Inflammatory Diseases

Inflammatory Bowel Diseases

The inflammatory bowel diseases (IBD) Crohn's disease (CD) and ulcerative colitis (UC) are chronic inflammatory diseases whose pathogenesis is not completely understood (Williams et al. 2012) but seems to be linked to autoimmune phenomena in a genetically prone background, following an abnormal immune response to colonic bacteria, and facilitated by a Western-type diet. IBD are associated with marked atherosclerosis and increased cardiovascular risk. Infection and chronic inflammation impair and alter lipoprotein metabolism and cause a variety of changes in plasma concentrations of lipids and lipoproteins (Borba et al. 2006; de Carvalho et al. 2008). An increase in inflammatory cytokines may result in a decrease in LPL enzyme activity, leading to a characteristic lipoprotein profile with decreased HDL-C levels as seen in patients with IBD that have high circulatory levels of inflammatory cytokines (Williams et al. 2012; Sappati Biyyani et al. 2010).

CD is a chronic inflammatory bowel disease that can affect any region of the gastrointestinal tract (Grand et al. 1995) with increased chronic inflammatory cell infiltrates in the mucosal lesions. The excessive local production of soluble mediators from activated monocytes and polymorphonuclear leukocytes has been implicated in mediating the tissue injury (Weiss 1989). Important among these mediators are oxygen free radicals. The chronic gut inflammation promotes an imbalance between oxidant and antioxidant mechanisms at the tissue level (Buffinton and Doe 1995) and may even compromise circulating antioxidant concentrations. A chronic inflammatory state is a risk factor for accelerated atherogenesis (van Leuven et al. 2007). A recent exploratory analysis demonstrated that CD is associated with an acceleration of the atherosclerotic process, as illustrated by an increased carotid intima-media thickness (IMT) in CD patients compared to healthy controls. In addition, CD patients were characterized during an inflammatory exacerbation by profoundly decreased levels of HDL combined with biochemical changes of the HDL particles, such as association with serum amyloid A, suggesting that early detection of atherosclerosis and subsequent cardiovascular prevention in patients with CD might be warranted (Romanato et al. 2009).

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