Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previously, we reported that the sensitivity of plasma DNA for patients with pulmonary emboli was 83 to 88 percent. To confirm these findings in a more comprehensive study, we collected plasma samples from 137 consecutive patients undergoing 148 ventilation-perfusion lung scans for pulmonary embolism. DNA was measured using a counter-immunoelectrophoresis technique that used high titer precipitating double-stranded DNA antibody from a patient with systemic lupus erythematosus. In addition to 17 patients (17 lung scans) excluded for not having plasma collected, 32 patients (37 lung scans) were excluded for having either a condition other than pulmonary embolism that could be associated with plasma DNA or for having nonacute symptoms. Eighteen of 22 patients with a diagnosis of pulmonary embolism (defined by either a high probability lung scan or abnormal pulmonary angiogram) had detectable plasma DNA. Only four of 27 patients without pulmonary embolism (defined by either a normal lung scan or normal pulmonary angiogram) had plasma DNA detected. Based on these results, plasma DNA had a sensitivity of 82 percent and a specificity of 85 percent for this condition. Plasma DNA is a promising test for pulmonary embolism and could help physicians interpret equivocal lung scan findings and thereby clarify difficult decisions such as the need for pulmonary angiography.
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PMID:Plasma DNA. A simple, rapid test for aiding the diagnosis of pulmonary embolism. 229 62

Hemoptysis in systemic lupus erythematosus (SLE) may occur in up to 17% of cases. The vast majority of the cases are secondary to bacterial, tuberculosis or opportunistic infections. Also uremia, pulmonary embolism and lung hemorrhage must be considered. The majority of the above referred entities are usually alarming events in any patient with SLE. In contrast, we describe a patient with inactive SLE, who developed hemoptysis secondary to Paragonimus sp., which was treated "easily" with praziquantel. Fluke infection must be considered in the differential diagnosis of hemoptysis in SLE.
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PMID:Paragonimiasis: an infrequent but treatable cause of hemoptysis in systemic lupus erythematosus. 231 24

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

Since most patients with thrombophilia in Israel are referred for diagnosis to our center, it was possible to estimate the relative frequency of the hereditary disorders leading to thrombophilia. 107 unrelated patients were evaluated over 4 years. Diagnoses were established in 23 patients (21.5%) while in 84 (78.5%) no abnormality was detected. Antithrombin III deficiency was found in 8 patients (7.5%), dominant protein C deficiency in 6 (5.6%), recessive homozygous protein C deficiency in 1, protein S deficiency in 3 (2.8%) and dysfibrinogenemia in 1. Four additional patients (3.7%) had a lupus anticoagulant. The frequency of deep vein thrombosis and pulmonary embolism was similar in patients with and without a definite diagnosis. Thrombosis of visceral or cerebral vessels and a positive family history were more frequent among patients in whom a definite diagnosis was made. In both groups there was a substantial lag between the time of presentation of the first thrombotic episode and the time of evaluation. Since the number of referred patients with thrombophilia has gradually increased over the period of the study, it is at present impossible to establish the prevalence of the various hereditary disorders leading to thrombophilia in the population.
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PMID:The relative frequency of hereditary thrombotic disorders among 107 patients with thrombophilia in Israel. 252 86

Fifteen patients (9 females and 6 males) with the "lupus type" circulating anticoagulant have been studied. The underlying disease was an auto-immune disorder in 11 cases and a malignant hemopathy in 4 cases. The manifestations frequently associated with the lupus inhibitor, such as thrombosis, thrombocytopenia and false-positive VDRL test were analysed. Hemorrhagic syndrome occurred only when thrombocytopenia or acquired abnormality of Willebrand's factor was present. Thrombotic events (8 cases) were frequent. Deep venous thrombosis was complicated with pulmonary embolism in 4 patients. Platelet abnormality, decreased fibrinolytic response or acquired Willebrand's syndrome were found in all patients with a thrombotic event. These different manifestations followed diverging courses in some patients with persistent thrombocytopenia although the anticoagulant had disappeared in 3 cases, negativation of the false-positive VDRL test while the anticoagulant remained unchanged in 1 case, occurrence of a thromboembolic episode although the anticoagulant had disappeared in 1 case.
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PMID:[Course of the manifestations associated with the antiprothrombinase circulating anticoagulant]. 293 5

From the age of 17 a young man had recurrent venous thrombosis, with pulmonary embolism on two occasions. Laboratory investigations showed increased DNA binding, thrombocytopenia, positive antinuclear antibodies, and immunoglobulin A deficiency. A plasminogen activator deficiency was suspected because the euglobulin lysis time was considerably prolonged. Variant lupus was diagnosed. He had a severe myocardial infarct at the age of 20 and subsequent investigations showed the presence in serum of the lupus anticoagulant and antibodies to cardiolipin. The presence of these antiphospholipid antibodies explains the features of his illness and establishes that this case fits into a subset of systemic lupus erythematosus characterised by thrombotic events.
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PMID:Myocardial infarction in a young man with systemic lupus erythematosus, deep vein thrombosis, and antibodies to phospholipid. 308 42

Anticardiolipin antibodies were determined in 96 psychiatric patients treated chronically with chlorpromazine by an enzyme-linked immunosorbent assay using anti-IgM and anti-IgG (fab'2 fragment) as the second antibody. Fifty-four of these patients had an IgM-lupus anticoagulant, and the remaining 42 were followed as controls. Elevated IgM-anticardiolipin antibodies (ACA) levels were detected in 31 patients with the lupus anticoagulant and in 5 controls (p less than 0.001). During a median followup of 5 years, single episodes of deep vein thrombosis or pulmonary embolism occurred in three patients; one had the lupus anticoagulant and the other two had low-level ACA. Contrary to the reported experience in systemic lupus erythematosus and related autoimmune disorders, chlorpromazine-induced lupus anticoagulant and anticardiolipin antibodies levels appear not to be associated with an increased incidence of thrombosis.
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PMID:Chlorpromazine-induced anticardiolipin antibodies and lupus anticoagulant: absence of thrombosis. 312 8

A 16-year-old girl meeting the criteria for SLE is described. Salient features of the clinical course included active glomerulonephritis with dense subepithelial deposits on electron microscopy, pulmonary embolism, axillary vein thrombosis, arthritis, serositis and fever. Disease activity correlated with the presence of lupus anticoagulant as measured by VDRL and partial thromboplastin time (PTT). Her serum was consistently negative to ANA, anti-DS-DNA, anti-SS-DNA, ENA, anti-Ro, anti-La, and LE cells for the entire 4-year course. She responded remarkably to prednisone and azathioprine. Reappearance of VDRL and elevated PTT preceded exacerbation of disease activity and served as a serological guide for modifying medical treatment.
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PMID:Antinuclear antibody-negative systemic lupus erythematosus (SLE) and severe renal involvement: close correlation between disease activity and appearance of circulating anticoagulant. 312 93


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