Systemic lupus erythematosus (SLE) is a chronic multisystem disorder of presumed autoimmune origin. Although recognized in antiquity, it is only in the latter half of this century that the spectrum of this disease has become well-described. Before the introduction of corticosteroids, SLE was frequently a rapidly fatal disease. The use of corticosteroids, antimalarial (AM) drugs, and immunosuppressive therapies and improvements in medical treatments in general (e.g., antihypertensives, antimicrobials, renal replacement therapy) have all contributed to a dramatic improvement in the long-term survival of patients with SLE. Although early studies showed a less than 50 survival rate at 5 years,44 contemporary reports suggest 5, 10, and 20-year survival rates of 93, 85, and 68, respectively.2 Because SLE has evolved as a chronic inflammatory disorder, many new clinical problems have emerged in these patients. One important problem is that of accelerated atherosclerosis and, in particular, premature coronary artery disease (CAD), which results in significant mortality and morbidity in these patients. The aim of this article is to summarize the current evidence regarding the clinical and subclinical spectra of this problem. The authors also explore what is known about the complex interaction between disease, therapy, and conventional CAD risk factors that appears to underlie the susceptibility these patients have for this complication. A practical approach to screening and prevention in such patients is also discussed.

EXPLOR_STEP=$WICRI_ROOT/Sante/explor/ChloroquineV1/Data/Main/Exploration

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{{Explor lien
   |wiki=    Sante
   |area=    ChloroquineV1
   |flux=    Main
   |étape=   Exploration
   |type=    RBID
   |clé=     ISTEX:EB09350E3E6C89CBBA3943F4A61755925F1B2109
   |texte=   PREMATURE ATHEROSCLEROSIS IN SYSTEMIC LUPUS ERYTHEMATOSUS
}}