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)

The purpose of this study was to determine the association between beta 2-glycoprotein I (beta 2GPI)-dependent anticardiolipin antibodies (aCL) and beta 2GPI-independent aCL and their respective relevance to adverse pregnancy outcomes. Therefore, we prospectively studied 210 normal pregnant women, utilizing a modified enzyme-linked immunosorbent assay method for beta 2GPI-dependent and -independent aCL. Seven of the 210 pregnant women (3.3%) demonstrated evidence for beta 2GPI-independent immunoglobulin G (IgG)-aCL. Two patients, who also appeared positive for beta 2GPI-dependent IgG-aCL, were proven to be false positives. Amongst the 210 patients, not one was thus positive for beta 2GPI-dependent aCL. Women with beta 2GPI-independent aCL demonstrated no adverse pregnancy outcomes. These results suggest that the presence of beta 2GPI-independent aCL is not associated with the presence of beta 2GPI-dependent aCL, though it may give rise to false positive results. Since the presence of beta 2GPI-independent aCL does not appear to be associated with adverse pregnancy outcomes, beta 2GPI-dependent assays may represent better markers of miscarriage risk.
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PMID:beta 2-Glycoprotein I-dependent and -independent anticardiolipin antibodies in healthy pregnant women. 784 14

The present study was conducted to elucidate the clinical significance of autoantibodies in infertility. Among 203 cases of infertility, 27 cases (A group) were positive for antinuclear antibodies (ANA), and 18 cases (B group) were positive for antiphospholipid antibodies (APA) regardless of the presence of ANA. The progress of pregnancy over time in the study period was clarified in 13 cases in A group and 12 cases in B group. Although only luteal support was given to the A group, appropriate for gestational age babies were obtained in all cases except 3 cases in which there occurred early abortion. In B group, babies were obtained successfully in 8 cases by steroid-aspirin therapy, but intrauterine fetal death occurred in the second trimester in 2 cases, and in the other 2 cases early abortion occurred. In cases positive for the antibody (beta 2(-)ACA) to cardiolipin, fetal distress did not occur in any of the 3 cases. On the other hand, in cases positive for the antibody (beta 2(+)ACA) to the cardiolipin-beta 2-glycoprotein I complex and/or lupus anticoagulant (LA), marked fetal distress occurred in all except one of the 7 cases. In conclusion, there was little correlation between ANA, beta 2(-)ACA and infertility, suggesting that the cause of infertility is the induction of placental circulating disorder by beta 2(+)ACA and LA.
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PMID:[Effect of autoantibodies on women with infertility]. 784 38

Recent evidence suggests that lupus anticoagulants are immunologically distinct from the anticardiolipin antibodies. Nevertheless, the associated clinical complications exhibited by the two groups of antibodies are similar. They have been shown to have a strong association with a history of arterial and venous thrombosis, thrombocytopenia and neurological disease in patients with SLE or lupus-like disorders. The association between antiphospholipid antibodies and recurrent fetal loss is suggested by the currently available data but is not firmly established. Patients with lupus and antiphospholipid antibodies and an established history of recurrent fetal wastage are at high risk for experiencing subsequent fetal loss, but it is not yet known whether the same is true for patients without a history of fetal loss. The association of thrombosis, neurological disease, thrombocytopenia, and fetal loss in patients with non-SLE disorders has not been as extensively studied. Only recently have investigators such as Ginsberg and colleagues begun to show in prospective studies that there may, in fact, be a statistically significant risk of thrombotic events in otherwise healthy individuals with antiphospholipid antibodies. Many of the diverse minor manifestations reported in individual patients, case series, or cross-sectional studies such as livedo reticularis, leg ulcers, and hemolytic anemia may, alternatively, be due to coincidence or chance. Efforts to elucidate the mechanisms of thrombosis in patients with antiphospholipid antibodies is an area of active research. Most efforts have been based on the effects of these antibodies on endothelial cell and platelet function as well as on the fibrinolytic system. In addition, it has recently been shown that binding of antiphospholipid antibodies to phospholipids requires the serum "co-factor" beta 2-glycoprotein I. In patients with SLE selected for the presence of the lupus anticoagulant, thrombosis, or fetal loss, Viard and associates found that 17 of 47 (36%) patients had anti-beta 2-glycoprotein I antibodies. They were able to show, in their small retrospective study, that there was an association between the presence of these antibodies and anticardiolipin activity, lupus anticoagulant activity, and thrombotic events, but not with spontaneous abortion. Of patients with SLE and thrombosis (9 of 47) eight of nine were positive for anti-beta 2-glycoprotein I antibodies, seven of nine were positive for anticardiolipin antibodies, and eight of nine were positive for the lupus anticoagulant. The known inhibitory effect of beta 2-glycoprotein I on platelet aggregation, on platelet prothrombinase activity, and on the intrinsic pathway of coagulation supports the hypothesis that implicates beta 2-glycoprotein I in the pathogenesis of unwanted thrombotic events.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinical syndromes associated with lupus anticoagulants. 805 30

In some individuals, the presence of antibodies to negatively charged phospholipids, currently measured as the lupus anticoagulant, and anticardiolipin antibodies is associated with certain clinical features, particularly a predisposition to both arterial and venous thromboses, thrombocytopenia, and spontaneous abortion. This syndrome is seen in patients with systemic lupus erythematosus (SLE). However, methods for measuring anticardiolipin antibody, especially epitope of anticardiolipin antibody which is not considered cardiolipin itself, but rather a complex of cardiolipin and beta 2-glycoprotein I are not well defined. Although many hypotheses have been proposed to explain the relation between antiphospholipid antibodies and thrombosis, the pathogenesis of thrombosis remains unclear. In this article, some problems in assaying anticardiolipin antibody, characteristics of antiphospholipid antibodies and the clinical significance of these antibodies are reviewed and discussed.
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PMID:[Assay of anticardiolipin antibodies and its clinical significance]. 837 1

The pathogenesis of the antiphospholipid syndrome remains uncertain. Antibodies that react with phospholipids may not be directly responsible for cellular injury, but may be part of the immune network through which autoantibodies with pathogenic potential are generated. The latter may recognize proteins such as beta 2-glycoprotein I that form complexes with phospholipids, proteins whose functions depend upon interaction with phospholipids such as protein C and its cofactors, altered lipoproteins such as oxidized low-density lipoproteins, or other molecules that share only antigenic similarity. Thus, a spectrum of autoantibodies that recognize different lipid-protein complexes may develop in these patients and contribute to the observed clinical heterogeneity of the syndrome. Current techniques do not permit identification of the subset of patients with antiphospholipid antibodies at risk for thrombosis or abortion and there are no prospective, controlled trials addressing the prophylaxis or treatment of affected individuals. Identification of the cellular targets of antibodies to lipid-protein moieties is needed to identify patients at risk for these complications and as a means to monitor therapy.
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PMID:The antiphospholipid-protein syndrome. 861 97

There has been a recent, dramatic surge in interest in antiphospholipid antibodies and associated clinical disorders, especially focal ischemic cerebrovascular disease. Antiphospholipid antibodies are a heterogeneous group of antibodies with varying specificities. Coagulation assays will detect lupus anticoagulants while enzyme-linked immunosorbent assays detect anticardiolipin antibodies. There are numerous potential links between antiphospholipid antibodies and coagulation disorders, including interaction of antiphospholipid antibodies and a cofactor, beta 2-glycoprotein I, which itself is involved in coagulation mechanisms. While the specific mechanism of antiphospholipid antibody-related coagulopathy is unknown, it is clear that antiphospholipid antibodies are associated with an immune-mediated prothrombotic state. Patients with the highest titers of IgG antiphospholipid antibodies have a relatively high risk of recurrent thrombotic events, especially stroke, deep venous thrombosis, and spontaneous abortion. Because of limited controlled, prospective data, current therapy remains empiric and directed at coagulation mechanisms, immune mechanisms, or both.
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PMID:Cerebrovascular disease with antiphospholipid antibodies: immune mechanisms, significance, and therapeutic options. 896 22

Antiphospholipid antibodies are a wide ranging, heterogeneous family of autoantibodies, formerly believed to be directed to anionic phospholipids. Recent research, however, has confirmed that they are directed to plasma proteins bound to suitable (phospholipid) anionic surfaces. The most well-known and best characterized antigens are beta 2-glycoprotein I, recognized by anticardiolipin antibodies, and prothrombin, recognized by most lupus anticoagulants. Lupus anticoagulants are generally identified on the basis of their capacity to prolong the phospholipid-dependent coagulation tests. Two types of lupus anticoagulants, anticardiolipin-type A, and antiprothrombin antibodies, whose presence is associated with different coagulation profiles, have been identified. Anticardiolipin-type A and antiprothrombin antibodies may be detected also by specific immunoassays. The capacity of several methodologies to detect antiphospholipid antibodies reflects chiefly their immunological and functional heterogeneity. Since most of the laboratory methods have not yet been standardized, the results of studies on the clinical relevance of antiphospholipid antibodies must be analyzed with caution. The association between antiphospholipid antibodies with peculiar clinical manifestations such as venous and arterial thrombosis, recurrent miscarriage, and thrombocytopenia, characterizes the so-called "antiphospholipid syndrome". Retrospective and cross-sectional studies have confirmed the role of anticardiolipin antibodies and lupus anticoagulants as risk factors for both venous and arterial thrombosis, the most common clinical manifestations of the antiphospholipid syndrome. Prospective studies performed in different patient populations have confirmed the association between anticardiolipin antibodies and lupus anticoagulants with venous, and possibly, arterial thrombosis, although information on the predictive value of the various laboratory tests with respect to thrombosis is still limited. It is hoped that the development and standardization of assays that selectively identify antiphospholipid antibodies associated with increased risk of thrombosis will lead to therapeutic strategies able to prevent thromboembolic complications of the antiphospholipid syndrome.
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PMID:[Clinical significance and predictive value of laboratory tests in thrombosis associated with antiphospolipid antibodies]. 933 16

We report a 40-year-old Japanese woman with antiphospholipid antibody syndrome (APS) associated with myasthenia gravis (MG). She had a history of miscarriage at the age of 27 followed by pulmonary embolism 3 weeks later. At the age of 40, she developed diplopia, bilateral ptosis and easy fatigability. Serum anti-acetylcholine receptor antibody and tensilon test were positive. She was diagnosed as having MG. The laboratory test revealed mild thrombocytopenia, prolonged activated partial thromboplastin time (aPTT) and positive findings for both beta 2-glycoprotein I-dependent anticardiolipin antibody and lupus anticoagulant. She fulfilled the diagnostic criteria of APS, but did not the criteria proposed by American Rheumatism Association for SLE. An extended total thymectomy was performed after administration of oral prednisolone and low-dose aspirin. This is a patient who had APS associated with MGs: both are known to result from autoimmune abnormality. The clinical and laboratory manifestations of APS were ameliorated after removal of the thymus, suggesting that thymectomy alleviates APS symptoms.
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PMID:[A case of antiphospholipid syndrome associated with myasthenia gravis]. 939 64

The objective of this study was to assess the clinical significance of autoimmune anticardiolipin antibody that can react with cardiolipin only in the presence of beta2-glycoprotein I (beta2-glycoprotein I-dependent anticardiolipin antibody) in the pathogenesis of early recurrent abortion. A total of 72 early recurrent spontaneous aborters and 175 normal healthy women were analysed for the occurrence of beta2-glycoprotein I-dependent anticardiolipin antibody in serum samples by an enzyme-linked immunosorbent assay specific for the detection of beta2-glycoprotein I-dependent anticardiolipin antibody. The incidence of beta2-glycoprotein I-dependent anticardiolipin antibody in the early recurrent spontaneous aborters was essentially the same as that of normal women. Thus, the beta2-glycoprotein I-dependent anticardiolipin antibody seemed to have little, if any, implication in the pathogenesis of early recurrent spontaneous abortion.
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PMID:Beta2-glycoprotein I-dependent anticardiolipin antibody in early recurrent spontaneous abortion. 974 Apr 73

The authors have determined the prevalence of antibodies of cofactor dependent anticardiolipin and beta 2-glycoprotein I and lupus anticoagulant and the frequency of false positive VDRL test in systemic lupus erythematosus. The aim of this retrospective study was to assess the presence of these antibodies and symptoms of antiphospholipid syndrome. The serum samples were examined by modified ELISA method for detecting of cofactor dependent anticardiolipin. The antibodies to beta 2-glycoprotein I were examined by ELISA. The lupus anticoagulant and VDRL test were performed by routine laboratory method. The authors have found that 19 of 58 patients with systemic lupus erythematosus had cofactor dependent anticardiolipin, 10 patients had antibodies to beta 2-glycoprotein I and 4 patients had positive VDRL test. 5 of 34 plasma samples were lupus anticoagulant positive. 19 patients with systemic lupus erythematosus had 14 neuropsychiatric disorders, 9 cardiovascular diseases, 7 thrombocytopenia, 6 histories of recurrent abortion and fetal loss, 5 livedo reticularis and 3 thromboembolic events in all of them had detected antibodies to cofactor dependent anticardiolipin, while these complications were diagnosed in 39 anticardiolipin negative patients much more rarely. The results of this retrospective study suggest that significant association exists between the presence of cofactor dependent anticardiolipin and symptoms of antiphospholipid syndrome in systemic lupus erythematosus.
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PMID:[Clinical significance of antiphospholipid autoantibodies in lupus erythematosus]. 979 52


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