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.
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.
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DOI：
10.1590/s0482-50042010000500007
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发表时间：
2010-09
影响因子：
--
通讯作者：
Reichlin M
中科院分区：
文献类型：
--
作者：
Fesmire J;Wolfson-Reichlin M;Reichlin M
系统性红斑狼疮过早发生动脉粥样硬化已有广泛报道。抗脂蛋白脂酶抗体可能是导致这种疾病的原因之一。评估狼疮患者颈动脉斑块中自身免疫抗体引起的冠状动脉风险程度。我们比较了114例记录的狼疮患者与111例性别和年龄匹配的正常对照。酶联免疫吸附法测定抗脂蛋白脂酶、抗氧化低密度脂蛋白和抗低密度脂蛋白。还测量了LDL-Trig和HDL-Trig。通过双侧颈动脉超声测量斑块。45.6%的患者A-LPL检测阳性，34.4%的患者A-OXLDL检测阳性。44%的正常对照检测为A-LPL阳性，20%为A-OXLDL阳性。在抗体水平增加的亚组中，风险急剧增加。A-LPL和A-OXLDL > 0.40的患者（n = 12）显示冠状动脉风险相关性：A-LPL × LDL-Trig，0.7008，p = 0.0111; USBL ×总胆固醇= 0.62205，p = 0.0308; LDL-Trig ×心肌梗死（MI）= 0.76562，p = 0.0037;总甘油三酯× MI = 0.78191，p = 0.0027）; LDL-Trig/LDL-胆固醇× MI = 0.80493，p = 0.0016; A-OXLDL × USBL = 0.71930，p = 0.0084。仅在抗体水平升高的亚组中，SLEDAI与风险变量的相关性高度显著（SLEDAI × A-OXLDL = 0.70366，p = 0.0107）。在一些SLE患者中，A-LPL启动LDL突变的发展，随后是抗体产生、斑块形成和冠状动脉风险。
Premature development of atherosclerosis in systemic lupus erythematosus has been widely reported. Anti-lipoprotein lipase antibody may be one cause contributing to this disorder. To assess the extent of coronary risk due to autoimmune antibodies in terms of carotid plaque in lupus patients. We compared 114 documented lupus patients with 111 normal controls matched for sex and age. Anti-lipoprotein lipase, anti-oxidized low density lipoprotein, and anti-low density lipoprotein were measured by enzme-linked immunoabsorbent assay. LDL-Trig and HDL-Trig were also measured. Plaque was measured by bilateral carotid ultrasound. 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 >.40 (n = 12) showed coronary risk correlations of: A-LPL × LDL-Trig, 0.7008, p = 0.0111; USBL × total cholesterol = 0.62205, p = 0.0308; LDL-Trig × myocardial infarction (MI) = 0.76562, p = 0.0037; total triglycerides × MI = 0.78191, p = 0.0027); LDL-Trig/LDL-cholesterol × MI = 0.80493, p = 0.0016; A-OXLDL × USBL = 0.71930, p = 0.0084. Correlations of SLEDAI with risk variables were highly significant only in subgroups of elevated antibody levels (SLEDAI × A-OXLDL = 0.70366, p = 0.0107). A-LPL initiates the development of LDL mutations, followed by antibody production, plaque formation and coronary risk in some SLE patients.
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影响因子：
--
作者：
Carvalho, Jozélio Freire de;Viana, Vilma Santos Trindade;Bonfá, Eloísa
通讯作者：
Bonfá, Eloísa
影响因子：
37.8
作者：
März, W;Scharnagl, H;Winkelmann, BR
通讯作者：
Winkelmann, BR
影响因子：
--
作者：
Reichlin, M;Fesmire, J;Wolfson-Reichlin, M
通讯作者：
Wolfson-Reichlin, M
影响因子：
3
作者：
Cicorella, Nicola;Zanolla, Luisa;Vassanelli, Corrado
通讯作者：
Vassanelli, Corrado
DOI：
10.1161/01.atv.10.3.325
发表时间：
1990-05-01
期刊：
ARTERIOSCLEROSIS
影响因子：
--
作者：
PALINSKI, W;YLAHERTTUALA, S;WITZTUM, JL
通讯作者：
WITZTUM, JL