Autoantibodies to lipoprotein lipase and dyslipidemia in systemic lupus erythematosus
Autoantibodies to lipoprotein lipase and dyslipidemia in systemic lupus erythematosus
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DOI：
10.1002/art.10624
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发表时间：
2002-11-01
影响因子：
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通讯作者：
Wolfson-Reichlin, M
中科院分区：
文献类型：
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作者：
Reichlin, M;Fesmire, J;Wolfson-Reichlin, M
目标。目的探讨系统性红斑狼疮(SLE)等风湿性疾病患者血清中牛脂蛋白脂酶(LPL)与血清免疫球蛋白(Ig G)的结合及其与血清中甘油三酯水平的关系。用双抗体夹心酶联免疫吸附测定法测定了SLE和其他风湿病患者血清中的免疫球蛋白G与LPL的结合。对SLE患者和对照组的空腹血样进行血脂谱检测。对105例SLE患者的血清进行了LPL反应，其中49例(47%)为阳性。类风湿性关节炎(RA)80例，干燥综合征(Sjogren‘s综合征)30例，多发性肌炎和皮肌炎30例，进行性系统性硬化症(SSD)31例，LPL阳性分别为10例(13%)、3例(10%)、12例(40%)和13例(42%)。亲和纯化的抗双链DNA(DsDNA)抗体和5株抗dsDNA单抗中的4株均与LPL结合。去除抗dsDNA的免疫球蛋白与LPL的结合表明SLE具有第二抗LPL活性。抗LPL抗体检测SLE患者空腹血脂水平与血清总甘油三酯、载脂蛋白B、载脂蛋白E浓度呈显著正相关。LPL抗体出现在47%的SLE患者和类似比例的多发性肌炎或系统性硬化症患者中。在RA或干燥综合征患者中，这些抗体的患病率较低。据推测，SLE患者甘油三酯水平升高的部分原因是抗LPL，这种脂质异常可能导致已知的SLE患者存在过早的动脉粥样硬化。
Objective. To demonstrate the binding of bovine lipoprotein lipase (LPL) by IgG from sera obtained from patients with systemic lupus erythematosus (SLE) and other rheumatic diseases, and the relationship of anti-LPL to triglyceride levels in SLE.Method. Binding of LPL by IgG from sera obtained from patients with SLE and other rheumatic diseases was measured by an enzyme-linked immunosorbent assay technique. Lipid profiles for fasting blood samples obtained from SLE patients and control subjects were determined.Results. Sera obtained from 105 patients with SLE were assessed for reactivity with LPL, and 49 (47%) of the results were positive. Sera obtained from patients with rheumatoid arthritis (RA) (n = 80), Sjogren's syndrome (n = 30), polymyositis and dermatomyositis (n = 30), and progressive systemic sclerosis (n = 31) were also studied, and 10 (13%), 3 (10%), 12 (40%), and 13 (42%), respectively, were positive for reactivity with LPL. It was determined that all affinity-purified antidouble-stranded DNA (dsDNA) antibodies and 4 of 5 monoclonal anti-dsDNA antibodies bound to LPL. The binding of IgG depleted of anti-dsDNA to LPL indicates a second anti-LPL activity in SLE. Measurements of fasting lipid levels in SLE patients with anti-LPL revealed a strong positive correlation of antibody levels and total serum triglycerides, apolipoprotein B, and apolipoprotein E concentrations.Conclusion. Antibodies to LPL occurred in 47% of SLE patients and in a similar percentage of patients with polymyositis or systemic sclerosis. The prevalence of these antibodies was less in patients with RA or Sjogren's syndrome. It is hypothesized that the elevated triglyceride levels in SLE patients are in part attributable to anti-LPL, and this lipid abnormality could contribute to the premature atherosclerosis known to be present in patients with SLE.