In pediatric systemic lupus erythematosus, active disease is associated with depressed HDL and elevated VLDL/triglycerides, while corticosteroid therapy is associated with increased total cholesterol, VLDL, and triglycerides.
Observational
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.
Ilowite et al. (Fri,) conducted a observational in Pediatric systemic lupus erythematosus. Corticosteroid therapy vs. Before corticosteroid therapy (active disease) was evaluated on Dyslipoproteinemia patterns. In pediatric systemic lupus erythematosus, active disease is associated with depressed HDL and elevated VLDL/triglycerides, while corticosteroid therapy is associated with increased total cholesterol, VLDL, and triglycerides.