Introduction: Lipid oxidation is a definite feature of atherosclerosis, and oxidized low-density lipoprotein (oxLDL) is not only highly immunogenic but toxic to several cell types. Beta-2-glycoprotein-I (β2GPI) dampens oxLDL toxicity by forming binary oxLDL/β2GPI complexes. We evaluated whether circulating oxLDL/β2GPI complexes are associated to atherosclerosis-related events (ARE) and to venous thromboembolism (VTE). Methods: In a cross-sectional case–control study, cases were (a) 57 consecutive patients (male/female [M/F] 33/24, mean age 57 [10] years) attending a thrombosis unit for ARE (myocardial infarction [MI] n = 20, peripheral vascular disease n = 7, and ischemic strokes n = 30); (b) 52 consecutive patients (M/F 22/30, mean age 55 [17] years) attending the same unit for unprovoked (VTE); (c) normal controls comprised 90 participants (M/F 35/55, mean age 41 [15] years); and (d) oxLDL/β2GPI complexes were measured by immunoassay and resulting levels divided into quartiles. Results: The odds ratio (OR) of ARE was greater in the fourth and second quartiles than in the first quartile (8.5 and 6.0, respectively); the OR of developing MI was greatest in the fourth quartile (17.8). By multivariable analysis with age, sex, smoking, lipid status, statin, and ARE phenotypes as independent variables and oxLDL/β2GPI as the dependent variable, only MI predicted oxLDL/β2GPI ( P < .0001). Conclusions: OxLDL/β2GPI may be regarded as a marker of ARE, in particular of MI.
Antibodies to adult human endothelial cells cross-react with oxidized low-density lipoprotein and β2
-glycoprotein I (β2
-GPI) in systemic lupus erythematosus
