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)

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

Adequate anticoagulation treatment in patients with deep vein thrombosis reduces the risk of thrombus extension or embolization to less than 5%. Thrombolytic treatment may possibly prevent subsequent postthrombotic syndrome. Heparin is the initial treatment of choice for most patients with deep vein thrombosis. The dose is adjusted according to the results of tests such as the whole blood clotting time, thrombin clotting time, activated partial thromboplastin time or plasma heparin concentration. The most commonly used test is the activated partial thromboplastin time which should be maintained at 1 1/2 to two times the control level. Initially the test should be performed two to three times daily and when optimal adjustment has been established, clotting studies are required only at 24-hour intervals. In general, treatment with intravenous heparin should be continued for seven to ten days. Thereafter, for secondary prophylaxis, treatment with oral anticoagulants is carried out for six to eight weeks for symptomatic lower leg thrombosis, for twelve weeks in the case of proximal venous thrombosis and pulmonary embolism. Oral anticoagulant therapy with warfarin should be given overlapping the last few days of heparin with the dose adjusted to prolong the prothrombin time to 1.3 to 1.5 times control. Initially, the prothrombin time should be monitored weekly, thereafter at intervals of two to three weeks. If oral anticoagulant therapy is contraindicated, secondary prophylaxis with subcutaneous heparin given twice daily in doses sufficient to prolong the activated partial thromboplastin time to 1 1/2 times control is an effective and safe alternative. The major side effect of oral anticoagulant therapy, as well as that of heparin, is bleeding.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Therapy of deep vein thrombosis. 269 42

Marked circadian variations in the activated partial thromboplastin time (APTt) during continuous heparin infusions for thromboembolic episodes have been reported in a French study. The aim of the present study was to test if these variations could be reproduced in a Swedish population. The frequency spectrum variations in APTt values were analysed with the Prony and the statistical Pearson product momentum correlation coefficient methods. In seven patients with pulmonary embolism, APTt was checked every fourth hour during 48 h of continuous, constant heparin treatment. In only one patient was a distinct circadian variation of APTt values seen. In six patients with venous leg thromboses, treated with s.c. heparin, marked variations in APTt were noticed over periods of 12 h. These variations paralleled the regular s.c. injections of heparin every twelfth hour. The results of the present study could not confirm the marked circadian variations in APTt reported in an earlier French study during continuous heparin infusions, except in one patient.
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PMID:Changes of activated partial thromboplastin time during constant intravenous and fixed intermittent subcutaneous administration of heparin. 272 83

The aim of our work was to study in a population of high risk patients with hemorrhagic and or thrombotic disease, the preventive or therapeutic effect of a low molecular weight heparin fraction, CY 216 (Choay, France), particularly in surgery. CY 216 was given to 9 patients for the treatment of a thrombosis (pulmonary embolism, acute ischemia, deep venous thrombosis) and to 40 patients in prevention of thrombosis. In this second group, 28 had a high thromboembolic risk such as valvular prosthesis, cardiac arrythmia, coronary artery bypass, etc. For all the patients, CY 216 was injected sub-cutaneously twice or three times a day at the mean dose of 1.5 mg/kg/d, equivalent to 300 U anti-Xa Choay/24 h, and always injected 24 hours before surgery. The biological tests used were: blood cells count, platelet count, prothrombin time, activated partial thromboplastin time, heparinemia levels by two technics: anti-factor-Xa activity and anti-factor IIa activity. None thrombotic complication was observed in the 40 patients prophylactically treated and a constant improvement of thrombosis was noted for the 9 patients with thrombo-embolic disease. In 3 patients, bleeding complications were observed: for 2 patients, all the coagulation tests were normal and anti-Xa activities were less than 0.55 U/ml; in one patient, the bleeding time was prolonged (15 minutes Ivy Incision) and returned to normal when the CY 216 was stopped. Concerning the biology, there was no modification except for anti-Xa activity which mean was 0.30 U/ml (01-07). However, this test is unable to predict either thrombotic or hemorrhagic events.
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PMID:[Prophylactic and therapeutic use of a low molecular weight heparin fraction, CY 216]. 283 83

Intravenous heparin is the initial treatment of choice for most patients with acute pulmonary embolism or proximal deep vein thrombosis. The primary objective of initial heparin therapy in such patients is to prevent recurrent venous thromboembolism. The efficacy of intravenous heparin for this purpose has been established by randomized clinical trials in patients with pulmonary embolism, and more recently, in patients with proximal vein thrombosis. Heparin is given as an initial intravenous bolus of 5000 units, followed by a maintenance dose of 30,000-40,000 units per 24 h by continuous intravenous infusion. A recent randomized trial in patients with proximal vein thrombosis indicates that failure to achieve an adequate anticoagulant response (APTT greater than 1.5 times control) is associated with a high risk (25%) of recurrent venous thromboembolism. Intravenous heparin administered in doses that prolong the activated partial thromboplastin time (APTT) to 1.5 or more times the control value is highly effective, and associated with a low frequency (2%) of recurrent venous thromboembolism. Heparin is continued for 7-10 days, overlapped with warfarin sodium during the last 4-5 days. Multiple randomized clinical trials indicate that this approach is highly effective. An alternative approach is to commence heparin and oral anticoagulants together at the time of diagnosis, and to discontinue heparin on the fourth or fifth day. A recent randomized trial in patients with submassive venous thrombosis or pulmonary embolism suggests that 4-5 days of initial heparin therapy is effective and safe, but this approach must be evaluated by further randomized trials before it is recommended for patients with extensive proximal vein thrombosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Heparin therapy for venous thrombosis and pulmonary embolism. 306 31

BRL 26921 (Eminase registered trade mark in Belgium, Germany and The Netherlands) is the p-anisoyl derivative of the primary (human) lys plasminogen-streptokinase activator complex (APSAC). The acyl-enzyme has the theoretical advantage of causing fibrinolysis in situ in the presence of fibrin clotbound plasminogen. It was administered to 34 patients with severe pulmonary embolism (PE) in an open multicentre study. PE was suspected on clinical, blood gas, ECG, and radiographic data. Pulmonary angiograms performed pre- and post-treatment confirmed the diagnosis and were assessed using the Miller Index (MI). Fibrinogen, plasminogen, alpha-2-antiplasmin, fibrinogen degradation products (FDP), activated partial thromboplastin time (APTT), partial thromboplastin time (PTT) were closely monitored before and after each administration of APSAC. Median angiographic improvement was 50% (range 0-94%). The following adverse events were reported: bleeding at puncture sites (n = 12), haematuria (n = 1), epistaxis (n = 3), fever (n = 2). A blood transfusion was given in one patient with an inguinal haematoma. Systemic fibrinogenolysis occurred in 20/28 patients.
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PMID:Thrombolytic treatment of pulmonary embolism with APSAC. 306 87

This open controlled study compared the effects of subcutaneous administration of two types of heparin in two groups of 40 patients each with deep vein thrombosis. One group received calcium heparin and the other received low molecular weight heparin for 40 days in each case. Patients receiving low molecular weight heparin showed a greater increase in inhibition of activated factor X than those receiving calcium heparin. Both drugs slightly reduced activated partial thromboplastin time. No patient experienced pulmonary embolism during the study. At the end of the study, maximum venous outflow was significantly higher in patients given low molecular weight heparin than in those given calcium heparin. No major side-effects were observed. This study showed that: (a) the anti-thrombotic effect of low molecular weight heparin was greater than for calcium heparin; and (b) low molecular weight heparin improved maximum venous outflow in approximately half of the patients, possibly by promoting or accelerating recanalization of the vessel.
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PMID:Deep vein thrombosis of the legs: new therapy by means of low molecular weight heparins. 306 22

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

To quantify physician practices in the care of patients with presumed pulmonary embolism or deep venous thrombosis, we analyzed heparin sodium orders, the intensity of anticoagulation, and complications in 65 patients with the diagnosis of deep venous thrombosis or pulmonary embolism. All patients were given heparin, for a mean (+/- SEM) period of 8.8 +/- 0.4 days. A high percentage of patients (60%) did not have a single partial thromboplastin time (PTT) greater than 1.5 times control within the first 24 hours of heparin therapy. Not until day 8 were 90% of PTTs in therapeutic range. We identified five common practices that led to delays in achieving a PTT greater than 1.5 times the laboratory control: (1) failure to start heparin therapy at the time of initial clinical suspicion, (2) choice of a heparin sodium bolus (mean, 5861 +/- 365 U) and continuous infusion (1026 +/- 148 U/h) insufficient to elevate the PTT to greater than 1.5 times control, (3) delay in obtaining the first PTT (mean, 11.7 +/- 1 h after start of heparin therapy), (4) insufficient heparin dosing in response to a low PTT, and (5) excessive and prolonged reductions in heparin therapy in response to a PTT greater than three times control, leading to subtherapeutic levels in 56% of subsequent PTTs. We think that poor understanding of heparin kinetics, overcautious behavior of physicians, and high heparin requirements in this selected population account for the findings.
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PMID:Physician practices in the treatment of pulmonary embolism and deep venous thrombosis. 337 15

Venous thromboembolism produces chronic sequelae in the legs and occasional immediate mortality due to pulmonary embolism. Because it occurs in certain high risk situations (for example, after surgery) its prevention is a practical proposition. This has been attempted using many different approaches. Administration of low dose heparin with or without dihydroergotamine to enhance venous return has been one of the most widely tested regimens. There is little doubt that this can prevent, in many patient groups, postoperative deep venous thrombosis and fatal pulmonary embolism, with a low incidence of adverse reactions. Some particularly high risk postoperative patient groups (for example, those undergoing hip surgery) warrant more aggressive measures to prevent thrombosis. Surveys have shown that increasing use is being made of this approach, and it is hoped that all surgeons will adopt a policy that will reduce postoperative venous thrombosis and pulmonary embolism. A reduction in the incidence of venous thromboembolism in large acute myocardial infarction is achieved by low dose heparin, although early mobilization is important. In addition, many of the patients at risk merit full dose anticoagulation to prevent intracardiac thromboembolism. Established venous thrombosis is treated effectively by intravenous heparin, followed by warfarin to keep the prothrombin time at 1.2 to 1.5 times control, as assessed using rabbit thromboplastin; most patients need three months of treatment. Anticoagulation is warranted for pulmonary embolism, with fibrinolytic therapy reserved for patients with massive embolism and hemodynamic compromise. Embolectomy is a heroic measure, which may occasionally be lifesaving.
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PMID:Preventive and therapeutic approach to venous thromboembolic disease and pulmonary embolism--can death from pulmonary embolism be prevented? 353 67


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