenotype, which produce transforming growth factor (TGF-) and IL-5. Activation of Th1 cells produce the down-regulatory cytokines IL-10 and TGF-.

    9. Environmental Precipitants Factors: NSAIDs use (?altered intestinal barrier), and Early appendectomy (increase UC incidence) Smoking (protects against UC but increases the risk of CD).

    10. CD: PATHOLOGY Early Findings: Aphthous ulcer. The presence of granulomas Late findings: Linear ulcers. The classic cobble stoned appearance may arise. Transmural inflammation Sinus tracts, and strictures. Fibrosis.

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