Effect of anti-beta 2glycoprotein I lupus anticoagulants on fibrin polymerization and fibrinolysis

Anti-beta 2-Glycoprotein I(beta 2GPI) antoantibodies are the prominent labo ratory feature of Hughes syndrome. By prolonging some coagulation tests in the presence of exogenous phospholipids (PL), they behave as classical Lupu s Anticoagulants (LA). We investigated the effect of 3 affinity-purified an ti-beta 2GPI IgG preparations from patients with Hughes syndrome on fibrin polymerization and fibrinolysis of normal plasma, measured by comparing the optical densities of assay mixtures in the presence of the autoantibodies or normal IgG. The presence of anti-beta 2GPI Ige in diluted Russell Viper Venom Time (dRVVT) assays, carried out using a PL dilution of 1 : 8 or 1 : 64, resulted in a delay in the onset of polymerization by 30-40 and 60-70 s , respectively. Fibrin polymerization was complete after 250 s for both ant i-beta 2GPI IgG and normal IgG, The inhibitory effect of the anti-beta 2GPI antibodies was not observed in the presence of excess FL, as expected for LA. Anti-beta 2GPI IgG increased the plateau level of polymerization when d RVVT was performed in the presence of 1.5nM recombinant tissue plasminogen activator, but did not impair the fibrinolytic process, which was almost co mplete after 250 min. The antoantibodies did not delay the onset of fibrin polymerization in tests carried out using recombinant tissue factor. On the contrary, the autoantibodies enhanced polymerization in prothrombin time a ssays, and accelerated it in tissue thromboplastin inhibition tests, with n o effect on fibrinolysis. These data provide evidence that anti-beta 2GPI L A may act as either anticoagulants or procoagulants in different in vitro c oagulation tests.