Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thromboembolism is a well-known complication of the hypercoagulable state associated with antiphospholipid (aPL) antibodies. Acute respiratory failure (ARF) with diffuse pulmonary infiltrates has been reported in only a few patients with aPL antibodies. We describe a 49 year old patient with spiking fever, livedo reticularis, mild haemoptysis and ARF. Chest radiography revealed diffuse bilateral pulmonary infiltrates, and high resolution computed tomography (CT) revealed patchy distribution of areas of ground-glass attenuations. Pulmonary emboli were excluded with angiography. Lung biopsy revealed diffuse microvascular thrombosis, without capillaritis. High serum levels of anticardiolipin (aCL) antibodies were found. The patient's condition improved dramatically after intravenous infection of 1 g methylprednisolone on three consecutive days, followed by 50 mg prednisone orally. The rapid improvement following the administration of glucocorticosteroids suggests that anticardiolipin associated microvascular thrombosis, without inflammatory lesions, may depend on an interference with beta2-glycoprotein I (beta2=GPI) by anticardiolipin.
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PMID:Diffuse microvascular pulmonary thrombosis associated with primary antiphospholipid antibody syndrome. 907 75

Antibodies against phospholipid-binding plasma proteins, such as beta2-glycoprotein I (beta2-GPI) and prothrombin, are associated with thromboembolic events in patients with systemic lupus erythematosus and also in subjects with no evident underlying diseases. We wanted to examine whether increased levels of antibodies to negatively-charged phospholipids (cardiolipin), to phospholipid-binding plasma proteins beta2-GPI and prothrombin and to oxidised low-density lipoprotein (LDL) were associated with risk of deep venous thrombosis or pulmonary embolism in subjects with no previous thrombosis. The antibodies were measured in stored serum samples from 265 cases of deep venous thrombosis of the lower extremity or pulmonary embolism occurring during a median follow-up of about 7 years and from 265 individually matched controls. The study subjects were middle-aged men participating in a cancer prevention trial of alpha-tocopherol and beta-carotene and the cases of thromboembolic events were identified from nationwide Hospital Discharge Register. The risk for thrombotic events was significantly increased only in relation to antiprothrombin antibodies. As adjusted for body mass index, number of daily cigarettes and history of chronic bronchitis, myocardial infarction and heart failure at baseline, the odds ratio per one unit of antibody was 6.56 (95% confidence interval 1.73-25.0). The seven highest individual optical density-unit values of antiprothrombin antibodies were all confined to subjects with thromboembolic episodes. In conclusion, the present nested case-control study showed that high autoantibody levels against prothrombin implied a risk of deep venous thrombosis and pulmonary embolism and could be involved in the development of the thrombotic processes.
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PMID:High antibody levels to prothrombin imply a risk of deep venous thrombosis and pulmonary embolism in middle-aged men--a nested case-control study. 936 81

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

We studied the prognostic significance of antiphospholipid antibodies for recurrence of venous thromboembolism (VTE), in 71 patients admitted for acute VTE (deep-vein thrombosis or pulmonary embolism) in a single internal medicine unit. Lupus anticoagulant (LA), antibodies directed against beta 2-glycoprotein I (beta 2GPI) and antibodies against both beta 2GPI and a mixture of phospholipids (cardiolipin, phosphatidylserine and phosphatidic acid) (APAs) were measured. The patients were followed-up (mean 4.9 years) to determine the time to the next VTE. We found LA in nine patients, anti-beta 2GPI antibodies in seven patients and APAs in six patients. The cumulative risk of recurring VTE was higher in patients with beta 2GPI-binding antibodies (hazard ratio 12.6, 95% CI 1.5-104.9; p = 0.0029). The risk associated with APAs was 11.5 (95% CI 1.3-98.9; p = 0.0049) and that for LA was 3.7 (95% CI 0.9-15.6; p = 0.055). The risk of VTE recurring was higher both in patients with antibodies directed against beta 2GPI, and in patients with antibodies directed against beta 2GPI and a mixture of phospholipids, than in patients without these antibodies.
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PMID:Antibodies against phospholipids and beta 2-glycoprotein I increase the risk of recurrent venous thromboembolism in patients without systemic lupus erythematosus. 957 94

To establish the prevalence of antibodies against beta2-glycoprotein I (beta2GPI) in unselected patients with venous thromboembolism, as well as the association with antiphospholipid antibodies (aPL) and a history of previous thromboembolism, we investigated the presence of these antibodies in 227 consecutive patients with acute deep vein thrombosis or pulmonary embolism, of whom 63 were carriers of aPL with or without lupus anticoagulant (LA), and seven were carriers of LA alone. The presence of antibodies against beta2GPI was demonstrated in 19 patients [8.4%; 95% confidence interval (CI), 4.5-11.3%]. All of them belonged to the group of 63 patients with aPL (30.2%). A history of a previous thromboembolism was identified in 11 of the 19 patients with anti-beta2GPI antibodies (57.9%) and in 45 of the 208 patients without these antibodies [21.6%; odds ratio (OR)=4.98; 95% CI, 1.89-13.1; p<0.0005]. In the subgroup of patients with aPL and/or LA, the rate of recurrent thromboembolism among patients with anti-beta2GPI antibodies (11 of 19, 57.9%) was significantly higher than that observed in patients without these antibodies (15 of 51, 29.4%; OR=3.3; 95% CI, 1.1-9.83; p=0.28). We conclude that in patients with acute venous thromboembolism the prevalence of antibodies against beta2GPI is unexpectedly high. The presence of these antibodies seems to identify a subgroup of patients with antiphospholipid antibodies who have a peculiarly high risk of thrombotic recurrences. Further prospective studies are indicated to better define the role of anti-beta2GPI antibodies in the development of recurrent thromboembolism.
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PMID:Anti-beta2-glycoprotein I antibodies in patients with acute venous thromboembolism: prevalence and association with recurrent thromboembolism. 1059 29

Anti-beta2-glycoprotein I antibodies are considered as a specific marker for the antiphospholipid syndrome. In contrast to lupus circulating anticoagulant and anticardiolipin (aCL) antibodies, they are usually not found at significant levels in infections. We report a case of pulmonary embolism in an adult with varicella. Transient significant levels of aCL antibodies and of IgM anti-beta2-GPI antibodies were observed. No other prothrombotic factor, including free protein S antigen deficiency, was found. The direct pathogenic role of these transient antibodies on the thrombotic event may then be suspected. They are probably associated with VZV acute infection and are absent two months after varicella.
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PMID:Pulmonary embolism and transitory anti-beta2-GPI antibodies in an adult with chicken pox. 1103 26

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

The antiphospholipid syndrome is a relatively common acquired cause of venous thrombosis. Up to 20% of cases of deep vein thrombosis, with and without pulmonary embolism, may be associated with antiphospholipid antibodies. These antibodies are typically detected in lupus anticoagulant assays and tests for anticardiolipin antibodies. Most antiphospholipid antibodies are directed against several phospholipid-binding plasma proteins. The most common antigens are beta2-glycoprotein I and prothrombin. Immunoassays using these purified antigens are now available. In addition to being markers for thrombotic risk, antiphospholipid antibodies have been shown to directly contribute to hypercoagulability in animal models and in various in vitro studies. Prevention of recurrent venous thrombosis in patients with the antiphospholipid syndrome requires long-term anticoagulation. The optimal intensity of warfarin therapy is an ongoing issue, but most clinicians currently favor a target INR in the 2.0 to 3.0 range. In certain patients, antiphospholipid antibodies may interfere with determination of the INR, requiring other approaches to monitor and adjust the warfarin dose. Low-dose aspirin is typically recommended for primary prevention of thrombosis in asymptomatic patients with moderate to high levels of antiphospholipid antibodies, although strong supporting data are lacking.
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PMID:Venous thrombosis in the antiphospholipid syndrome. 1922 5

A 67-year-old woman was admitted to the hospital for lethargy, fever, hemolytic anemia, thrombocytopenia, and consciousness disturbance. Direct Coombs test was positive, and anti-cardiolipin beta2-glycoprotein I antibody was detected. She was diagnosed with antiphospholipid syndrome complicated with autoimmune hemolytic anemia (AIHA). She demonstrated variable consciousness disturbance, inability to distinguish right from left, dysgraphia and dyscalculia. Multiple cerebral infarctions, especially dominant cerebral hemisphere infarctions, were observed on magnetic resonance imaging. A ventilation-perfusion scan demonstrated the presence of a ventilation-perfusion mismatch in both lung fields, and multiple veinous embolisms in the right femoral, bilateral the great saphenous and popliteal veins. Therefore, pulmonary embolism and thrombophlebitis were diagnosed. Based on these findings, it was necessary to distinguish this diagnosis from thrombotic thrombocytopenic purpura (TTP). As ADAMTS-13 activity was within the normal range, TTP was denied. Thereafter, the patient was treated with 1 mg/kg of prednisolone for AIHA, 3 mg of warfarin, and 3500 units of low-molecular-weight heparin for thrombosis, and her condition improved.
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PMID:[Antiphospholipid syndrome with autoimmune hemolytic anemia which mimics thrombotic thrombocytopenic purpura]. 2046 25