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Atherosclerosis and systemic lupus erythematosus

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Abstract

The description of late-stage mortality and morbidity has been an important contribution to the understanding of systemic lupus erythematosus (SLE) in the past decade. Among the major factors in this clinical spectrum of SLE is the development of accelerated atherosclerosis. This condition has been recognized clinically with the documentation of myocardial infarction and angina in young women with SLE. This accelerated atherosclerosis has also been recognized at postmortem examinations. The exact mechanism for accelerated atherosclerosis remains unclear. However, disease activity with its immunologic events, the anticardiolipin syndrome, and the effect of corticosteroids in promoting hyperlipidemia contribute to its development. It appears that SLE may be a risk factor, in addition to the usual risk factors for the development of atherosclerosis. It has recently been shown that antimalarials may prevent some of the hyperlipidemia caused by corticosteroids. As evidence for the presence of subclinical atherosclerosis in these patients is accumulating, earlier diagnosis and treatment of events may be possible, and preventive measures may be instituted earlier.

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Authors and Affiliations

  1. Western Division, University of Toronto, Director Centre of Prognosis Studies in The Rheumatic Diseases and The University of Toronto Lupus Clinic, The Toronto Hospital, 399 Bathurst Street, 1-318, M5T 2S8, Toronto, Ontario, Canada

    Murray Urowitz MD

  2. University of Toronto, Deputy-Director Centre of Prognosis Studies in The Rheumatic Diseases and The University of Toronto Lupus Clinic, The Toronto Hospital, Toronto, Ontario, Canada

    Dafna Gladman MD (Professor of Medicine)

  3. Central Manchester Healthcare NHS Trust and the University of Manchester, UK

    Ian Bruce MB, MRCP (Consultant Rheumatologist and Honorary Clinical Lecturer)

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  1. Murray Urowitz MD
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  2. Dafna Gladman MD
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  3. Ian Bruce MB, MRCP
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Urowitz, M., Gladman, D. & Bruce, I. Atherosclerosis and systemic lupus erythematosus. Curr Rheumatol Rep 2, 19–23 (2000). https://doi.org/10.1007/s11926-996-0064-9

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  • DOI: https://doi.org/10.1007/s11926-996-0064-9

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