Anti-phospholipid antibodies are directed against a complex antigen that includes a lipid-binding inhibitor of coagulation: beta 2-glycoprotein I (apolipoprotein H).
In systemic lupus erythematosus (SLE), various forms of vascular lesions develop, in some of which microthrombosis is demonstrated histopathologically. These vascular changes have been considered to be induced by an immune complex, especially by denatured DNA and antiDNA complex, followed by complement activation and vascular injury . It has also been reported that these vascular lesions develop in close association with antiphospholipid (PL) antibodies (aPLAs) which may cross-react with a single-strand DNA, cardiolipin or the epitopes which are responsible for lupus anticoagulant activity . The term antiphospholipid syndrome has been applied to this condition, including SLE and other connective tissue diseases. Thrombocytopenia, thrombosis and recurrent fetal loss are considered to be major clinical manifestations of this syndrome . It has been suggested that the pathogenic mechanisms underlying thrombosis in these conditions are as follows: inhibition of PGI2 synthesis from vascular endothelial cells , stimulation of thromboxane A2 synthesis by platelets , inhibition of antithrombin III or thrombomodulin/protein C in the coagulation system , or inhibition of beta2-glycoprotein I (apolipoprotein H) which is a cofactor for cardiolipin and interferes with the coagulation pathway . All of these mechanisms are the targets of aPLAs, and result in platelet aggregation. However, their precise interaction with platelet membranous PLs remains unclear. Therefore, in this study, we investigated the reaction pattern of aPLA-positive sera from SLE patients using a solvent-extracted platelet lipid fraction on thin layer chromatography (TLC) plates. Serum was obtained from 18 patients by venopuncture at their first visit and stored at 2 0 ~ until use. Clinically, these patients had developed four types of vascular lesions in which microthrombotic lesions were demonstrated histopathologically (Table 1). Control sera were