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)

Prothrombin time (PT) is routinely used to monitor oral anticoagulant treatment in patients with the antiphospholipid antibody syndrome (APS). The fact that PT is a phospholipid (PL)-dependent coagulation test raises the possibility that lupus anticoagulant (LA) might interfere with this test, thus complicating the control of anticoagulant treatment. The effect of 6 affinity-purified preparations of anti- (a)beta2-glycoprotein I (GPI) antibodies with LA activity on the PT was tested. Instead of prolonging PT as expected, the abeta2-GPI antibodies reduced the PT of both normal plasma and anticoagulated plasma by a mean of 2.4 seconds and 5.6 seconds, respectively. This effect was also observed using other 5 commercially available preparations of thromboplastin. The abeta2-GPI-mediated reduction in PT was dose-dependent and was lost upon removal of beta2-GPI. The failure of abeta2-GPI antibodies to express LA activity in PT was found to depend on the fact that calcium ions were added together with PL at the beginning of the assay. In fact, modification of the standard diluted Russell viper venom time (dRVVT) test by adding calcium ions together with PL resulted in a loss of abeta2-GPI anticoagulant activity. The procoagulant effect was not as evident in an assay that used stimulated monocytes as a source of thromboplastin. These results show that abeta2-GPI antibodies exhibit an 'in vitro' procoagulant effect in PT and an anticoagulant effect in dRVVT only when the interaction with their antigen and PL occurs in the absence of calcium ions.
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PMID:Procoagulant effect of anti-beta2-glycoprotein I antibodies with lupus anticoagulant activity. 1057 96

Antiphospholipid antibodies (APAs) are considered risk factors in patients with thromboembolic diseases. Although the incidence of such acquired coagulation disturbances in adults are well described, only few data exist for children. Therefore, in a first step to collect new data we analyzed the presence of different APAs in 202 consecutive children and compared them with two groups of adults. The children screened for APA were exclusively those who did not have any thromboembolic complications or a tendency for thrombophilia due to other underlying diseases such as systemic lupus or malignancy in their past or present medical history. Consecutive blood samples were evaluated from routine laboratory specimens. The two groups of adults comprised 200 patients after deep vein thrombosis and 200 patients without thromboembolic events that served as controls. Four lupus anticoagulant (LA) screening tests were determined: the dilute Russell's viper venom test; a lupus anticoagulant-sensitive activated partial thromboplastin time reagent; a second lupus-sensitive activated partial thromboplastin time; and the Kaolin clotting time. Furthermore, three different antiphospholipid antibodies ELISA assays against cardiolipin (ACA), beta2-glycoprotein I, and phosphatidyl-serine, were determined. The children had a much higher prevalence for LA than did the adults. On the other hand, their values for ACA were significantly lower than in adults with a history of thromboembolism. Findings in children were similar to the normal adult group. This has to be taken into account when evaluating children with thromboembolic diseases.
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PMID:Antiphospholipid antibodies in children without and in adults with and without thrombophilia. 1129 Dec 89

We examined activated partial thromboplastin time, kaolin clotting time, mixing with normal plasma in kaolin clotting time, dilute Russell's viper venom time, dilute Russell's viper venom time at high lipid concentrations, anti-phospholipid antibodies, and anti-cardiolipin-beta2-glycoprotein I complex antibody in 135 patients with prolongation of activated partial thromboplastin time and diagnosed 86 patients positive for lupus anticoagulant. The sensitivity of activated partial thromboplastin time and dilute Russell's viper venom time/dilute Russell's viper venom time-high lipid concentrations ratio for lupus anticoagulant were markedly high, but the specificity of activated partial thromboplastin time for lupus anticoagulant was not markedly high. The specificity, but not the sensitivity, of kaolin clotting time-mixing with normal plasma in kaolin clotting time was markedly high. In summary, dilute Russell's viper venom time to dilute Russell's viper venom time-high lipid concentrations ratio gave high sensitivity as well as specificity, being the only assay to confirm this. Of the patients positive for lupus anticoagulant, 25% were positive for anti-phospholipid antibodies and 17% were positive for anti-cardiolipin-beta2-glycoprotein I complex antibody. Of the lupus anticoagulant-positive patients with thrombosis, 45% were positive for anti-phospholipid antibodies, 35% were positive for anti-cardiolipin-beta2-glycoprotein I complex antibody, 60% were positive for both anti-phospholipid antibodies and anti-cardiolipin-beta2-glycoprotein I complex antibody, and only 17% were negative for anti-phospholipid antibodies and anti-cardiolipin-beta2-glycoprotein I complex antibody. These findings suggest that lupus anticoagulant can be diagnosed by dilute Russell's viper venom time/dilute Russell's viper venom time-high lipid concentrations ratio, and that thrombosis in lupus anticoagulant-positive may be predictable from both anti-phospholipid antibodies and anti-cardiolipin-beta2-glycoprotein I complex antibody. Plasma tissue type plasminogen activator level in lupus anticoagulant patients was significantly increased, and plasma tissue type plasminogen activator and fibrin-D-dimer levels in lupus anticoagulant-positive patients with thrombosis were significantly higher than in those without thrombosis, suggesting that the diagnosis of thrombosis by hemostatic markers might be important in lupus anticoagulant.
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PMID:Coagulation tests and anti-phospholipid antibodies in patients positive for lupus anticoagulant. 1089 74

Anti-beta 2-glycoprotein I antibodies bind to endothelial cells through beta 2-GPI. The antibodies are present in patients with systemic lupus erythematosus and antiphospholipid syndrome and are associated with the pathogenesis of the disease. Anti-endothelial cell antibodies that react with constitutive antigens on ECs are present in patients with vasculiditis and other diseases. Both types of antibodies can activate ECs. Frequent findings in APLS and vasculitis are fibrin deposits and thromboembolic phenomena. These indicate that the coagulation system is activated. However, the mechanism of activation is not clear. ECs generate tissue factor upon stimulation with various substances. In the present study we report that monoclonal anti-beta 2-GPI antibodies and AECAs, derived from a patient with primary APLS and a patient with Takayasu's arteritis, respectively, induce a potent tissue factor in ECs. The production of TF activity, TF antigen and TF mRNA is dose and time dependent. The TF activity was induced also by F(ab)2 but not by Fc fragments and was abolished completely by pre-incubation with ant-TF antibodies. The TF that is induced in ECs by AECAs with and without beta 2-GPI specificity may activate the coagulation and thereby play a major role in the pathogenesis of fibrin deposition and thrombus formation in diseases that are associated with the presence of these antibodies.
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PMID:Anti-beta 2-glycoprotein I antibodies and anti-endothelial cell antibodies induce tissue factor in endothelial cells. 1090 14

An abnormal increase in anti-beta2-glycoprotein I antibodies (abeta2GPI) is capable of producing thrombosis and the vasculopathy-simulating antiphospholipid antibody (aPL). However, it is rarely described in cerebral ischemia without an association with aPL. The authors report a middle-aged man who experienced recurrent cerebral ischemia and diffuse cerebral stenosis without the apparent traditional cardiovascular risk factor. He was free of antiphospholipid/cofactor syndrome (APCS) and systemic lupus erythematosus (SLE). An increase of blood abeta2GPI was detected in serial measurements. The aPL, Venereal Disease Research Laboratory (VDRL) test, Coombs' test, and antinuclear factor were negative. Activated partial thromboplastin time was normal. This patient is a reminder to consider abeta2GPI in an unexplained recurrent cerebral thrombosis and cerebral artery stenosis even when the typical clinical manifestation or laboratory data of APCS is absent.
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PMID:An unusual increase of blood anti-beta 2-glycoprotein-I antibody but not antiphospholipid antibody in cerebral ischemia--a case report. 1122 90

The GAIT (Genetic Analysis of Idiopathic Thrombophilia) Project is a family-based study dedicated to elucidating the genetic basis of hemostasis-related phenotypes and thrombosis risk. In this paper, we have examined several lesser-studied hemostasis-related phenotypes in the 21 GAIT families: levels of vitamin B 12, serum folate, whole blood folate, alpha2-antiplasmin, prekallikrein, beta2-glycoprotein I, soluble P-selectin, factor XIII A and B subunits and a new coagulation measurement based on thromboplastin time in the presence or absence of thrombomodulin. Using the variance component method, we estimated the relative contributions of genetic and environmental influences on these phenotypes. In addition, we calculated the genetic correlations between thrombosis risk and each of these phenotypes. All 12 phenotypes showed significant genetic contributions with genes accounting for 22% to 78% of the variance after correction for covariate effects. Four phenotypes (three traits involving thromboplastin-thrombomodulin mediated coagulation time and serum folate) exhibited significant genetic correlations with thrombosis. Thus, some of the genes that influence quantitative variation in these physiological phenotypes also influence the risk of thrombosis. The high heritabilities and significant genetic correlations between thrombosis and some risk factors suggest that joint consideration of correlated quantitative phenotypes will aid in identifying susceptibility genes.
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PMID:Thromboplastin-thrombomodulin-mediated time and serum folate levels are genetically correlated with the risk of thromboembolic disease: results from the GAIT project. 1184 58

Nodular regenerative hyperplasia (NRH) of the liver is a local hyperplastic response of hepatocytes, probably due to vascular abnormalities. Since it was shown in a few case reports that NRH may be associated with antiphospholipid antibodies (APA) we wanted to analyze the relevance of APA in patients with this disease. Sera from 13 patients with histologically defined NRH were tested for APA by an in-house ELISA using as antigens cardiolipin (CL), beta2-glycoprotein I (beta2-gp I), phosphatidylserine (PS), and thromboplastin (TP), a mixture of different phospholipids and phospholipid-binding proteins. As controls, sera from patients with serologically and histologically defined autoimmune liver diseases (primary biliary cirrhosis n = 14; autoimmune hepatitis n = 14) without histological evidence for NRH as well as from 14 healthy blood donors were analyzed. 77% of the NRH patients had APA. In 46% they were directed against CL. In contrast, only 14% of the patients with autoimmune liver diseases and 14% of the healthy controls had anti-CL antibodies (p < 0,05). Antibodies to beta2-gp I and TP did not discriminate between NRH and autoimmune liver diseases. Anti-PS antibodies were not observed. These data indicate that determination of anti-CL antibodies in NRH may help to identify a subgroup of patients in whom an 'organ-specific antiphosholipid syndrome' of the liver may be involved in the pathogenesis.
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PMID:Nodular regenerative hyperplasia (NRH) of the liver--a manifestation of 'organ-specific antiphospholipid syndrome'? 1263 4

The role of humoral autoimmunity in virus-induced vascular thrombosis is still not clear. We encountered a patient who experienced cerebral ischemia in his early course of Japanese encephalitis. At the beginning, an increase of blood immunoglobulin G isotype of anti-beta2-glycoprotein I antibody, a prolonged activated partial thromboplastin time and thrombocytopenia resembling antiphospholipid antibody syndrome were found, and these abnormalities disappeared when the patient recovered later. A molecular mimicry between the T(2688)LRVLE in Japanese encephalitis virus and hexapeptide-TLRVYK may contribute for the patient's anti-beta2-glycoprotein I antibody generation. Therefore, an increase of procoagulative antibody, such as anti-beta2-glycoprotein I antibody, may display a crucial role for cerebral thrombosis associated with infectious pathogens such as Japanese encephalitis virus. The interaction between autoimmunity induction by infectious agents and procoagulation in the occurrence of vascular thrombosis may be more important than has been understood in previous studies.
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PMID:An increase of blood anti-beta2-glycoprotein I antibody in Japanese encephalitis associated with cerebral ischemia. 1565 May 47

A chemical worker working with urea-formaldehyde resin hazard for 20 years suffered cerebral ischemia in association with an increase of blood beta2-glycoprotein I-dependent anticardiolipin antibody (aCL)-IgG and IgM isotype, and a prolongation of activated partial thromboplastin time (aPTT). Major histocompatibility complex antigen showed DR4 positivity. On follow-up for over 6 years, aCL-IgG and aPTT decreased to reference range but aCL-IgM was still abnormally high despite a cessation of exposure. This patient highlights the induction of antibody-mediated thrombosis in chronic chemical exposure, especially in an individual with subclinical autoimmune disorder. The role of environment for coagulopathic vascular thrombosis is warranted for investigation.
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PMID:An increase of anticardiolipin antibody in association with stroke and chronic chemical exposure. 1670 28

Prothrombin (PT) is a target for antibodies with lupus anticoagulant (LA) activity. Anti-prothrombin antibodies (aPT) were recently identified as antibodies directed toward a phospholipid-binding protein. aPT are a new serologic marker of antiphospholipid syndrome. The objective was to detect aPT in a group of 46 patients with acute ischemic stroke in order to correlate their presence with clinical diagnosis, laboratory and neuroradiological findings. We tested aPT, lupus anticoagulant (LA), anticardiolipin (aCL), and anti-beta2-glycoprotein I antibodies (anti-bbeta2-GPI) in 46 young women with acute ischemic stroke aged 34-45 years and 43 patients with nonischemic neurologic diseases and 141 normal controls. Anti-prothrombin antibodies were detected by calcium-containing aPT ELISA, aCL and anti-beta2-GPI by ELISA. All samples were screened using the activated partial thromboplastin time (aPTT); the dilute Russell viper venous time (dRVV) coagulation test was performed. The results were statistically analyzed. Anti-prothrombin antibodies were found in 26 (57%) of 46 stroke patients. Out of 43 patients with nonischemic neurological disorders, 2 (4.18%) were positive for aPT. aPT were detected in one (0.70%) of the normal controls. Ten stroke patients (21%) were positive for IgG aPT only, 9 stroke patients (18.2%) for IgM aPT only, and 8 stroke patients (16.9%) for both IgG and IgM isotypes of aPT. Two nonischemic neurological disorders patients (4.18%) presented IgM isotype of aPT. Patients with ischemic stroke presented aPT much more frequently than the healthy controls (OR 182.00 [95% CI 23.382-1416.6]. p < 0.0001). Patients with ischemic stroke presented aPT much frequently than the nonischemic neurological disorders patients (OR 26.650 [95% CI 5.743-123.66], p < 0.0001). When IgG or IgM aPT were considered separately, they were more frequently found in patients with ischemic stroke than in healthy control group (OR 38.889 [95% CI 4.817-313.95], p < 0.0001) and (OR 34.054 [95% CI 4.178-277.5], p < 0.0001), respectively. Simultaneous positive titers for both isotypes of aPT (IgG and IgM) were more frequently found in patients with ischemic stroke than in healthy control group (OR 29.474 [95% CI 3.573-243.12], p < 0.0001). Eleven stroke patients (43%) were negative for aCL, LA and anti-beta2-GPI, but positive for aPT (OR 0.03287 [95% CI 0.001794-0.6022], p < 0.001). aCL, LA and anti-beta2-GPI were not found both in nonischemic neurological disorders patients and in healthy controls.
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PMID:Detecting anti-prothrombin antibodies in young women with acute ischemic stroke. 1948 Mar


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