Vasculitis

Behc¸et's disease (BD) is a systemic vasculitis, most common in the Mediterranean area and in Asia, which can involve nearly every organ system and results from the interplay between infectious agent exposure and genetic factors. High production of cytokines, T and B lymphocyte activation, autoantibody production, and hypercoagulable/prothrombotic state are all characteristics of BD. Evidence for accelerated atherosclerosis in BD has been observed, but the relationship between cardiovascular risk factors and accelerated atherosclerosis in patients with BD is still controversial (Messedi et al. 2011). A study published by Messedi and colleagues demonstrated that in BD patients, HDL concentration and their subfraction levels are decreased. The same study reported that the percentage of HDL2 subpopulation was also decreased and HDL3 subfraction was significantly higher. The LDL-C/ HDL-C ratio and CRP level were increased, and HDL and its subfractions were correlated with CRP and TG levels, suggesting that all these parameters may be considered as important predictors of cardiovascular events in BD patients (Messedi et al. 2011). This study confirms what seen in some previous studies in which, compared to control subjects, BD patients were characterized by reduced levels of HDL (Cimen et al. 2012; Musabak et al. 2005; Orem et al. 2002).

Kawasaki disease (KD) is an acute vasculitis that predominantly occurs in infancy and early childhood. It is commonly thought that KD results from the exposure of a genetically predisposed individual to an as-yet unidentified, possibly infectious environmental trigger. Coronary artery aneurysms or ectasia develops in approximately 15–25 % of affected children (Dhillon et al. 1996; Newburger et al. 1991; Cheung et al. 2004). There is increasing evidence to suggest that children with a history of KD might be predisposed to premature atherosclerosis and a significant association between carotid IMT and systemic arterial stiffness in children after KD has been demonstrated (Cheung et al. 2007). This syndrome is associated with significant abnormalities in lipid profile. In one of the first studies on this subject, it was shown that in the earliest days of illness, mean plasma concentrations of total cholesterol and HDL cholesterol are profoundly depressed, whereas mean triglyceride concentration is very high. Total cholesterol values rapidly return to normal and remain stable for more than 3 months after the onset of illness. HDL concentration recovered more slowly after illness onset, and mean HDL was significantly lower than expected more than 3 years after illness onset (Newburger et al. 1991). The persistence of low HDL for many years suggests a more lasting effect of KD on endothelial function, perhaps attributable to diminished activity of lipoprotein lipase. This enzyme resides on the capillary walls of most tissues and functions at the luminal surface of the vascular endothelium (Eckel 1989). This observation is confirmed, at least in part, in later studies on the lipid derangement in KD (Cheung et al. 2004; Chiang et al. 1997; Cabana et al. 1997). The results showed that during the acute phase, the concentrations of plasma HDL-C, apoA-I, and apoA-II were significantly reduced and the reduction of HDL was mainly related to the lowering of esterified and unesterified cholesterol in HDL2 (Chiang et al. 1997). In parallel, another study demonstrated that the lipid changes involved not only HDL-C concentration but also HDL composition. The authors showed that children with KD have extremely low serum HDL-C and apoA-I levels at the time of the acute illness and that serum amyloid A (SAA) is present in the acute stage and is associated mainly with HDL particles of HDL3 density (Cabana et al. 1997). Moreover, a more recent study demonstrated a significant induction of MCP-1, CCR2, and iNOS expression in THP-1 macrophages in vitro by the serum of children with a history of KD, showing that this induction correlated positively with serum high-sensitivity C-reactive protein (hs-CRP) and LDL and negatively with HDL-C levels (Cheung et al. 2005).

 
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