Efeitos de autoanticorpos antilipoproteína lipase, antilipoproteína de baixa densidade e antilipoproteína de baixa densidade oxidada sobre o metabolismo lipídico e aterosclerose no lúpus eritematoso sistêmico

Abstract

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 lipoproteintriglyceride (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.

Novel Insights in Systemic Lupus Erythematosus and Atherosclerosis

“…Antibodies against OxLDL, although not usually determined in clinical practice, have also been correlated with lupus activity and cIMT ( 145 ).…”

Association of serum levels of antibodies against MMP1, CBX1, and CBX5 with transient ischemic attack and cerebral infarction

“…Antibody markers may be more sensitive than antigen markers because repeated exposure of a small amount of an antigen to immune cells results in the production of a large amount of the antibody. Therefore, increasing numbers of antibody markers, such as those against oxidized LDL for atherosclerosis [58], p53 antibodies for cancer [59], and glutamic acid decarboxylase antibodies for type-1 DM [60], have been developed for practical use. However, antibody markers have some limitations.…”

Accelerated atherosclerosis in patients with SLE—mechanisms and management

“…A recent study suggests that anti-oxLDL antibodies develop after of anti-lipoprotein lipase autoantibodies are detected and are responsible for increased atherosclerotic risk in an SLE cohort with high disease activity 32 . The underlying mechanism behind why IgG anti-oxLDL antibodies are atherogenic is unclear, but decreased immune complex clearing (e.g., SLE nephritis) or the presence of aggregated oxLDL in the subendothelial space could explain the increased atherosclerotic risk.…”