Patients with systemic lupus erythematosus are at increased risk for premature atherosclerosis. We examined one possible etiologic factor, dyslipoproteinemia, both before and after corticosteroid therapy. We identified 2 distinct patterns of dyslipoproteinemia. One is attributable to active disease; the other is attributable, in part, to corticosteroid therapy. The dyslipoproteinemia of active disease consists of depressed high density lipoprotein cholesterol and apoprotein A-I with elevated very low density lipoprotein cholesterol and triglyceride, while the dyslipoproteinemia after corticosteroid therapy consists of increased total cholesterol, very low density lipoprotein cholesterol, and triglyceride. The possible pathophysiologic mechanisms responsible for these patterns, as well as the possible roles in premature atherosclerosis seen in systemic lupus erythematosus patients, are discussed.Premature atherosclerosis and its sequelae, myocardial infarction and cerebrovascular accident, have recently been recognized as complications of systemic lupus erythematosus (SLE) (1-7). Possible etiologies include dyslipoproteinemia, vasculitis, hypertension, and increased tendency for thrombosis associated with the presence of circulating anticoagulant (1-8).Dyslipoproteinemia is common in adult SLE patients (9); however, the relationships of disease activity, diet, corticosteroid therapy, and concurrent renal, liver, and pancreatic disease have not been studied well. To differentiate the roles of corticosteroids and disease activity in the dyslipoproteinemia of SLE, we studied newly diagnosed pediatric patients both before and after high-dose systemic prednisone therapy.
PATIENTS AND METHODSPatients. Ten successive pediatric patients (younger than 21 years of age) newly diagnosed as having SLE were enrolled after informed consent was obtained. Nine fulfilled the requirements of the American Rheumatism Association revised diagnostic criteria (10). The other (patient 5) had anticardiolipin, high-titer speckled antinuclear, anti-Smith, and anti-double-stranded DNA antibodies, circulating lupus anticoagulant, hypocomplementemia, and recurrent pulmonary emboli. He was not treated with corticosteroids. Eight patients underwent percutaneous renal biopsy prior to therapy. Results are shown in Table 1. In all 10 patients at diagnosis, and in 8 patients at 4-8 weeks after institution of 1-2 mg/kg/day of prednisone, fasting plasma lipid profiles (see below) were obtained. Dietary intake was quantified by 3-day diet record, and this was supplemented with 24-hour recall