Anti-β2-glycoprotein I autoantibodies influence thrombin generation parameters via various mechanisms

AbstractIntroduction Antiphospholipid syndrome (APS) is a systemic autoimmune disease characterised by recurrent thrombotic events, pregnancy loss and thrombocytopenia the presence of antiphospholipid antibodies (APL). The exact pathomechanism APS still unknown, thus we investigated effect anti-β2-glycoprotein I (anti-β2GPI) on thrombin generation in different plasma samples. Methods For separation anti-β2GPI IgG, overall 12 patients were selected. criteria existence lupus anticoagulant, anti-CL anti-β2GPI, latter exceeding at least 25 times upper reference limit. We purified IgG from affinity chromatography added to normal pooled, heterozygous forms inherited thrombophilia samples (prothrombin G20210A, factor V Leiden). To further specify mechanism effect, also used deficient plasmas assay. Results In pooled plasma, significantly prolonged Lag Time according anticoagulant contrast, it elevated Peak Thrombin significantly, which suggests procoagulant effect. antibody was able exert this multi-faceted both FVLeiden prothrombin G20210A polymorphism, however, prolonging more remarkable latter. By using plasmas, found that FVII required for prolongation, while intrinsic factors are needed elevation Thrombin. Conclusion autoantibodies their thrombophilic via various mechanisms.