Effects of autoimmune antibodies anti-lipoprotein lipase, anti-low density lipoprotein, and anti-oxidized low density lipoprotein on lipid metabolism and atherosclerosis in systemic lupus erythematosus.

INTRODUCTION Premature development of atherosclerosis in systemic lupus erythematosus has been widely reported. Anti-lipoprotein lipase antibody may be one cause contributing to this disorder. OBJECTIVE To assess the extent of coronary risk due to autoimmune antibodies in terms of carotid plaque in lupus patients. PATIENTS AND METHODS We compared 114 documented lupus patients with 111 normal controls matched for sex and age. Anti-lipoprotein lipase (A-LPL), anti-oxidized low density lipoprotein (A-OXLDL), and anti-low density lipoprotein (A-LDL) were measured by enzme-linked immunoabsorbent assay. Low density lipoprotein-triglyceride (LDL-Trig) and high density lipoprotein-triglyceride (HDL-Trig) were also measured. Plaque was measured by bilateral carotid ultrasound. RESULTS 45.6% of patients tested positive for A-LPL, and 34.4% for A-OXLDL. 44% of normal controls tested positive for A-LPL, and 20% for A-OXLDL. Risk increased sharply in subgroups with increased antibody levels. Patients with A-LPL and A-OXLDL > 0.40 (n = 12) showed coronary risk correlations of: A-LPL x LDL-Trig = 0.7008, P = 0.0111; bilateral ultrasound vs total cholesterol = 0.62205, P = 0.0308; LDL-Trig vs myocardial infarction (MI) = 0.76562, P = 0.0037; total triglycerides vs MI = 0.78191, P = 0.0027); LDL-Trig/LDL-cholesterol vs MI = 0.80493, P = 0.0016; A-OXLDL vs USBL = 0.71930, P = 0.0084. Correlations of SLEDAI with risk variables were highly significant only in subgroups of elevated antibody levels (SLEDAI x A-OXLDL = 0.70366, P = 0.0107). CONCLUSION A-LPL initiates the development of LDL mutations, followed by antibody production, plaque formation and coronary risk in some SLE patients.