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PubMed1988

Mechanisms of the development of acquired antithrombin III deficiency in the experimental nephrotic syndromes.

In the experiments on white rats was studied the role of excessive thrombinogenesis in the development of acquired antithrombin III deficiency in the experimental nephrotic syndrome. It was determined that excess thrombin generation induced the marked acceleration of 125I-antithrombin III clearance from blood stream in consequence formation of thrombin antithrombin III complexes with the following limited proteolysis of the inhibitor by enzyme. These results give evidence that apart from proteinuria the excess thrombin generation accompanied by nephrotic syndrome play a part in the development of acquired deficiency of antithrombin III in this experimental pathology.

Animals↗
PubMed1988

Antithrombin III deficiency.

A moderate reduction of plasma antithrombin activity is an uncommon but clinically important cause of severe thromboembolic disease. In recent years the molecule responsible for the major part of this activity (antithrombin III) has been extensively characterised and the mode of inheritance of familial deficiencies worked out. Over 30 autosomally dominant inheritable variants have been described, the gene for normal human antithrombin III has been sequenced and this information has provided important insights into the reaction of antithrombin with thrombin and the catalytic role of heparin. Further information has been derived by analogy with other serine proteinase inhibitors, in particular alpha 1 antitrypsin. Recombinant DNA methods have been used to produce functionally active AT III which may, in the future, replace human chromatographically-separated AT III as the treatment of choice for clinically important deficiency states. Newer diagnostic techniques, using restriction fragment length polymorphisms and synthetic oligonucleotide probes, hold the promise of more accurate diagnosis and diagnosis in the antenatal period in families possessing some of the fully characterised variants.

Antithrombin III Deficiency↗
PubMed1989

[Perioperative management of congenital antithrombin III deficiency].

We describe perioperative management of a patient with congenital antithrombin III (ATIII) deficiency, who had an oral surgical operation under general anesthesia. The patient had a history of thrombosis. Preoperative plasma ATIII activity was 52% of the normal value. ATIII concentrates had been administered to prevent perioperative thrombosis. During the operation, the plasma ATIII level was maintained at 128%, and there was no episode of abnormal hemostasis. But, he complained of pain in his left leg probably due to thrombosis on the third day after operation, when his plasma ATIII activity was supposed to be approximately 70%. It is recommended that the plasma ATIII level is maintained, at least, above 80% for one week after the operation.

Adult↗
PubMed1990

Elimination of antithrombin III concentrate in healthy pregnant and preeclamptic women with an acquired antithrombin III deficiency.

The activity elimination half-life of heat-treated antithrombin III (AT III) concentrate was studied in 5 healthy pregnant and 5 preeclamptic women with a documented AT III deficiency. Healthy pregnant women received 1500 units over 20 minutes. Serial blood specimens were obtained over the next 12 hours. The mean (+/- SEM) activity elimination half-life of AT III was 29.4h +/- 3.4h. Preeclamptic subjects had a mean baseline AT III activity of 70.5 +/- 2% (range 61 to 75%). Their activity eliminator half-life after 3000 units of AT III concentrate was 8.5 +/- 1.2h. There was a direct relationship between the pre-concentrate AT III activity level and the AT III activity elimination half-life (r = 0.79, p = 0.01) for all subjects. Based upon parameters calculated from the first infusion, the AT III activity of preeclamptic subjects was maintained by a constant infusion at approximately 100% for 96h. At the conclusion of the infusion, the activity elimination half-life was again measured. A dramatic increase in the activity elimination half-life was demonstrated (433.6h). We conclude that the activity elimination half-life of AT III concentrate is increased during normal pregnancy and further increased in preeclamptic women with an acquired deficiency.

Antithrombin III↗
PubMed1990

Occult antithrombin III deficiency: a potentially lethal complication of the postphlebitic limb.

Chronic venous insufficiency is a frequent sequel to lower extremity venous thrombosis. A relatively uncommon, but potentially lethal, cause of the thrombosis is congenital antithrombin III deficiency. Recognition and treatment of this occult deficiency is critical. The following report describes a family treated by the authors for this problem. In one generation of nine siblings, three males had documentation of the disease with functional antithrombin III levels in the range of 50% to 60%. Before evaluation for the deficiency one female sibling died at the age of 20 years as a consequence of a proven pulmonary embolus. Antithrombin III levels in another female sibling, who was free of symptoms, were normal (80% to 120%). Four other siblings who were free of symptoms (one female, three males) refused evaluation. All three men with the deficiency had severe, chronic, bilateral, lower extremity, venous insufficiency manifested by pain, varicosities, edema, pigmentation, and ulceration. Despite chronic warfarin therapy, one experienced recurrent pulmonary embolization with eventual loss of perfusion of the entire right lung. Ascending venography in the symptomatic males with the deficiency revealed evidence of recurrent and diffuse venous thrombosis with partial recanalization. Recurrent lower extremity venous thrombosis consequent to antithrombin III deficiency causes a particularly fulminant postphlebitic syndrome with characteristic venographic findings. Although potentially lethal if unrecognized and treated simply as venous insufficiency, chronic therapy with warfarin offers palliation and prolongs life.

Adult↗
PubMed1985

Antithrombin III deficiency: an etiology of Budd-Chiari syndrome.

This report documents a unique case of Budd-Chiari syndrome associated with antithrombin III deficiency and massive thrombus in the superior vena cava and right atrium. This aberration of the coagulation mechanism is proposed as an etiologic factor in the pathogenesis of hepatic venous obstruction whenever the cause is obscure. Antithrombin III was restored to a level adequate to permit thrombus extraction with cardiopulmonary bypass and relief of portal hypertension with a mesoatrial shunt. The protocol for reversing this hypercoagulable state with fresh frozen plasma and warfarin (Coumadin) is discussed, and technical innovations employed in the management of this complex problem are described.

Antithrombin III Deficiency↗
PubMed1982

[Prevention of thrombosis by Hemoclar. Preliminary results of a test in a patient with antithrombin III deficiency].

We report here preliminary results of a study comparing the effect of Hemoclar and antithrombin III (AT III) in a patient with an AT III congenital deficiency. Both drugs inhibit thrombin generation in the patient's plasma. Unlike AT III, Hemoclar also inhibits factor Xa generation. This led us to propose the use of Hemoclar, which acts via an AT III independent pathway, to prevent thrombosis in A III deficient patients.

Adult↗
PubMed1988

Surgery in patients with congenital antithrombin III deficiency.

A retrospective study is presented of 23 patients with congenital antithrombin (AT) III deficiency who underwent 57 operations of various types. Thromboprophylaxis was given in 28 operations. Dextran was used in most cases, sometimes in combination with specific AT III concentrate. No patient given AT III concentrate alone or in combination with other methods had signs of thromboembolism. Deep venous thrombosis followed four of the operations with prophylaxis (3 patients). After the 29 operations without prophylaxis there were three cases of deep venous thrombosis, one with clinical signs of pulmonary embolism and another with superficial thrombophlebitis. Despite its inherent drawbacks, this retrospective study indicated that AT III concentrate can effectively prevent postoperative thromboembolism. But as the selection criteria for thromboprophylaxis are difficult to evaluate, a prospective study should be of great value.

Adult↗
PubMed1989

Congenital antithrombin III deficiency: insights into the pathogenesis of the hypercoagulable state and its management using markers of hemostatic system activation.

Hereditary antithrombin III (ATIII) deficiency predisposes patients to venous thrombosis. The prothrombin fragment F1+2 radioimmunoassay demonstrates that many asymptomatic patients with this disorder not receiving antithrombotic therapy have elevated plasma factor Xa activity. The hemostatic system hyperactivity as measured by this assay could be specifically corrected by rising plasma ATIII levels of several persons into the normal range. This indicates that the prethrombotic state can be defined as an imbalance between the production and inhibition of factor Xa enzymatic activity. The effects of warfarin on factor Xa enzymatic activity in persons with congenital ATIII deficiency have also been evaluated. At equivalent intensities of oral anticoagulation, the mean plasma F1+2 level in patients with ATIII deficiency was significantly elevated as compared with anticoagulated persons without this inherited thrombotic disorder. It is concluded that the effect of warfarin on hemostatic system activation is modulated by the endogenous heparan sulfate-ATIII mechanism. This suggests that the F1+2 radioimmunoassay can be employed to improve the understanding of the hypercoagulable state associated with antithrombin III deficiency as well as to develop more effective treatment strategies to prevent thromboembolic events in patients with this disorder.

Antithrombin III Deficiency↗
PubMed1978

Antithrombin III deficiency in diabetes mellitus: influence on vascular degenerative complications.

Plasma Antithrombin III (At III), a natural inhibitor of coagulation, was determined using a single radial immunodiffusion technique. In 116 diabetics, plasma At III levels were significantly decreased (26.6 +/- 0.4 mg/100 ml) compared with those in 64 controls (31.0 +/- 0.3 mg/100 ml, P less than 0.001). An elevation of plasma fibrinogen degradation products in 42 per cent of our patients, and a positive linear relationship between platelet counts and At III levels ( r = 0.29, P less than 0.01), provided additional evidence for chronic disseminated intravascular clotting in diabetes mellitus. Diabetic retinal complications were more frequent in patient with low plasma At III levels (50.6 per cent of cases) than in those exhibiting At III concentrations within a normal range: 32.4 per cent of cases (X2 = 6.09, P less than 0.02). It is postulated that the low levels of At III encountered in diabetes result from excessive consumption, and that the deficiency may be responsible for the onset and/or aggravation of intravascular clotting. At III deficiency may therefore contribute to vascular degenerative complications, particularly those leading to diabetic retinopathy.

Adolescent↗
PubMed1977

Antithrombin III deficiency causing postsplenectomy mesenteric venous thrombosis coincident with thrombocytopenia.

The most commonly recognized cause of mesenteric venous thrombosis following splenectomy is hypercoagulation secondary to reactive thrombocytosis. A case is reviewed in which hypercoagulation followed splenectomy for idiopathic thrombocytopenic purpura (ITP) in spite of persistent thrombocytopenia. Episodic mesenteric venous occlusion occurred due to antithrombin III deficiency. This hypercoagulable state may be the cause of primary acute mesenteric venous occlusive disease. Symptoms and signs suggesting thrombosis in the portal circulation demand immediate coagulation studies since even in the thrombocytopenic patient thrombotic proglems can occur. Surgical intervention is the treatment of choice for segmental small bowel ischemia; warfarin therapy is indicated when there is evidence of antithrombin III deficiency.

Adult↗
PubMed1984

Heparin cofactor II determination--levels in normals and patients with hereditary antithrombin III deficiency and disseminated intravascular coagulation.

A technique is described to completely remove antithrombin III (AT) from small amounts of human plasma by immunoaffinity chromatography on antibodies against human AT linked to Sepharose 4B. The level of heparin cofactor II (HCII) was not affected by the immunoadsorption. HCII activity was then determined by measuring the rate of human thrombin inhibition by 3 ways: a) activation with heparin in AT-free plasma, b) activation with dermatan sulfate in normal plasma and c) activation with dermatan sulfate in AT-free plasma. The normal range of HCII varied between 0.7-1.5 U/ml, as compared to a normal plasma pool containing by definition 1 U/ml. Highly significant correlations between assays as obtained from 40 normal plasmas proved the suitability of the 3 assays, although the progressive thrombin inhibition by AT, when not removed, contributed about one fifth to the thrombin inhibition by HCII in the presence of dermatan sulfate. There were also highly significant correlations between HCII activity and antigen, as determined by rocket immunoelectrophoresis using specific antibodies against HCII. Levels of HCII and AT were examined in 7 patients with hereditary AT deficiency and 7 patients with disseminated intravascular coagulation (DIC). In hereditary AT deficiency, whereas the AT activity was reduced by half, levels of HCII activity and antigen were in the normal range. In DIC, a parallel decrease of HCII and AT suggests that HCII may participate in the inhibition of thrombin released during DIC and thus provides an inhibitor reserve, once the AT level becomes subnormally low.

Antigens↗
PubMed1981

Antithrombin III deficiency appearing as mesenteric vein thrombosis.

Mesenteric vein thrombosis is a relatively uncommon but devastating problem. Absence of any of the generally accepted etiologic factors of mesenteric vein thrombosis has lead to the diagnosis of "primary" mesenteric vein thrombosis in 25-55% of all cases. In this report we identify a young man with antithrombin III deficiency presenting as "primary" mesenteric vein thrombosis with massive bowel infarction. It again raises the possibility that other cases of "primary" mesenteric vein thrombosis may have been associated with this coagulopathy. Factors influencing antithrombin III levels are discussed in relation to diagnosis of the familial deficiency state in a patient with mesenteric vein thrombosis. The association of intra-abdominal venous occlusion and antithrombin III deficiency is emphasized.

Adult↗