The Significance of the Chronic Anticoagulant Treatment in Recurrent Thromboembolic Caused by Hereditary Antithrombin III Deficiency

1975 ◽  
Author(s):  
I. Nagy ◽  
H. Losonczy
Keyword(s):  
Functional Activity ◽  
Antithrombin Iii ◽  
Young Patients ◽  
The Other ◽  
Anticoagulant Treatment ◽  
Vein Thrombosis ◽  
Modified Method ◽  
Recurrent Venous Thromboembolism ◽  
Antithrombin Iii Deficiency ◽  
Deep Vein

It has been known since the publication of Egeberg (1965, 1970) and Marciniak (1974) that herditary antithrombin III deficiency could be the cause of recurrent venous thromboembolism.The authors observed in 5 cases of severe repeated venous thrombosis in young patients an antithrombin III decrease, which proved to be a hereditary abnormality. In the case of a 15 years old girl the late introduced anticoagulant treatment could not save the life of the patient, she died after repeated deep vein thrombosis. In the other cases the long-lasting anticoagulant treatment resulted in a perfect clinical improve, while the behaviour of antithrombin III was different; in some cases its quantity (determined by radial -immunodiffusion) and functional activity (examined by modified method of Gerendás and Rák) remained decreased, while in the other cases its functional activity increased during the anticoagulant treatment as it was found by Marciniak, too.It is most likely, that there are two types of hereditary antithrombin III decrease; in one of them the quantitative and functional decrease goes parallel, in the other there is mainly a functional decrease, which improves during the chronic anticoagulant treatment. The authors demonstrated the significance of the prolonged anticoagulant treatment in the patients with hereditary antithrombin III decrease.

Congenital Antithrombin III Deficiency in 3 Families (7 Affected Members)

1979 ◽  
Author(s):  
J. Conard ◽  
M. Samama ◽  
M. H. Horellou ◽  
B. Cazenave ◽  
P. Griguer ◽  
...  
Keyword(s):  
Deep Vein Thrombosis ◽  
Antithrombin Iii ◽  
Oral Anticoagulants ◽  
Vena Cava ◽  
Oral Contraception ◽  
Vein Thrombosis ◽  
Heparin Treatment ◽  
At Iii ◽  
Antithrombin Iii Deficiency ◽  
Deep Vein

A congenital Antithrombin III (AT III) deficiency affecting 7 members of 3 families is reported.The first throrabo-embolic accidents were observed between the age of 22 and 35 : they were spontaneous or occured after delivery or oral contraception. in one patient, a deep vein thrombosis was observed during heparin treatment. in 2 cases, recurrent pulmonary embolic episodes required vena cava ligation. No thromboembolic accident was observed during oral anticoagulation.AT III was measured by an amidolytic method and by the Mancini method on plasma and serum ; the antithrombin activity was determined on serum by the von Kaulla method. in 7 patients, a decreased AT III was found by all the methods performed. The AT III level was around 50 % in patients treated or not by oral anticoagulants One patient was studied during heparin treatment and then under oral anticoagulants : AT III levels were lower under heparin.

Antithrombin-III Deficiency Causing Deep Vein Thrombosis And Pulmonary Embolism In A Young Male

1981 ◽  
Author(s):  
K Genth ◽  
J Schaefer ◽  
J Frank ◽  
W Krämer ◽  
B Weinei ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Deep Vein Thrombosis ◽  
Pulmonary Artery ◽  
Antithrombin Iii ◽  
Clinical Symptoms ◽  
Venous Pressure ◽  
Vein Thrombosis ◽  
At Iii ◽  
Antithrombin Iii Deficiency ◽  
Deep Vein

A 34 year old male was admitted to the hospital with typical clinical symptoms of acute pulmonary embolism caused by deep vein thrombosis in the upper leg detected by phlebography. Pulmonary embolism was verified by the lung-perfusion-scintigram. The patient developed an infarct pneumonia with hemoptoe. Episodic thromboembolic phenomena occurred due to antithrombin-III deficiency (AT-III). The method, using homogenic substrates exhibited low AT-III activity of 8.6 IU/ml(25°C) due to a familiar AT-III deficit. Fiberoptic pulmonary catheter was placed into the pulmonary artery to measure pulmonary artery pressure (PAP, PCP), right ventricular pressure (RVP) and to determine cardiac output (CO) using the dye dilution technique. Heart rate (HR), central venous pressure (CVP) and aortic pressure (AOP) were recorded continuously. Patient received immediately fibrinolytic therapy, initiated by an initial dose of streptokinase (SK)(250 000 IU/20 min.), followed by a maintenance dose (100 000 IU/h), lasting 3 days. M-mode echocardiography detected before SK a moderate enlarged right ventricle and a small left ventricle, indicating a low output. After SK these values were improved. In conclusion, this case demonstrated a serious thromboembolic disorder, related to AT-III deficit. SK-therapy improved the hemodynamic situation.

Congenital Antithrombin III Deficiency in 3 Families (7 Affected Members).

1979 ◽  
Author(s):  
J. Conard ◽  
M. Samama ◽  
H.H. Horellou ◽  
B. Cazenave ◽  
P. Griquer ◽  
...  
Keyword(s):  
Deep Vein Thrombosis ◽  
Antithrombin Iii ◽  
Oral Anticoagulants ◽  
Vena Cava ◽  
Oral Contraception ◽  
Vein Thrombosis ◽  
Heparin Treatment ◽  
At Iii ◽  
Antithrombin Iii Deficiency ◽  
Deep Vein

A congenital Antithrombin III (AT III) deficiency affecting 7 members of 3 families is reported.The first thrombo-embolic accidents were observed between the age of 22 and 35: they were spontaneous or occured after delivery or oral contraception. In one patient, a deep vein thrombosis was observed during heparin treatment. In 2 cases, recurrent pulmonary embolic episodes required vena cava ligation. No thromboembolic accident was observed during oral anticoagulation.AT III was measured by an amidolytic method and by the Mancini method on plasma and serum ; the antithrombin activity was determined on serum by the von Kaulla method. In 7 patients, a decreased AT III was found by all the methods performed. The AT III level was around 50% in patients treated or not by oral anticoagulants.One patient was studied during heparin treatment and then under oral anticoagulants: AT III levels were lower under heparin.

A Case of Hereditary Antithrombin III Deficiency Manifested by Myocardial Infarction and Deep Vein Thrombosis

2002 ◽  
Vol 32 (6) ◽  
pp. 521 ◽  
Author(s):  
Ki Young Kim ◽  
Keon Woong Moon ◽  
Doo Soo Jeon ◽  
Joo Youn Choi ◽  
Dae Hyung Jeon ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Deep Vein Thrombosis ◽  
Antithrombin Iii ◽  
Vein Thrombosis ◽  
Antithrombin Iii Deficiency ◽  
Deep Vein

D-Dimers, Thrombin Antithrombin III Complexes and Prothrombin Fragments 1 + 2: Diagnostic value in Clinically Suspected Deep Vein Thrombosis

1991 ◽  
Vol 65 (01) ◽  
pp. 028-032 ◽  
Author(s):  
B Boneu ◽  
G Bes ◽  
H Pelzer ◽  
P Sié ◽  
H Boccalon
Keyword(s):  
Deep Vein Thrombosis ◽  
Antithrombin Iii ◽  
High Sensitivity ◽  
Diagnostic Value ◽  
Predictive Values ◽  
Vein Thrombosis ◽  
High Negative Predictive Value ◽  
Deep Vein ◽  
D Dimer ◽  
Mercury Strain Gauge

SummaryThis study was performed to determine the accuracy of D-Dimer fibrin derivatives, thrombin-antithrombin III (TAT) complexes and prothrombin fragments 1 + 2 (F 1 + 2) determinations for the diagnosis of deep vein thrombosis (DVT). One hundred and sixteen consecutive patients referred to the angiology unit of our hospital for a clinically suspected DVT were investigated. They were submitted to mercury strain gauge plethysmography and to ultrasonic duplex scanning examination; in cases of inconclusive results or of proximal DVT (n = 35), an ascending phlebography was performed. After these investigations were completed, the diagnosis of DVT was confirmed in 34 and excluded in 82. One half of the patients were already under anticoagulant therapy at the time of investigation. The 3 biological markers were assayed using commercially available ELISA techniques and the D-Dimer was also assayed with a fast latex method. The normal distribution of these markers was established in 40 healthy blood donors. The most accurate assay for the diagnosis of DVT was the D-Dimer ELISA which had both a high sensitivity (94%) and a high negative predictive value (95%). The D-Dirner latex, TAT complexes and F 1 + 2 were far less sensitive and provided negative predictive values which ranged between 78 and 85%. In spite of positive and significant correlations between the levels of ihe 3 markers, their association did not improve their overall accuracy for detecting D\/L Therefore, with the exception of the D-Dimer ELISA, these markers were of little value for the diagnosis of DVT in this specific population.

Sign in / Sign up

Export Citation Format

Share Document