Lipid peroxidation as risk factor for endothelial dysfunction in antiphospholipid syndrome patients.

Abstract

The aim of this study was to evaluate oxidative stress markers and it relations to endothelial damage as risk factor for thrombosis in patients with primary (PAPS) and secondary (SAPS) antiphospholipid syndrome (APS) in correlation to traditional risk factors. Flow-mediated (FMD) and nitroglycerine (NMD)-induced dilation of the brachial artery were studied in 140 APS patients (90 PAPS, 50 SAPS) and 40 controls matched by age, sex, and conventional risk factors for atherosclerosis. Markers of oxidative stress, lipid hydroperoxydes (LOOH), advanced oxidation protein products (AOPP), total sulfhydryl groups (tSHG), and paraoxonase 1 activity (PON1) were determined by spectrophotometric method. Oxidative stress dominates in APS patients. LOOH and AOPP correlate to lipid fractions (p<0.05), unlike PON1, tSHG that correlated to antiphospholipid antibody positivity (p<0.05). FMD was lower in APS patients comparing to controls (p<0.001). Cholesterol is independent variable for FMD impairment in control group (p=0.011); LOOH in PAPS (p=0.004); LOOH, aCL, and triglycerides in SAPS patients (p=0.009, p=0.049, and p=0.012, respectively). Combined predictive of aCL and LOOH is better for FMD impairment than LOOH alone in both PAPS and SAPS patients (AUC 0.727, p=0.001, 95% CI 0.616-0.837 and AUC 0.824, p˂0.001, 95% CI 0.690-0.957, respectively). Lipid peroxidation is independent predictor for endothelial dysfunction in APS patients. We demonstrated synergistic effect of aCL and LOOH as risk for endothelial impairment in both PAPS and SAPS patients.