Clinical studies
Dyslipoproteinemia in systemic lupus erythematosus: Effect of Corticosteroids

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Abstract

The increased incidence of atherosclerotic coronary artery disease in patients with systemic lupus erythematosus (SLE) may be due to a dyslipoproteinemia caused by corticosteroid administration. To determine whether lipoprotein lipid levels are abnormal in SLE and the relation of lipoprotein levels to corticosteroid use, lipid and apolipoprotein levels were measured in 46 female patients with SLE and 30 matched control subjects. The patients with SLE had higher levels of plasma triglyceride (134 versus 73 mg/dl; p <0.001), cholesterol (201 versus 168 mg/dl; p <0.001), and low-density lipoprotein cholesterol (121 versus 94 mg/dl; p <0.001) than control subjects. The levels of high-density lipoprotein cholesterol, high-density lipoprotein subfraction 3 cholesterol, and apolipoprotein Al were similar in the two groups, but high-density lipoprotein subfraction 2 cholesterol was lower in the patients with SLE (10.2 versus 18.2 mg/dl; p <0.001). When patients with SLE treated with prednisone (n = 32) were compared to patients with SLE not treated with prednisone (n = 14), the former had higher triglyceride (158 versus 87 mg/dl; p <0.001), cholesterol (214 versus 170 mg/dl; p <0.001), and low-density lipoprotein cholesterol (130 versus 103 mg/dl; p <0.001) levels. The patients with SLE not treated with prednisone had lipid levels similar to those in control subjects except that high-density lipoprotein cholesterol was lower (49.7 versus 59.0 mg/dl; p <0.05). The daily prednisone dosage in the treated patients with SLE correlated with levels of cholesterol (r = 0.38, p <0.02), high-density lipoprotein cholesterol (r = 0.40, p <0.02), and high-density lipoprotein subfraction 3 cholesterol (r = 0.47, p <0.01). Thus, female patients with SLE have a dyslipoproteinemia of the type that would place them at an increased risk for coronary artery disease. Corticosteroids, used in the treatment of SLE, seem to play a role in the pathogenesis of the observed lipoprotein abnormalities.

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This work was supported in part by Grant HL-38225-01 from the National Institutes of Health and General Clinical Research Center Grant RR-02719. A portion of this work was presented at the American Rheumatism Association meetings, June 1985, Dr. Ettinger is a Brookdale National Fellow in Geriatric Medicine.

Current address: Department of Medicine, Bowman Gray School of Medicine, Winston-Salem, North Carolina 27103.