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)

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

Antiphospholipid antibodies, that is, lupus anticoagulants and anticardiolipin antibodies, are associated with thrombosis and obstetric complications in the antiphospholipid syndrome. Venous thrombosis occurs mostly in the lower limbs, with or without pulmonary embolism, and cerebral ischemia and transient ischemic attacks are the most common arterial events. Overall, the prevalence of thrombosis is about 30%, the rate of first event approximates 1%/year, and that of recurrence of patients not receiving anticoagulation is about 10-29%/year. The presence of lupus anticoagulants carries an odds ratio for thrombosis ranging from 5 to 16, and that of anticardiolipin antibodies from nonsignificant to 18. The detection of anti-beta2-glycoprotein I, but not antiprothrombin, antibodies might also help to identify antiphospholipid-positive patients at risk of thrombosis. Unfractionated or low-molecular-weight heparin followed by oral anticoagulation represents the current treatment of both arterial and venous thrombosis. However, uncertainty still exists about the optimal duration and intensity of oral anticoagulation following the first event. Several therapeutic clinical trials are currently being conducted, which soon clarify these issues. The prevalence of obstetric complications is about 15-20%. The presence of lupus anticoagulants carries an odds ratio for recurrent miscarriages and fetal death ranging from 3.0 to 4.8, whereas that of anticardiolipin antibodies goes from 0.86 to 20. Unfractionated or low-molecular-weight heparin in combination with low-dose aspirin represents the current standard of treatment of pregnant antiphospholipid-positive women to prevent recurrent obstetric complications. Upon treatment, the live birth rate increases from 0-40% to 70-80%.
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PMID:Antiphospholipid antibodies and thrombosis: strength of association. 1276 50

Hypertension is known as a cause of endothelial cell damage and it activates humoral immunity. Therefore, it may modulate the anti-beta2-glycoprotein I antibody (abetaGPI) to commit for thrombosis. To elucidate the relation between abetaGPI and hypertension in cerebral ischemia, the blood abetaGPI level was examined in healthy subjects, hypertensive subjects, and patients with cerebral ischemia with and without hypertension, respectively. The results showed that the blood abetaGPI level increased in cerebral ischemia patients with hypertension rather than hypertensive subjects, and patients without hypertension rather than healthy individuals. However, the blood abetaGPI level showed no difference between healthy individuals and hypertensive subjects, nor cerebral ischemia patients with and without hypertension. The serum globulin level did not change among them. Therefore, abetaGPI displays a vital role for cerebral ischemia in both hypertensive and normotensive subjects. An activation of humoral immunity involving abetaGPI warrants further investigation in cerebral ischemia.
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PMID:Anti-beta2-Glycoprotein I antibody and hypertension in cerebral ischemia. 1497 6

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

Peripheral artery disease (PAD) is mostly related to atherosclerosis. Autoimmunity and, in particular, antibodies to cardiolipin (aCL) and phospholipid cofactors such as beta2-glycoprotein I (beta2-gpI) might influence the development of atheroma. Beta2-glycoprotein I (beta2-gpI) has been found in atheroma. It has previously been shown that immunoglobulin A (IgA) anti-beta2-gpI antibodies are associated with a risk of cerebral ischemia and myocardial infarction. This case control study aimed to determine whether elevated levels of aCL/anti-beta2-gpI antibodies are associated with a risk of symptomatic PAD (sPAD). Cases comprised a nonselected population of patients with sPAD (intermittent claudication or critical ischemia). Patient recruitment was based on arteriography changes. Controls were selected from patients admitted to orthopedic wards as a result of fractures or muscle-ligamentous disorders. Age, sex, race, hypertension, smoking, diabetes mellitus, and hypercholesterolemia were evaluated as risk factors in both groups. IgG/IgM/IgA aCL and anti-beta2-gpI were detected by enzyme-linked immunoabsorbant assays (ELISA). To estimate the grade of association of antibodies with sPAD, odds ratios (OR) were calculated. Logistic regression was utilized for adjustment of confounding factors. Seventy-seven cases and 93 controls were studied. The mean age was 61.5 years for cases and 47.5 years for controls (p <0.001). Among the risk factors evaluated, the presence of hypertension showed the strongest association with sPAD (OR 12.1; 95%CI 5.8-30). The presence of IgA anti-beta2-gpI was independently associated with sPAD (OR 5.4; 95%CI 1.8-15.8; p = 0.01). IgA aCL was strongly associated with the outcome (nonadjusted OR 11.5 after Agresti correction). IgA aCL and IgA anti-beta2-gpI antibodies were not associated with any known risk factors for sPAD or with arteriography changes. The occurrence of these autoantibodies might represent one of the links between autoimmunity and atherosclerosis in patients with sPAD.
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PMID:Autoantibodies to the atheroma component beta2-glycoprotein I and risk of symptomatic peripheral artery disease. 1762 83

Abnormal increases of antiphospholipid antibody and plasma homocysteine levels are recently emerging as nonlipidic risk factors for cerebral atherogenesis and thrombosis. Both antiphospholipid antibody and homocysteine share many similar bioeffects in hemostasis, but their interaction is still inconsistent. In this study, we examined the relation between the plasma homocysteine level and lupus anticoagulant, anticardiolipin antibody, and anti-beta2-glycoprotein I antibody in patients with noncardiac cerebral ischemia. Systemic lupus erythrematosus patients were excluded. The results showed a higher frequency of moderate hyperhomocysteinemia in patients with an abnormal increase of lupus anticoagulant only. Neither the serum folate and cobalamin levels nor methylenetetrahydrofolate reductase allele mutation contributes to this result. Accordingly, homocysteine interacts with lupus anticoagulant to promote cerebral atherosclerosis and ischemia. The role of vasculopathic or prothrombotic autoantibody generation in response to specific pathological change such as hyperhomocysteinemia warrants further investigation.
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PMID:Hyperhomocysteinemia relates to the subtype of antiphospholipid antibodies in non-SLE patients. 1791 Nov 91