| Background:Systemic lupus erythematosus(SLE), primary antiphospholipid syndrome(APS) and systemic vasculitides are involvement of many important organ systems and cause of high mortality incidence.The pathologic finding of them occur throughout the body and are manifested by inflammation ,blood vessel abnormalities and thrombophilias that encompass bland vasculopathy and vasculitis, and immune-complex deposition. It is a predominate of antibodies due to vascular endothelial injury. Among of them , antiphospholipid antibodies are a heterogeneous group of antibodies and antiendothelial cell antibodies (AECA) may play a direct part in the pathophysiology of thrombosis, vasculitis and disease activity have gained increasing attention. Many of the autoantibodies associated of the aPL syndrome recognise certain phospholipids-binding plasma proteins, not phospholipids alone-ie, different autoantibodies have different effects. Thrombophilia is an important of pathophysiology in vasculitis associated of AECA. In general, mechanisms of autoautibodies-medi-ated thrombosis may be divided into two general types: (1) autoantibody interference with haemostatic reactions occurring onmembrane suefaces, and (2) autoantibody engagement of antigens on cell surfaces leading to transduction of a signal and altered cell activity. At present, SLE, APS and systemic vasculitides due to thrombosis is not clearly. It is not peculiar index that is supervised thrombophilia and disease activity in internal and external. In external, it is only now established autoantibody-mediated vascular endothelial injury model using thorough study of thrombosis.Objective:Through SLE, APS and various forms of vasculitis diseases activity and thrombosis in clinical and to determine the prevalence of antiphospholipid antibodies and AECA, To elucidate the role of these antibodies relationships with markers of disease activity and thrombosis, to establish monitored systemic of antibody test to use disease activity and thrombosis. At the base of this, to establish autoantibody-mediated vascular endothelial injury model using thorough study of thrombosis.Methods:1. Clinical evaluation on the patients who fulfilled the international10criteria of SLE,APS and various forms of vasculitis to find out the relationships between disease activity and thrombosis, also the relationships between the involved organs with the disease mortality.2. The sera of patients were screened for the presence of anticardiolipin antibodies(aCL), anti P 2-glycoprotein 1 antibodies(a(3 2GP1), antiprothrombin antibodies(aPT),antiplatelet GPIIb/lIIa antibodies(aIIb/IIIa) and lupus anticoagulants by using enzyme-linked immunosorbent assay(ELISA).3. Endothelial cells obtained from Human umbilical vein were cultured. The third passage was used and plated in 96-well microtitre plates, ELISAs for anti-endothelial cell antibodies(AECA) were performed. Also, AECA were detected by immunofluorescence using HUVEC as substrate. The APA positive sera of patients with SEE accompanying by thrombosis and the AECA positive sera of patients with Bechet's disease were screened. Then, the purified IgG was prepared by affinity chromatography using protein G columns. After that, HUVEC were incubated with these antibodies, and the proportion of apoptotic cells was detected by annexin V/PI double-staining by flow cytometry. Morphology of apoptotic Cells were observed by fluorescence staining.Result1. Disease activity in SLE with thrombotic events was significantly higher than the patients without thrombotic events.(t test, P<0.05). Compared with patients without thrombosis, pulmonary hypertension, elevation of Cholesterol and LDL, thrombocytopenia occurred more frequently in patients with thrombosis. Disease activity index such as ulceration of Oral and vulva, erythema nodosa,, fever, erythrocyte sedimentation rate ,C-reactive pr...
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