Premature Atherosclerosis in Systemic Lupus Erythematosus: Pathogenesis and Therapeutic Considerations

Systemic lupus erythematosus (SLE) is a chronic inflammatory disease of unknown cause that can affect any organ, and is characterized by a wide range of autoantibodies. Several studies of large cohorts of SLE patients have reported an increased prevalence of symptomatic subclinical cardiovascular disease (CVD). It is currently believed that accelerated atherosclerosis in SLE results from a combination of numerous risk factors. In addition to a high prevalence of traditional risk factors, inflammatory processes in SLE are considered to be important in atherogenesis. Chronic activation or damage to the endothelium in SLE may trigger the inflammatory cascade and thereby promote atherogenesis. Several forms of endothelial insult are being recognized in SLE, including hypercholesterolemia, hyperhomocysteinemia, mechanical stress from hypertension, increased oxidative stress and immunologic injury as a result of immune complex deposition. This review updates the modifiable risk factors in SLE. The main focus is on the potential utility of these risk factors. The putative mechanisms of accentuated risk as a result of underlying inflammation, and evidence for association with premature atherosclerosis are discussed. Strategies that may be useful in preventing the progression of atheroma in this population include close monitoring and aggressive treatment of the traditional risk factors as in patients with high risk of CVD. The role of antioxidants and immunomodulators are also explored.

Key words:  atherosclerosis , homocysteine , hyperlipidemia , oxidative stress , risk factors , systemic lupus erythematosus

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