Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149871 (deep vein thrombosis)
 12,364 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A radioimmunoassay (RIA) had been developed for the determination of antithrombin III (AT III) in man. The detection limit was 25 microgram/dl. AT III-RIA level and biological activity (anti-Xa) was significantly correlated (r = 0.737, P less than 0.001). Plasma levels in 36 healthy males (mean +/- SD, 19.9 +/- 2.5 mg/dl) and 21 healthy females (19.1 +/- 2.4 mg/dl) were similar. Serial AT III measurements in normal menstruating females showed lower levels during midcycle and higher concentrations during menstruation. In carcinomas, the AT III levels were lower than normal, particularly in hepatocellular carcinoma. In cirrhosis of liver, the levels were markedly decreased and in some patients were below that found in congenital AT III deficiency. Patients with deep vein thrombosis and patients with heart valve replacement had lower levels than normal, while patients with cerebral vascular occlusion had normal levels. The possible use of AT III as a diagnostic tool of post-operative deep vein thrombosis was demonstrated in one patient after hysterectomy. The increased sensitivity, specificity and precision of this type of assay offer distinct advantages over existing methods of AT III estimation.
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PMID:The determination of antithrombin III by radioimmunoassay and its clinical application. 43 3

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

1. We describe a patient who developed deep vein thrombosis after commencing treatment with the synthetic androgen, mesterolone (Pro-Viron). 2. To investigate the potential thrombogenic action of this drug, a 21 day course of mesterolone (100 mg/day) was given to nine healthy male volunteers. 3. No significant change after treatment occurred in any of the blood tests performed (clotting times, Factor VIII coagulant activity, Factor VIII related antigen, antithrombin III activity, fibrinogen, fibrinogen-fibrin degradation products, plasminogen, euglobulin lysis time, urokinase sensitivity, platelet count, haematocrit, whole blood viscosity and plasma viscosity). 4. We conclude that in a conventional dose taken for 3 weeks mesterolone does not produce a consistent measurable prothrombotic state, nor does it enhance fibrinolysis.
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PMID:Mesterolone: thrombosis during treatment, and a study of its prothrombotic effects. 76 Jul 33

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

Some traditional coagulation assays and several new molecular markers of hemostatic activation were measured in 37 patients with spinal cord injury (SCI). Twenty one of the patients (57%) developed deep vein thrombosis (DVT). The radiofibrinogen uptake test (RFUT) was used to diagnose DVT. Thirty eight percent of quadriplegic and 88% of paraplegic patients developed DVT (p < 0.005). No significant differences were found in platelet counts, mean platelet volumes, fibrinogen levels, von Willebrand factor (Ag) levels, platelet factor 4 and beta thromboglobulin concentrations between the groups with and without DVT. Fibrinopeptide A, thrombin/antithrombin III (TAT) complexes and plasma D-dimer levels were significantly higher in the patients with thrombosis. Most patients with DVT had elevated TAT complex levels up to three days before the RFUT became positive. D-dimer levels were highest after the diagnosis had been made.
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PMID:Thrombosis in spinal cord injury. 129 Jan 64

Patients over 40 years of age who undergo elective orthopaedic surgery have a relatively high risk for developing post-surgical deep vein thrombosis (DVT). Prophylactic use of heparin or low molecular weight heparins can reduce the incidence of post-operative DVT by up to 80%. It is not known whether prophylaxis is achieved by inhibition of prothrombin activation or catalysis of thrombin inhibition in vivo. We determined the changes in concentrations of factor VII zymogen and thrombin-antithrombin III (the latter as an index of prothrombin activation) in the plasmas of 129 patients randomized to receive two daily subcutaneous injections of placebo or 30 mg of Enoxaparin after elective knee surgery. Enoxaparin reduced the frequency of post-surgical DVT by 70%. The concentration of factor VII zymogen had decreased by approximately 50% within 24 h after the knee surgery, followed by a gradual increase to near presurgical values. Additionally, post-Enoxaparin plasmas had statistically significant higher concentrations of factor VII zymogen than post-placebo plasmas. Post-Enoxaparin plasmas had significantly lower concentrations of endogenous thrombin-antithrombin III than comparable post-placebo plasmas. Finally, post-Enoxaparin plasmas inactivated exogenous factor Xa and thrombin more effectively than comparable post-placebo plasmas. As Enoxaparin moderated the generation of endogenous thrombin-antithrombin III after elective knee surgery, inhibition of prothrombin activation in vivo by Enoxaparin may be important for its prophylactic antithrombotic effect.
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PMID:The low molecular weight heparin Enoxaparin inhibits the consumption of factor VII and prothrombin activation in vivo associated with elective knee replacement surgery. 132 19

This study compared how Enoxaparin and unfractionated (UF) heparin influenced in vivo coagulation in patients randomized to receive, by twice daily subcutaneous injections, either 30 mg of Enoxaparin or 7500 I.U. of UF heparin after elective hip surgery. These two regimens were equally effective in reducing the incidence of post-operative deep vein thrombosis DVT. We compared the concentrations of endogenous thrombin-antithrombin III in pre- and post-surgical plasmas to determine how each prophylactic regimen influenced prothrombinase activity in vivo, and found the same concentrations of endogenous thrombin-antithrombin III in post-heparin and post-Enoxaparin plasmas. However, significantly higher concentrations of endogenous thrombin-antithrombin III were found in pre- and post-surgical plasmas of patients who developed post-operative DVT than the levels found in comparable plasmas of patients who remained DVT-negative, regardless of the drug received for prophylaxis. Human factor Xa was added to an equal volume of each patient's plasmas and the amount of added enzyme inactivated by antithrombin III measured using an enzyme-linked immunosorbent assay for factor Xa-antithrombin III. Post-heparin and post-Enoxaparin plasmas inactivated approximately 4 times more factor Xa than the pre-surgical plasmas, regardless of the clinical outcome. Thus, before and after surgery, a higher than normal in vivo prothrombinase activity may be a significant risk factor for developing post-operative DVT.
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PMID:Prophylactically equivalent doses of Enoxaparin and unfractionated heparin inhibit in vivo coagulation to the same extent. 132 20

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

Lower rates of deep vein thrombosis have been noted following total hip replacement under epidural anesthesia in patients receiving exogenous epinephrine throughout surgery. To determine whether this is due to enhanced fibrinolysis or to circulatory effects of epinephrine, 30 patients scheduled for primary total hip replacement under epidural anesthesia were randomly assigned to receive intravenous infusions of either low dose epinephrine or phenylephrine intraoperatively. All patients received lumbar epidural anesthesia with induced hypotension and were monitored with radial artery and pulmonary artery catheters. Patients receiving low dose epinephrine infusion had maintenance of heart rate and cardiac index whereas both heart rate and cardiac index declined significantly throughout surgery in patients receiving phenylephrine (p = 0.0001 and p = 0.0001, respectively). Tissue plasminogen activator (t-PA) activity increased significantly during surgery (p < 0.005) and declined below baseline postoperatively (p < 0.005) in both groups. Low dose epinephrine was not associated with any additional augmentation of fibrinolytic activity perioperatively. There were no significant differences in changes in D-Dimer, t-PA antigen, alpha 2-plasmin inhibitor-plasmin complexes or thrombin-antithrombin III complexes perioperatively between groups receiving low dose epinephrine or phenylephrine. The reduction in deep vein thrombosis rate with low dose epinephrine is more likely mediated by a circulatory mechanism than by augmentation of fibrinolysis.
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PMID:The hemodynamic and fibrinolytic response to low dose epinephrine and phenylephrine infusions during total hip replacement under epidural anesthesia. 144 77

Plasma thrombin-antithrombin III (T-AT) complexes are reputed to be an indirect manifestation of thrombin generation, and a role for their determination in the diagnosis of deep vein thrombosis (DVT) has been advocated. In order to evaluate the accuracy of T-AT complexes assay for DVT diagnosis, in 166 consecutive outpatients with clinical suspicion of the disease, plasma concentration of T-AT complexes was measured immediately before venography by means of an enzyme-linked immunosorbent assay kit. The result of the T-AT complexes assay was elevated in 29 of the 48 patients with DVT (sensitivity, 60%). The T-AT complexes levels were within the normal range in 104 of the 118 patients with normal venograms (specificity, 88%). The positive and the negative predictive value were 67% and 85%, respectively. The authors conclude that the T-AT complexes assay is of little value for the diagnosis of DVT in outpatients.
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PMID:Failure of thrombin-antithrombin III complexes in the diagnosis of deep vein thrombosis. 146 85


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