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.

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.

scholarly journals Successful treatment with rivaroxaban of an extended deep vein thrombosis complicated by pulmonary embolism in a patient with familial antithrombin III deficiency: a case report

2019 ◽  
Vol 4 (1) ◽  
pp. 1-5
Author(s):  
Marianna Appignani ◽  
Adolfo Sciartilli ◽  
Marcello Caputo ◽  
Enrico Di Girolamo
Keyword(s):  
Deep Vein Thrombosis ◽  
Inferior Vena Cava ◽  
Complete Resolution ◽  
Inferior Vena ◽  
Antithrombin Iii ◽  
Vena Cava ◽  
Vein Thrombosis ◽  
Increased Risk ◽  
At Iii ◽  
Deep Vein

Abstract Background  Patients with low levels of antithrombin III (AT III) are at an increased risk of developing arteriovenous thromboembolic disease. Case summary  We report a case of a 28-year-old woman who presented with a 1-week history of spontaneous right calf pain and swelling. A heterozygous AT III deficiency, phenotypically expressed as deep vein thrombosis, was reported in the patient’s mother and sister. Blood workup revealed residual AT III activity at 58% with normal protein C and protein S levels. Computed tomographic angiography (CTA) revealed subsegmental bilateral pulmonary embolism (PE) and deep vein thrombosis in the right leg extending into the inferior vena cava up to the confluence of the left renal vein. Placement of an inferior vena cava filter was not considered. Given the patient’s haemodynamic stability, anticoagulant therapy with 15 mg of rivaroxaban twice a day was initiated instead. Echocardiography after 10 days of treatment revealed complete resolution of the thrombus located in the inferior vena cava, while CTA revealed complete resolution of the PE. Discussion  Patients with AT III deficiency are likely to be heparin-resistant and will require higher heparin doses or the administration of AT III replacement therapy for the treatment of thrombosis, both of which are associated with an increased risk for haemorrhagic complications. Direct factor Xa inhibition by rivaroxaban provided an alternative mechanism for anticoagulation, which was found to be particularly useful in this patient with familial AT III deficiency, deep vein thrombosis, and PE.

Patients with APC Resistance Compared with Those with Other Clotting Inhibitor Deficiencies Show Later Onset of Venous Thrombosis During Oral Contraception

1995 ◽  
Vol 1 (4) ◽  
pp. 274-276 ◽  
Author(s):  
Antonio Girolami ◽  
Paolo Simioni ◽  
Sandra Zanardi ◽  
Luigi Scarano ◽  
Bruno Girolami
Keyword(s):  
Deep Vein Thrombosis ◽  
Protein C ◽  
Antithrombin Iii ◽  
Activated Protein C ◽  
Protein S ◽  
Oral Contraception ◽  
Vein Thrombosis ◽  
Apc Resistance ◽  
At Iii ◽  
Deep Vein

The prevalence of deep vein thrombosis in female patients with antithrombin III (AT III), protein C, or protein S deficiency who are on oral contraception has been compared with that of patients with activated protein C (APC) resistance. In the latter case the prevalence was lower (36.4%) than in the AT III deficiency group (71.4%) but similar to that seen in the protein C and protein S group (25%).' Furthermore, venous thrombosis occurred with APC resistance much later than with AT III, protein C, or protein S defects. The time lag between onset of oral contraception and thrombosis (~16 cycles) was not statistically different from that seen in a group of women who were known to have no antithrombin III, protein C, or protein S defects. It appears that as far as the interaction with oral contraception is concerned APC resistance is a much less severe condition compared with other clotting inhibitor defects. Key Words: Oral contraceptive—Activated protein C resistance—Deep vein thrombosis.

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.

Predictive Value of Decreasing Antithrombin III in Deep-Vein Thrombosis

1980 ◽  
Vol 44 (03) ◽  
pp. 135-137 ◽  
Author(s):  
Thorkild Lund Andreasen
Keyword(s):  
Deep Vein Thrombosis ◽  
Predictive Value ◽  
Coronary Care Unit ◽  
Antithrombin Iii ◽  
Predictive Values ◽  
Vein Thrombosis ◽  
At Iii ◽  
Coronary Care ◽  
Time Of Admission ◽  
Deep Vein

SummaryAntithrombin III (At-III) was measured at the time of admission and two days later in 131 patients laid up in a coronary care unit. The patients were examined for deep-vein thrombosis (DVT) clinically and by means of 125I-fibrinogen scanning. 19 patients developed DVT. In 11 subjects with and 25 without DVT At-III decreased more than 10%. And in 7 with and 17 without DVT At-III decreased more than 15%. One person with DVT had subnormal At-III. By using decrease of At-III or subnormal initial At-III to predict DVT the following predictive value (PV) were found. Decrease ≤ 10%, PV pos.= 0.32 and PV neg. = 0.93. Decrease ≤ 15%, PV pos. = 0.32 and PV neg. = 0.90. The positive predictive values obtained were too low to let decreasing At-III give occasion for prophylactic anticoagulant treatment.

Deep Vein Thrombosis During Oral Contraception. An Analysis Of 57 Patients

1981 ◽  
Author(s):  
A Bergqvist ◽  
D Bergqvist ◽  
U Hedner
Keyword(s):  
Deep Vein Thrombosis ◽  
Fibrinolytic Activity ◽  
Vessel Wall ◽  
Oral Contraception ◽  
Vein Thrombosis ◽  
Release Capacity ◽  
At Iii ◽  
Estrogen Dose ◽  
The Right ◽  
Deep Vein

A phlebographic and haemostatic analysis has been made of 57 patients developing deep vein thrombosis while on combined oral contraceptives containing 30 or 50 μg estrogen. The diagnosis was based on ascending phlebography. One patient had bilateral, 18 rightsided and 38 leftsided thrombosis. The leftsided dominance was seen only in patients taking 50 μg estrogen daily. The thrombotic process was significantly more extensive and more proximally located in patients with leftsided thrombosis. Thirty-three percent of the rightsided and 8% of the leftsided thrombi embolised, a difference which is significant. Six to twelve months after the acute thromboembolic episode an analysis was made of platelet function, the coagulation and fibrinolytic systems. Only 5/57 patients had an excessive increase of f. VIII:C (>250%) and none had low AT III levels. Thirty-two percent of the patients had a defect in their vessel wall fibrinolysis (a defective release capacity and/or a decreased fibrinolytic activity within the vessel wall) and these patients developed rightsided thrombosis significantly more often.Judging from our findings a defective vessel wall fibrinolysis seems to be of pathogenetic significance for the development of deep vein thrombosis especially on the right side during oral contraceptive medication. The more extensive leftsided thrombi seemed to be dependent on the estrogen dose and not to the same extent associated with an impaired vessel wall fibrinolysis.

Deep Vein Thrombosis and Venous Thromboembolism in the Critically Ill

2017 ◽  
Author(s):  
Kathryn L. Butler ◽  
George Velmahos
Keyword(s):  
Pulmonary Embolism ◽  
Deep Vein Thrombosis ◽  
Venous Thromboembolism ◽  
Critically Ill ◽  
Oral Anticoagulants ◽  
Anticoagulation Therapy ◽  
Vena Cava ◽  
Vein Thrombosis ◽  
Vena Cava Filters ◽  
Deep Vein

Venous thromboembolism (VTE) poses unique diagnostic and therapeutic dilemmas in the intensive care unit (ICU). Immobility, inflammatory states, and trauma uniquely predispose surgical ICU patients to deep vein thrombosis and pulmonary embolism. Concurrently, the risks of perioperative and traumatic bleeding complicate management of VTE, with anticoagulation contraindicated in many scenarios. This review surveys the latest evidence in the diagnosis and management of VTE among critically ill surgical patients. It discusses evidence-based guidelines regarding diagnostic imaging, anticoagulation, prophylaxis, inferior vena cava filters, non–vitamin K oral anticoagulants, and surgical and catheter-based therapies. The review also examines the special challenges encountered when treating multisystem trauma patients.  Key words: anticoagulation therapy, deep vein thrombosis, pharmacoprophylaxis, pulmonary embolism, venous thromboembolism  

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