Atherogenesis and Vascular Disease in SLE

摘要: SLE is the classical model of a chronic multi-systemic immune-mediated inflammatory disease. It affects mainly young women, subgroup general population usually free cardiovascular risk. Although survival rates have improved dramatically, due to early diagnosis, treatment, and better management complications, death for patients with remain 3 5 times higher than in (Haque & Bruce, 2009). Nevertheless, whilst 5-year was below 50% 1950s, it nowadays above 90% (Nikpour et al., 2005). Atherosclerosis highly complex process autoimmunity, local systemic inflammation, endothelial dysfunction playing critical roles its initiation propagation. In particular case SLE, extremely intricate immune system deregulation involving all types cells up an increased autoantibody production seems play major role accelerated atheroma formation found these patients. Cardiovascular events are now cause morbidity mortality SLE. The acceptance importance vascular risk this context came from description bimodal pattern (Urowitz 1976), peak (within 1 year diagnosis) as consequence active lupus later (more years after attributable atherosclerosis. considered be coronary heart disease-risk equivalent, atherosclerosis (Aranow Ginzler, 2000; Bjornadal 2004; Manzi 1997; Esdaile 2001; Fischer al. Roman 2003; Ward, 1999). This can especially relevant where 50-fold increase over age gender-matched controls has been reported (Manzi 1997). fact, majority those women were aged less 55 at time their first cardiac event. Framingham factors do not explain entirely atherosclerotic burden Furthermore, traditional seem important predictors activity (Esdaile 2001). (see table 1). direct relation between conventional SLE-related actual incidence easy establish different reasons: most