Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02749 (beta2-glycoprotein I)
 836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antiphospholipid-protein antibodies (APA) include lupus-type anticoagulant (LA) and antibodies recognizing complexes of anionic phospholipids (e.g. cardiolipin) and proteins (e.g. prothrombin and beta2-glycoprotein I). The presence of APA is associated with an increased risk of both arterial and venous thrombosis. However, the pathogenic mechanism leading to thrombosis in patients with APA remains unclear. We studied 32 patients with systemic lupus erythematosus (SLE) who were divided into two groups depending on the presence (n = 19) or absence (n = 13) of APA. Healthy volunteers (n = 12) matched by age and sex served as controls. In all subjects LA and IgG class anticardiolipin antibodies (ACA) were determined. Thrombin generation was monitored ex vivo measuring fibrinopeptide A (FPA) and prothrombin fragment F1 + 2 (F1 + 2) in blood emerging from a skin microvasculature injury, collected at 30 second intervals. In subjects with antiphospholipid antibodies mean FPA and F1 + 2 concentrations were significantly higher at most blood sampling times than in controls. In some SLE patients with APA the process of thrombin generation was clearly disturbed and very high concentrations of fibrinopeptide A were detected already in the first samples collected. Two minutes after skin incision SLE patients without APA produced slightly more FPA, but not F1 + 2, as compared to healthy subjects. Mathematical model applied to analyze the thrombin generation kinetics revealed that APA patients generated significantly greater amounts of thrombin than healthy controls (p = 0.02 for either marker). In contrast, in the same patients generation of thrombin in recalcified plasma in vitro was delayed pointing to the role of endothelium in the phenomenon studied. In summary, these data show for the first time that in SLE patients with antiphospholipid-protein antibodies thrombin generation after small blood vessel injury is markedly increased. Enhanced thrombin generation might explain thrombotic tendency observed in these patients.
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PMID:Thrombin generation measured ex vivo following microvascular injury is increased in SLE patients with antiphospholipid-protein antibodies. 936 80

Anticoagulant activity is present in non-immunoglobulin (IgG) fractions from plasma of patients with antiphospholipid syndrome (APS). Plasma from six patients with primary or secondary APS was passed through a protein A sepharose 4B column. Anticoagulant activity in IgG samples and non-IgG samples was determined by both dilute aPTT based clotting assay and by dilute PT based clotting assay. Thrombin generation was determined by prothrombinase complex assay in the presence of IgG sample or non-IgG sample. Anticoagulant activity was detected in the IgG samples with the dilute aPTT based clotting assay and in non-IgG samples with the dilute PT based clotting assay. The activity was not detected in IgG samples with the dilute PT clotting assay. Forty percent of total thrombin generation was inhibited in the presence of non-IgG samples although thrombin generation was not inhibited in the presence of IgG samples and beta2-glycoprotein I. The anticoagulant activity detected by dilute PT based clotting assay and prothrombinase complex assay was non-IgG, phospholipid-Ca++-dependent and beta2-glycoprotein I-independent. The role of non-IgG anticoagulants should be determined as well as the role of LA Igs antibodies in the mechanisms of thrombosis.
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PMID:Anticoagulant activity in non-immunoglobulin fraction from plasma of patients with antiphospholipid syndrome. 983 16