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)

We describe a 43-year-old male patient with congenital antithrombin III deficiency requiring haemodialysis due to extension of venous thrombus from recurrent deep vein thrombosis. During dialysis with adequate heparinization, the patient often revealed clot formation in the extracorporeal circuit resulting in unexpected discontinuation of dialysis. When either a combination of antithrombin III concentrate plus heparin or the newly developed synthetic antithrombin preparation, MD805, was infused during dialysis, he could be uneventfully dialysed with either of the two regimens. The functional antithrombin III activity with MD805 increased to the same level as that obtained with antithrombin III concentrate, and it was possible to achieve an antithrombotic effect, as measured from the APTT and thrombin-antithrombin III complex with MD805 during and after dialysis. We thus found that MD805 could be used as an anticoagulant drug when an AT III-deficient patient required anticoagulation in the extracorporeal circulation.
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PMID:Choice of anticoagulant in a congenital antithrombin III (AT III)-deficient patient with chronic renal failure undergoing regular haemodialysis. 268 3

We studied the diagnostic value of recently introduced ELISA's for the determination of thrombin-antithrombin III (TAT) complexes, fibrin degradation products (FbDP), fibrinogen degradation products (FgDP) and total degradation products (TDP) for deep venous thrombosis (DVT) in plasma of 239 consecutive outpatients, suspected for DVT by their family doctor. DVT was confirmed by impedance plethysmography in 60 patients. Using the 95th percentile range of 42 healthy volunteers the sensitivity for the detection of DVT was: 37% for TAT, 95% for TDP, 92% for FbDP and 90% for FgDP. Specificity was: 88% for TAT, 16% for TDP, 20% for FbDP and 25% for FgDP. We conclude that these assays are of little value in the diagnosis of DVT in outpatients.
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PMID:Is quantitative determination of fibrin(ogen) degradation products and thrombin-antithrombin III complexes useful to diagnose deep venous thrombosis in outpatients? 269 21

18 elderly patients submitted to major surgery for malignancies or other disease were studied to assess the relationship between changes of blood coagulation factors and inhibitors in the early post-operative period and the appearance of lower limb deep vein thrombosis. A decrease in serum antithrombin III (AT III) Protein C antigen (PC: Ag) and Plasminogen activity (PLG) levels from the second to the fourth postoperative day, together with a simultaneous increase in serum fibrinogen (FG) and von Willebrand Factor (vWF:Ag) antigen levels was observed. In 8 patients, PC:Ag levels dropped below the limit considered at risk to develop DVT (less than 60 U/dl). A patient with the lowest PC:Ag levels had deep vein thrombosis From the analysis of data it was concluded that in the postoperative period, blood coagulation changes occur in elderly patients, predisposing to the risk of deep vein thrombosis.
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PMID:Evaluation of postoperative blood coagulation changes in elderly patients undergoing major surgery. 278 5

Deep venous thrombosis and pulmonary embolism are frequently diagnosed in patients encountered in a primary-care practice. Poor prognosis is related to acute sudden death and to recurrent thromboembolic disease. Anticoagulant therapy with heparin followed by coumarin derivatives is highly effective in preventing such recurrences, but the intensity of anticoagulation must be strictly monitored. Treatment with heparin, sufficient to prolong the activated partial prothrombin time to 1.5 to 2.0 times the control, should be continued for five to ten days, and oral anticoagulation should be overlapped with heparin for four to five days. The recommended therapeutic range for the prothrombin time during coumarin therapy is an INR of 2.0 to 3.0. The duration of anticoagulant treatment must be tailored to the individual patient. Patients with slowly resolving risk factors must be treated for at least three months after an acute deep vein thrombosis and for six months after a pulmonary embolism. Patients with tumors, antithrombin III, protein C or S deficiency should be treated indefinitely.
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PMID:[Prevention of recurrence of thromboembolic disease: maintenance of anticoagulant therapy]. 281 10

Eighteen items of clinical and laboratory information were measured on the day before operation in 85 patients who underwent elective major abdominal surgery. Postoperatively, deep venous thrombosis (DVT) was detected by 125I-fibrinogen scan in 23 patients. Stepwise logistic discriminant analysis was used to identify factors which predicted DVT. Seven such factors were identified, which were then used to construct a predictive index. In descending order of predictive power, they were: age, euglobulin lysis time (ELT), previous abdominal surgery, varicose veins, antithrombin III concentration, cigarette smoking, and platelet count. Pre-operatively, the predictive index correctly identified 91% of the patients in whom DVT developed, and wrongly allocated to the high-risk group 19% of those in whom it did not. A shortened version of the predictive index based only on age and ELT (I = -11.5 + 0.133 age + 0.006 ELT) was 91% sensitive and 63% specific in the prediction of DVT. In a prospective study of 43 patients, this shortened predictive index correctly identified pre-operatively 93% of patients in whom DVT developed, and wrongly allocated to the high-risk group only 17% of those in whom it did not.
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PMID:Pre-operative identification of patients at high risk of deep venous thrombosis after elective major abdominal surgery. 287 19

In 22 patients with suspected pulmonary embolism and 19 patients with suspected deep vein thrombosis, thrombin-antithrombin III complex (TAT) as an indicator of thrombin activation was measured using a newly developed ELISA. For comparison fibrinopeptide A (FPA), as a marker of an activated coagulation, as well as platelet factor 4 (PF4), and beta-thromboglobulin (beta-TG), as markers of platelet activation, were determined. In all patients in whom pulmonary embolism was confirmed by perfusion lung scan and in 15 of 16 patients in whom deep vein thrombosis was confirmed by phlebography, TAT exceeded the upper limit of normal (3.0 ng/ml). FPA was increased in 71% of the pulmonary embolism patients, PF4 in 53%, and beta-TG in 59%. The data for the patients with deep vein thrombosis were comparable. PF4 and beta-TG were increased in more than 25% of the normal controls, FPA in 17%, and TAT in 9%. TAT is very sensitive in detecting an activation of the coagulation system in patients with suspected thromboembolic events. The test, however, is not specific for thromboembolism; it only indicates an activation of the coagulation system. Acute pulmonary embolism or deep vein thrombosis would appear to be unlikely if TAT is normal. The measurement of TAT is easier and less susceptible to disturbances than that of FPA, PF4, and beta-TG.
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PMID:[Significance of the thrombin-antithrombin III complex in the diagnosis of pulmonary embolism and deep venous thrombosis--comparison with fibrinopeptide A, platelet factor 4 and beta-thromboglobulin]. 295 57

The fibrinolytic system was investigated in 120 patients with spontaneous or recurrent deep vein thrombosis (DVT) without any known organic disease able to explain by itself the occurrence of a thrombosis and without any known defect of antithrombin III, Heparin Cofactor II, Protein C, or Protein S. The assays included: Euglobulin fibrinolytic activity (EFA), tissue-type plasminogen activator related antigen (t-PA-Ag) and plasminogen activator inhibitor activity (PA inhibitor), which were measured before and after 10 min of venous occlusion (V.O.). On the basis of the results, the patients could be classified in 3 groups: good responders with an at least two-fold increase of EFA after venous occlusion (n = 76), poor responders with a lesser increase of EFA due to deficient release of t-PA (n = 12), and poor responders with a normal t-PA release but an increased level of PA-Inhibitor (n = 32). The poor responders due to deficient t-PA release (10% of total) had a higher incidence of recurrence of deep vein thrombosis, than the other groups (p less than 0.01). An overall correlation was found between the level of PA-Inhibitor activity and the triglyceride level (r = 0.40, p less than 0.01), suggesting that these elevations may be due to a common cause, at least in some of the patients. It is concluded that a poor fibrinolytic response to venous occlusion occurs in 35 percent of DVT patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Deficient t-PA release and elevated PA inhibitor levels in patients with spontaneous or recurrent deep venous thrombosis. 310 59

Protein C and protein S serve as natural anticoagulants. Deficiencies of these proteins are often associated with recurrent deep vein thrombosis and coumarin induced skin necrosis. These two proteins function by selectively inactivating factors Va and VIIIa, two of the "cofactors" of blood coagulation. Hence, inhibition of coagulation by this pathway complements the better known inhibition mediated by the antithrombin III-heparin system. These observations suggest that protein C and/or activated protein C may prove useful in controlling thrombosis and/or DIC. We have developed a Ca2+ dependent monoclonal antibody which allows the rapid isolation of human protein C. This rapid isolation has allowed us to demonstrate that activated protein C can protect baboons from the lethal effects of E. coli/endotoxin and that protein C supplementation can minimize fibrinogen consumption following tissue factor infusion into dogs.
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PMID:Protein C, isolation and potential use in prevention of thrombosis. 330 68

Careful interpretation of the vascular pathology is important in cases of intestinal ischemia caused by primary mesenteric vein thrombosis because it suggests antithrombin III (AT III) deficiency. This deficiency, an autosomal dominant hereditary disorder, predisposes the patient to venous thrombosis. Similar or acquired deficiencies may also predispose the patient to thrombosis. In hereditary AT III deficiency, 90% of the cases have thrombosis of the leg or iliac veins; 8.3% of the cases, thrombosis of the mesenteric veins. Additionally, some families have a tendency to develop mesenteric vein thrombosis specifically. In this case report, a daughter with probable AT III deficiency had a history of 3 episodes of deep vein thrombosis in the previous 5 years while taking oral contraceptives. Her father, with the same deficiency, died from massive intestinal infarction resulting from portal and mesenteric vein thrombosis. The 19-year old woman developed gradually worsening abdominal pain, signs of peritonitis, and hematemesis. A laparotomy revealed peritonitis that was due to segmental small-bowel infarction; the underlying pathologic condition was mesenteric vein thrombosis. Coagulation study results revealed AT III activity by chromogenic assay, 0.48 u/mL; AT III antigen, 0.5 u/mL; and protein C antigen, 1.15 u/mL. 10 days after discharge, she developed a hemicranial headache with nausea, vomiting, neck tenderness, and photophobia; she was readmitted. A CT scan showed a left posterior parietal cerebral infarct. Repeat AT III activity by chromogenic assay was 0.51 u/mL and AT III antigen level was 0.50 u/mL. Before anticoagulant therapy could be initiated, the patient died 7 days after readmission. The combined lowering of AT III activity and antigen levels to half of normal suggests AT III deficiency. Earlier diagnosis of this deficiency could have been made in light of the patient's own history of thrombosis and the paternal history.
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PMID:Mesenteric venous thrombosis due to antithrombin III deficiency. 333 17

An Israeli Arab family with type I antithrombin III (AT-III) deficiency with several affected symptomatic members in three generations is reported. The propositus presented with deep vein thrombosis and pulmonary emboli associated with gestation. The propositus infant presented at the age of 2 weeks with superior sagittal and rectus sinus thrombosis. Hereditary AT-III deficiency should be considered in infants with cerebral thrombosis, especially if they have a family history of thromboembolism. The role of prophylactic therapy by AT-III concentrates in these infants should be further assessed.
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PMID:Cerebral thrombosis in a newborn with a congenital deficiency of antithrombin III. 334 5


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