Antiphospholipid antibodies are associated with increased levels of selected oxidative stress biomarkers.

BACKGROUND: Antiphospholipid antibodies (aPLs) are detected in 1-5% of the general population. They include lupus anticoagulant (LAC), anticardiolipin antibodies (aCL) and anti-β2-glycoprotein I antibodies (aβ2GPI). APL increases thrombotic risk, but the pathogenesis of this effect is not fully understood. OBJECTIVES: The aim of this study was to evaluate oxidative and nitrosative stress biomarkers and their relation to certain rotational thromboelastometry (ROTEM) parameters as a risk factor for thrombosis in 32 patients in whom the presence of antiphospholipid antibodies was confirmed, but who had never experienced a thrombosis event (Group 1) in order to rule out any impact of thrombosis on stress parameters. The parameters were also assessed in a group of 23 healthy volunteers (Group 2). METHODS: To assess FRAP and thiol groups we used colorimetric method. The level of protein carbonylation, total pool of 3-nitrotyrosine in plasma proteins, 3-nitrotyrosine-containing fibrinogen as well as the acetyl-lysine-containing fibrinogen were estimated by ELISA. Lipid hydroperoxides were detected using the ferric-xylenol orange hydroperoxide assay. Additionally four ROTEM tests, i.e. INTEM, EXTEM, FIBTEM and APTEM, were performed. In statistical analysis the Mann-Whitney U-test, Student's t-test and logistic regression were used. RESULTS: TBARS (p = 0,002), LOOH (p = 0,035) and carbonyl groups (p = 0,018) were markedly higher in Group 1 compared to Group 2. Also the acetyl-lysine-containing fibrinogen were significantly higher in Group 1 (p = 0,0028). Other biomarkers did not differ markedly between the studied groups. The obtained results of ROTEM, were not consistent and did not clearly indicate hypercoagulable state. CONCLUSION: Study confirms increased levels of oxidative biomarkers in patients in whom the presence of antiphospholipid antibodies was confirmed, but who had never experienced a thrombosis event. Oxidative stress may an important role in the pathogenesis of APS and is not secondary to thrombosis.