Atherogenesis and autoimmune disease: the model of lupus

Abstract

Accelerated atherosclerosis is a major cause of morbidity and mortality in patients with systemic lupus erythematosus (SLE). Certain ‘classic’ risk factors are associated with atherosclerosis risk in SLE. However, these factors alone do not fully explain the excess risk observed. Atherosclerosis is increasingly recognized as a chronic inflammatory condition and in SLE, complement activation and immune complex formation may promote atheroma development. Similarly, autoantibody production, especially those in the anticardiolipin (ACLA) family are gaining increasing attention. The role of steroids may not be completely straightforward, low doses may have a beneficial anti-inflammatory role whereas higher doses may exacerbate metabolic factors. In contrast, antimalarials have a beneficial effect on lipids as well as anti-inflammatory and anti-platelet effects. The aetiology of atherosclerosis in SLE is therefore multifactorial. A better understanding of the interface of autoimmunity and atherogenesis in the context of SLE will benefit lupus patients and will also help us better understand the pathogenesis of atherosclerosis in general.