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)

The association of anticardiolipin antibodies (aCL) with unexplained vascular occlusive disease (VOD) is well known. We reviewed the records of 102 consecutive patients seen over a 9 months period who had positive IgG or IgM aCL to determine the frequency and types of VOD in this unselected group of patients. Lupus anticoagulant was detectable in 17 of 67 (25%) patients tested. VOD occurred in 80 of 102 (78%) aCL-positive patients comprised of 17 (16.7%) with systemic venous VOD or pulmonary embolism; 27 (26.5%) with cerebral VOD: 11 (10.8%) with systemic arterial VOD; 3 (2.9%) with coronary thrombosis; and 5 (4.9%) with visceral venous or arterial VOD. Of the 19 obstetric patients with positive aCL, 17 (89%) had at least one unexplained fetal loss and 8 of the 17 (47%) had multiple or recurrent fetal losses. Twelve (11.7%) of the 102 patients met the ACR criteria for systemic lupus erythematosus (SLE). Additionally, 12 (11.7%) patients were identified as nonSLE or undifferentiated connective tissue disease (CTD). The remaining 78 (76%) had no known underlying disease (primary antiphospholipid syndrome). We conclude that IgG and IgM aCL with or without lupus anticoagulant are associated with diverse types of VOD but cerebral VOD appears predominant. aCL-associated unexplained VOD occurs frequently in patients without evidence of CTD-65 of 80 (81%) in our series. Testing for aCL is essential for identifying patients with unexplained VOD, and it should be performed in prospective clinical studies of such patients to better define the pathogenic role of aCL in the natural history of unexplained VOD.
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PMID:The prevalence of vascular occlusive disease associated with antiphospholipid syndromes. 152 53

Thromboembolic events occur with a frequency of 3-5% in children with nephrotic syndrome (NS). Although numerous abnormalities in all phases of coagulation have been described in NS, the pathogenesis of clotting abnormalities remains poorly understood in this group of patients. We describe a child with long-standing NS in whom a severe deep venous thrombosis and pulmonary embolism secondary to acquired protein S deficiency and a strong lupus-type circulating anticoagulant developed. In addition, this patient had a markedly decreased plasma level of C4b binding protein. Although acquired protein S deficiency has been described in various clinical disorders including NS, our patient is unusual in having C4bBP deficiency, and his is the only reported pediatric case of NS complicated by thromboembolism in which a circulating anticoagulant has been implicated, to our knowledge.
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PMID:Deep venous thrombosis in a child with nephrotic syndrome associated with a circulating anticoagulant and acquired protein S deficiency. 183 4

Pulmonary hypertension due to recurrent thromboembolism is a rare disease but life-threatening. We evaluated 18 patients (11 female, 7 male) with this pathology between 1973 and 1991. We compared clinical features and evolution of our patients with the ones of the literature. The mean interval between beginning of symptoms and diagnosis was 5 years (range 1-10 years) and the most frequent symptom was increasing dyspnoea. In 2 of our patients there were well definite predisposing causes for thromboembolism (intracardiac catheters), 6 of the others had a previous episode of acute pulmonary embolism. Mean pulmonary arterial pressure was 50 mmHg and low output was present in 8 of these. Lung perfusion scintigraphy was diagnostic in 98% of cases showing segmental defects and pulmonary angiography confirms diagnosis revealing abrupt cut-off of cases showing segmental defects and pulmonary angiography confirms diagnosis revealing abrupt cut-off a major pulmonary artery. Angiographic evaluation of thrombus extent and location was difficult. In a small number of patients was found lupus anticoagulant, deficiency of protein C, of protein S and of antithrombin III. Mortality in medical treatment was 39% at a mean follow-up of 4-5 years. Progression of pulmonary hypertension was due to recurrent pulmonary embolism only in 30-40% of cases. The role of caval filter is not well established. Thromboendarterectomy shows immediate good results at short time but the long-term results are not known.
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PMID:[Thromboembolic pulmonary hypertension]. 184 71

Nonspecific pleuritis, i.e., inflammation of the visceral pleura, is recognized by the presence of pleural strands on the routine posteroanterior chest radiograph. The computed tomograph counterparts of these strands are seen as interlobular septal intrusions and lenticular or wedge-shaped subpleural opacities. The pleural reaction is nonspecific and may be found with asbestos exposure, traumatic hemorrhagic effusions, pulmonary embolism, viral pleurisy, malignant pleural effusions, and lupus or rheumatoid effusions. The asbestos-related pleural changes may be found alone or in association with parietal pleural plaque formation or with asbestotic lung fibrosis.
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PMID:Inflammation of the visceral pleura, a nonspecific asbestos-related pleural reaction: chest radiograph and computed tomograph correlation. 186 17

A retrospective study was undertaken of 120 children with systemic lupus erythematosus (SLE) seen in Paris and its immediate suburbs who fulfilled at least four of the American College of Rheumatology diagnostic criteria for SLE, and in whom the disease was diagnosed before the age of 16 and between January 1975 and December 1987. Eleven of these children (eight girls and three boys) all more than 10 years of age (mean follow up 8.1 years; range 3-13) had thrombotic episodes (9%). Thrombosis was one of the presenting signs in seven patients; in five it was associated with typical symptoms of SLE, and in the other two the thrombotic episode was isolated and diagnosis of SLE was delayed one and three years. Of a total of 16 thrombotic episodes (six of which were recurrent), 14 involved the leg veins, and in four there was associated pulmonary embolism. There were two episodes that affected cerebral arteries. The American College of Rheumatology diagnostic criteria for SLE as well as the incidence of lupus anticoagulant, positive direct Coombs test, and vasculitis in this group of patients was compared with the incidence in patients with SLE but no thrombosis. Only lupus anticoagulant was significantly associated with thrombotic episodes: eight of 11 (73%) of patients with SLE and thrombotic (arterial or venous) episodes had lupus anticoagulant compared with only 10 of 74 patients (14%) with no history of thrombotic events in the same age group.
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PMID:Thrombosis in systemic lupus erythematosus: a French collaborative study. 190 23

A young man who had suffered several episodes of deep-vein thrombosis of the legs since the age of 20 had a myocardial infarction at the age of 33, at which time both a prolonged partial thromboplastin time (PTT), compatible with a lupus anticoagulant (LA), and decreased fibrinolytic capacity (FC) were found. His sister presented with deep-vein thrombosis of a leg and subsequent pulmonary embolism when she was 18 years old. She had a miscarriage three years later and developed a hemolytic-uremic syndrome at the age of 35. The PT and FC were normal. Laboratory investigations of the parents revealed positive antinuclear antibodies in the mother's serum but no anomaly in the father. This study suggests a familial tendency to develop autoimmune disorders associated with LA and thromboembolic complications related to decreased FC.
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PMID:Different clinical presentations of a lupus anticoagulant in the same family. 190 97

The radiological manifestations of asbestos-related visceral pleural changes are described. Generally, visceral pleural reactions follow the mesothelial cells response to various injurious substances, including asbestos, and even saline. The changes are nonspecific. They may occur subsequent to pleural reactions associated with many conditions, which include tuberculosis, viral pleurisy, malignancy and lymphoma, lupus, or rheumatoid-induced effusions, cardiac failure, and pulmonary embolism, among other etiologies. The failure to absorb the fibrinous exudate on the visceral pleural surface can lead to the development of diffuse fibrosis of the serosal surface, interlobar pleural thickening, localized pleural filaments (strands), subpleural wedge, and lenticular-shaped masses, and could be the forerunner of lobular atelectasis (pseudotumor) formation. Some of the features are recognized on posteroanterior chest radiographs and the counterparts corroborated with the use of routine and high-resolution computed tomography studies.
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PMID:Radiological features of asbestos-related visceral pleural changes. 200 21

Most patients with lupus anticoagulant (LA) activity have coincident antibodies to a group of negatively charged phospholipids, and its is suggested that LA and anticardiolipin tests detect antibodies with overlapping specificities. Some discordance between the two assays has been described, however. One patient presenting with severe thrombotic disease (recurrent deep vein thrombosis, pulmonary embolism, inferior venocaval obstruction, myocardial infarction, and digital gangrene) showed strong LA activity in February 1987. An enzyme linked immunosorbent assay (ELISA) showed no binding to the negatively charged phospholipids cardiolipin, phosphatidylserine, and phosphatidic acid, but binding to zwitterionic phosphatidylethanolamine (PE) was demonstrated. Inhibition studies and affinity purification confirmed this finding. Interestingly, the serum did not bind to the kaolin cephalin clotting time reagent when used as antigen in an ELISA. The pathogenic significance of anti-PE antibodies and their relation to LA remains to be clarified. Further studies of the occurrence of anti-PE antibodies in patients with LA activity who have negative anticardiolipin tests are suggested.
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PMID:Antibody to phosphatidylethanolamine in a patient with lupus anticoagulant and thrombosis. 249 57

A 51 year-old man with a history of deep venous thromboses and recurrent pulmonary embolism on long-term anticoagulant treatment was admitted to our department because of insidious onset thrombocytopenia. He had neither a history nor clinical signs of abnormal bleeding. On admission, the platelet count was reduced to 21 x 10(9)/l, platelet associated IgG was increased, and bone marrow specimens showed megakaryocytic hyperplasia. Platelet survival was slightly shortened with enhanced platelet sequestration in a normal size spleen. Laboratory evaluation after discontinuation of anticoagulant treatment revealed persisting prolongation of both the prothrombin time and the activated partial thromboplastin time which could be attributed to the presence of a lupus-type circulating anticoagulant. Further relevant laboratory findings included an elevated titer of IgG anti-cardiolipin antibodies and a reduced euglobulin clot lysis activity after venous occlusion due to increased plasminogen activator inhibitor activity. In recent years, it has become apparent that a striking correlation exists between the presence of antibodies to phospholipids and thromboembolic disease and immune thrombocytopenia respectively. The present case report on the association of these autoantibodies with both, recurrent venous thromboembolism and severe thrombocytopenia, supports the hypothesis that anti-phospholipid antibodies may play a crucial part in the pathogenesis of these clinical conditions. A reduced vascular fibrinolytic capacity may be involved in the thrombophilic state induced by anti-phospholipid antibodies.
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PMID:[Anti-phospholipid antibody with recurrent venous thromboembolism and severe autoimmune thrombocytopenia]. 250 50

A predisposition to thrombosis in patients with procainamide-induced lupus anticoagulants is previously unrecognized. We describe two patients treated with procainamide who experienced acute thromboembolic events temporally associated with development of the lupus anticoagulant. One patient had a deep venous thrombosis and pulmonary embolism, while the other patient had a cerebrovascular accident. In both patients, coagulation parameters corrected with interruption of procainamide therapy. We suggest that thrombosis may complicate treatment with procainamide in patients who develop the lupus anticoagulant.
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PMID:Thrombosis associated with procainamide-induced lupus anticoagulant. 250 75


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