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)

Severe pulmonary embolism with thrombosis of the inferior vena cava was observed in a 16 year old girl with no risk factors and treated successfully by fibrinolytic therapy. Secondarily, despite heparino-therapy, upper limb venous thrombosis occurred. Investigation of the clotting factors in the patient and her family revealed a hereditary deficit of antithrombin III. The features of the haemotological diagnosis of this rare condition and the therapeutic implications are discussed.
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PMID:[Severe pulmonary embolism and recurrent thrombophlebitis caused by hereditary antithrombin III deficiency]. 11 39

One hundred patients were screened for hypercoagulability preoperatively and on the third, seventh, tenth, fourteenth, and twenty-first days postoperatively. Patients found to have hypercoagulability were treated with heparin, aspirin, and Coumadin. When the abnormality was present preoperatively, treatment was continued for the duration of the patient's life. Those patients in whom abnormalities developed postoperatively were given anticoagulants until cardiac catheterization 6 months following their operation. Twenty-four of the 100 patients had no coagulation abnormalities preoperatively or postoperatively. Fifteen patients were found to have abnormality prior to operation. Their predominant abnormality was low antithrombin III activity. Sixty-one patients became hypercoagulable postoperatively. Predominant abnormality in this group of patients was increased thrombin generation and increased platelet adhesiveness. Evaluation of patients in this study group revealed a decrease in the incidence of pulmonary embolism, an increase in the patency of vein grafts, and the elimination of anticoagulant therapy in 24 percent of the patients.
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PMID:Coagulation abnormalities in patients undergoing myocardial revascularization. 30 43

This investigation was undertaken to identify and correlate one factor that makes patients undergoing total hip replacement more susceptible to venous thrombosis and pulmonary embolism than those who have almost any other elective orthopaedic procedure, and to determine why the operation of total hip replacement has proved to be relatively resistant to antithrombotic prophylaxis compared with general surgical procedures. Using the depletion of antithrombin III as a marker of activation of the coagulation system, two groups of patients were compared: twenty-one who were subjected to hip arthroplasty and fourteen who underwent general surgical procedures. Both during and after operation the decrease in the quantity of antithrombin III in hip-arthroplasty patients was significantly greater (p less than 0.05) than the decrease in general surgical patients. Seventy-three per cent of hip-replacement patients had venographic evidence of recent thrombosis, 60 per cent of which were discontinuous femoral-vein thrombi. Femoral-vein thrombosis occurs frequently in hip-arthroplasty patients and is relatively resistant to current antithrombotic prophylaxis. The data presented suggest that during hip surgery there is a strong systemic activation of the clotting cascade that is associated with local vessel injury and local stasis in the femoral vein, an association not found in most general surgical procedures.
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PMID:The effect of total hip replacement and general surgery on antithrombin III in relation to venous thrombosis. 45 10

The most important side effects of oral contraceptives (OCs) and their incidence, together with advice and monitoring of the patient at risk, are pointed out. There is a mild increase in blood pressure in longterm contraceptive use caused by increased angiotensinogen production by the liver. It is significant only for women with a history of familial hypertension, diabetes mellitus, or pre-eclampsia. Smoking increases this risk. Urinary tract infections are 25-50% more frequent in pill users. Glucose tolerance is slightly decreased. Contraceptives' diabetogenic effect is higher in women with hereditary tendency for diabetes, latent diabetes, and/or obesity. They are contraindicated in latent diabetes. Findings are contradictory in their effects on cholesterol and triglyceride serum level, but the pill is contraindicated in lipid metabolism disorders. There is an increased incidence in cholecystitis and cholelithiasis in pill-users (70-80 additional cases/100,000 user years). Liver diseases, intrahepatic cholestasis, occur rarely and benign liver tumors have not conclusively been proved to be caused by the pill. A variety of laboratory findings have been related to contraceptive use and drug interactions occur with barbiturates, rifampicin, hydantoin, and phenylbutazone. Blood coagulation is increased, partially by increased production of various blood coagulation factors; but more importantly, by a decreased synthesis of antithrombin III, a natural protective mechanism against intravascular coagulation. This increases thrombosis risk. Risk doubles with simultaneous cigarette smoking. Various epidemiological studies indicate a 5-10 fold increase in thromboembolism and thrombophlebitis, deep vein thrombosis, and pulmonary embolism. There is a correlation between contraceptive use and cerebrovascular disorders and myocardial infarction. This risk increases with age and years of pill use. The pill is contraindicated with symptoms of thrombophlebitis and thromboembolism, sickle cell anemia, proposed surgery, and longterm immobilization. Overall risk factors are not too high. Recommendations for rational pill use related to age are given and further contraindications are mentioned.
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PMID:[Adverse effects of oral contraceptives]. 55 52

There are three categories of antithrombotic agents: drugs which prevent fibrin fromation (the anticoagulants and defibrinating enzymes), drugs which prevent platelet adhesion or aggregation (the antiplatelet drugs), and thrombolytic drugs which induce fibrin degradation. Clinical studies have now led to a better understanding of the relative value of these drugs in different thrombotic disorders. In addition, knowledge of the mechanism of action of some of these drugs has recently been much advanced. The anticoagulant drugs in clinical use are heparin and the oral anticoagulants. Heparin is a potent inhibitor of several steps on the intrinsic coagulation pathway through its effect on a plasma cofactor, antithrombin III. its action is immediate, but heparin must be given parenterally. Oral anticoagulants act more slowly, by reducing the hepatic synthesis of biologically active factors II, VII, IX and X, but can be given by mouth. Heparin is therefore most suitable for starting anticoagulant treatment, while oral anticoagulants are generally used for prolonged therapy. The value of the anticoagulants as antithrombotic agents has been best assessed by studying their effectiveness in preventing and treating venous thromboembolic disease. Oral anticoagulants have been repeatedly shown to prevent venous thrombosis and pulmonary embolism in patients at high risk of developing these complications. However, the increased risk of postoperative bleeding has prevented their widespread use for this purpose in surgical patients. Recently, the use of low doses of heparin, given subcutaneously before and after surgery, has been shown to markedly reduce the incidence of venous thrombosis and pulmonary embolism (including fatal pulmonary embolism) after major elective abdominal surgery, and to produce only a slight increase of postoperative bleeding. This represents a major advance in anticoagulant prophylaxis of venous thromboembolism insurgical patients. However, low dose heparin prophylasix is relatively ineffective in patients having hip surgery, and has not been evaluated in patients having other types of orthopaidic surgery. There is direct evidence that antocoagulant therapy prevents death and recurrent embolism in patients who have developed pulmonary embolism, and considerable indirect evidence that it prevents pulmonary embolism, and considerable indirect evidence that it prevents pulmonary embolism (and death from pulmonary embolism) in patients who have venous thrombosis. The incidence of further venous thromboembolism or bleeding during treatment appears to be minimised when heparin is given by continuous intravenous infusion in a dose sufficient to produce a moderate, but no excessive, prolongation of a heparin-sensitive, in vitro coagulation test. The tests most commonly used to monitor heparin therapy was based on either the whole blood clotting time or the activated partial thromboplastin time...
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PMID:Antithrombotic drugs: part I. 78 43

Antithrombin III (AT III) was determined in 290 patients with deep venous thrombosis and/or pulmonary embolism by immunological methods (radial immunodiffusion, Laurell technique) and by biological activity (heparin cofactor activity and anti-Xa activity). Patients with venous thrombosis had a significantly lower AT III concentration, as determined by the immunological methods or biological method (heparin cofactor activity), than normal persons without any history of venous thrombosis. A decreased level of AT III was found in 27 patients. In these patients the immunoreactive antithrombin III was decreased to the same degree as biological activity (heparin cofactor activity or anti-Xa activity). Thirteen out of these 27 patients belonged to 9 families and, hence, congenital AT III deficiency can be assumed in these cases. The aetiology was unknown in the other half. Patients with AT III deficiency are prone to spontaneous and/or recurrent venous thrombosis. A high incidence of pulmonary embolism and particularly, of fatal pulmonary embolism is remarkable. In more than half of the patients the first thrombotic event occurred before the age of 35. The treatment of choice in such patients is with oral anticoagulants of the coumarin group.
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PMID:[Antithrombin III deficiency and tendency to thrombosis (author's transl)]. 85 29

We observed the changes of molecular markers for hemostatic activation in a patient with acute pulmonary embolism treated with 2 x 10(7) unit tissue plasminogen activator (t-PA). Blood samples were obtained before, just after, at 30 min, 1, 2, 6, and 24 hours after the infusion. Molecular markers included thrombin-antithrombin III complex (TAT), plasminogen-alpha 2 plasmin inhibitor complex (PIC), and thrombomodulin (TM). Marked elevation of TAT was observed from immediately after the t-PA infusion to 6 hours after, although it had been observed for only 1 hour in our previous report on the cases of acute myocardial infarction. PIC level was significantly increased during t-PA infusion but returned to almost baseline value 6 hours after the end of t-PA infusion. This finding was almost the same as the one previously reported concerning acute myocardial infarction cases. TM level increased throughout the evaluation, and remained so, even on the 7th day after t-PA infusion. Our present data revealed a clear difference between the reactive TAT increases after t-PA therapy in acute myocardial infarction cases and in acute pulmonary embolism cases. Our present data also revealed a prolonged elevation of TM during the acute period of pulmonary embolism. It is therefore necessary to keep an eye on the changes of molecular markers for hemostatic activation after t-PA therapy in acute pulmonary embolism.
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PMID:[The changes in molecular markers for hemostatic activation after t-PA therapy in case of pulmonary embolism]. 131 73

Three groups of patients receiving oral anticoagulation treatment were evaluated. The groups consisted of patients with mechanical heart valve prosthesis (n = 60), patients after coronary bypass graft surgery (n = 60) and patients using oral anticoagulation after deep venous thrombosis or pulmonary embolism (n = 60). The patient groups were subdivided into three groups of 20 patients, each group receiving different levels of oral anticoagulation as indicated by the international normalized ratio (INR). Prothrombin fragment 1 + 2, thrombin-antithrombin III complexes and fibrin monomers were determined as coagulation activation makers. The prothrombin fragments 1 + 2 were INR dependent in all groups whereas the thrombin-antithrombin III values were only INR dependent in the group of patients with mechanical heart valve prosthesis. For fibrin monomers no correlation with the INR levels could be found. These results indicate that prothrombin fragment 1 + 2 is the only laboratory quantity of the three, which provides a suitable index of low thrombin activity during anticoagulation therapy.
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PMID:Comparison of markers of coagulation activation in patients under oral anticoagulation at different levels. 144 59

The clinical status of 418 consecutive thrombotic patients was assessed and they were investigated for deficiencies of the proteins involved in the modulation of blood coagulation and fibrinolysis. The whole cohort was divided into two groups according to the age at which the first thrombotic event occurred: group 1 younger than 45 years and group 2 older than 45 years. Deficiencies were significantly more frequent in the juvenile thrombotic population; in this subset of patients the prevalences of single deficiencies were: protein S (6.9%), protein C (4.9%), antithrombin III (3%), plasminogen (0.5%) and dysfibrinogenemia (0.3%). It was possible to diagnose 41 additional deficiencies in the relatives of the probands. The clinical picture and the presence, absence and type of predisposing factors were not statistically different in deficient and non-deficient patients. However, deficient patients experienced their first episode significantly earlier than non-deficient patients and had a significantly higher number of recurrences and pulmonary embolism episodes. From the analysis of the thrombosis-free survival curves, there is no doubt that age represents a strong cofactor in thrombotic risk-related deficiency.
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PMID:Clinical and biological aspects of juvenile thrombophilia. 146 39

Deep venous thrombosis and pulmonary embolism are relatively frequent occurrences in pregnancy and the postpartum period. The diagnosis of deep venous thrombosis and pulmonary embolism requires accurate objective tests because clinical diagnosis is unreliable. Procedures that expose the fetus to ionizing radiation must sometimes be performed to make an accurate diagnosis; current evidence suggests that the adverse effects to the fetus associated with such procedures are minimal. Heparin is the anticoagulant of choice during pregnancy and is used for both the treatment and prevention of venous thrombosis and pulmonary embolism. Patients with deficiencies of antithrombin III, protein C, or protein S as well as patients with antiphospholipid antibodies are at increased risk for thrombotic complications and require particular vigilance during pregnancy.
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PMID:Deep venous thrombosis and pulmonary embolism in pregnancy. 147 24


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