PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Antithrombin III Deficiency”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 127 records · Page 7Linked to original sources
PubMed1986

[Therapeutic management of pregnancy complicated by congenital antithrombin III deficiency associated with pregnancy nephropathy].

Thrombo-embolic complications in pregnant women who have congenital antithrombin III deficiency are usually prevented by giving injections of sub-cutaneous heparin from the beginning to the end of pregnancy and with the administration of concentrated doses of antithrombin III (A.T. III) at delivery and in the following days. When we discovered a severe pre-eclampsia at the 28th week of pregnancy in a patient who had congenital deficiency of A.T. III and who had a past history of very severe thrombo-embolic complications we administered concentrated A.T. III as well as continuing the heparin treatment and anti-hypertensive treatment during the pregnancy. Severe fetal distress made us carry out a caesarean operation after 32 weeks of amenorrhoea. Delivery and the post-partum period were conducted without any complications. The newborn baby, who did not have congenital A.T. III deficiency, is very well.

Adult↗
PubMed1996

Aortic thrombosis in a neonate with hereditary antithrombin III deficiency: successful outcome with thrombolytic and replacement treatment.

We report the case of a newborn male who presented an aortic thrombosis during the neonatal period and was subsequently diagnosed as having antithrombin III (AT III) hereditary deficiency type I. This hypercoagulable condition is known to predispose young adults to venous thrombosis, but in our patient the primary thrombotic incident affected the arterial vessels within the first few days of life. Combined treatment with thrombolytic agents and AT III concentrates recovered aortic permeability, suggesting that the use of AT III may be beneficial for the treatment of thrombotic complications during the first few days of life.

Angiography, Digital Subtraction↗
PubMed1984

Thrombosis of an aortic porcine xenobioprosthesis associated with familial antithrombin III deficiency.

Thrombosis of a porcine xenobioprosthesis in the aortic position associated with antithrombin III deficiency has not been reported. Admittedly a rare coagulation abnormality, it should be suspected in patients with previous tendencies or family history toward spontaneous thrombosis, especially in those with Scandinavian ancestry. Special precautions should be taken if a cardiac operation becomes necessary.

Antithrombin III Deficiency↗
PubMed1995

Portal vein thrombosis due to antithrombin III deficiency. A case report.

The authors report a case of intrahepatic portal vein thrombosis in a sixty-four-year-old Japanese man with antithrombin III deficiency who successfully underwent cholecystectomy and common bile duct exploration. To their knowledge, this is the first report of portal vein thrombosis due to primary antithrombin III deficiency.

Antithrombin III Deficiency↗
PubMed2000

Antithrombin III deficiency in a patient with multifocal osteonecrosis.

The authors examined a 35-year-old man who had multifocal osteonecrosis on the right and left femoral heads, left humeral head, and right scaphoid. The patient previously had a diagnosis of Type I congenital antithrombin III deficiency but had no other risk factors for osteonecrosis. This patient was thought to have systemic thromboembolism because of the increased blood coagulability resulting from antithrombin III deficiency. Thrombophilia (increased likelihood of thrombosis) and hypofibrinolysis (reduced ability to lyse thrombi) have been implicated as causative factors for osteonecrosis. This case shows a possible relationship between thrombophilic antithrombin III deficiency and multifocal osteonecrosis.

Adult↗
PubMed1985

Protection against venous thrombosis in an antithrombin-III deficient patient suffering from episodes of arterial thrombosis requiring major surgery. Effects of oral stanozolol in combination with subcutaneous heparin and intravenous AT-III.

In an antithrombin-III (AT-III) deficient patient suffering from recurrent episodes of venous and arterial thrombosis requiring major surgery an attempt was made to institute antithrombotic protection by long-term stanozolol treatment supplemented during periods of thrombogenic exposure with subcutaneous heparin and, when needed, infusion of AT-III as plasma or concentrate. Stanozolol raised the plasma levels of AT-III, demonstrating a sparing effect on the AT-III needed. Despite the repeated exposures to major surgery, protection against venous thrombosis was complete, but the arterial disease progressed and led to the demise of the patient.

Administration, Oral↗
PubMedDate not supplied

Deficient antithrombin III activity and enhanced fibrinolysis in patients with liver disease: evidence against a cause-effect relationship.

To investigate the pathogenesis of fibrinolysis in liver disease, antithrombin III (AT III) activity, prothrombin fragment (F1 + 2) and d-dimer (D-DI) were measured in 50 patients with liver disease and in 17 healthy controls. Moreover, 4 patients with cirrhosis were randomly assigned to receive either an intravenous infusion of AT III (at two different dosages) or placebo, with a crossover design. Increased levels of D-DI were detected in patients with cirrhosis and hepatocellular carcinoma in comparison both with control subjects and with patients with acute hepatitis or mild chronic liver disease. An inverse correlation was observed between AT III and D-DI (r = -0.755, P < 0.001, simple linear regression), while no correlation was found between D-DI or AT III and F1 + 2. The correlation of the deficiency of AT III activity by infusion of human AT III did not result in any significant change (P0.10, analysis of variance for repeated measures) of the plasma concentration of either D-DI or F1 + 2, in comparison to placebo. Thus, advanced forms of chronic liver disease, but not acute hepatitis and mild forms of chronic liver disease, are associated with increased plasma concentrations of markers of fibrinolysis, which are inversely correlated with AT III activity. However, the correction of the deficient AT III activity does not affect the plasma concentration of either D-DI or F1 + 2, thence not supporting the hypothesis that enhanced fibrinolysis in advanced liver disease is the result of low-grade disseminated intravascular coagulation.

Adult↗
PubMed1987

Extensive thrombus formation with heparin resistance during extracorporeal circulation. A new presentation of familial antithrombin III deficiency.

Extensive thrombus formation during extracorporeal circulation despite the administration of heparin sodium prompted investigation of a 15-year-old boy with a calcified right ventricular thrombus and a history of subacute bacterial endocarditis. In vitro studies confirmed the failure of heparin in standard doses to have an anticoagulant effect. Antithrombin III concentrations were low. The patient's mother, who had no history of thromboembolic disease, was also antithrombin III deficient. Resistance to heparin is a theoretical, but inconsistently documented, feature of antithrombin III deficiency. This deficiency state should be considered whenever heparin resistance is encountered, even in the absence of a personal and family history of thromboses.

Adolescent↗
PubMed1978

Acquired antithrombin III deficiency in patients with glomerular proteinuria.

Antithrombin III (AT II/III) was determined immunologically and by means of a heparin cofactor assay in plasma samples and 24-hour urine of 15 patients with various degrees of proteinuria, being predominantly of glomerular origin. In urine the AT II/III concentrations were significantly correlated to the concentrations of albumin, plasminogen and IgG. One third of the patients had AT II/III plasma levels below the normal range. The plasma levels showed a significant inverse correlation to the AT II/III and albumin clearance rates. Similarily, the plasminogen concentrations in plasma were decreased in two thirds of the patients, being inversely correlated to the renal plasminogen clearance values. It is proposed that AT II/III deficiency in the nephrotic syndrome is an important pathogenetic factor in venous thrombosis.

Adolescent↗
PubMed1986

Hereditary antithrombin III deficiency: case report and review of recent therapeutic advances.

We report on a newly diagnosed family with hereditary antithrombin III deficiency, with thromboembolic complications in the propositus. Both the propositus and his asymptomatic sister had decreased plasma levels of antithrombin III antigen and activity (28-52% of normal with good agreement between functional and immunologic assays). The propositus developed deep venous thrombosis, followed by massive pulmonary emboli despite heparin therapy and was treated with streptokinase and heparin with excellent results. Shortly thereafter, small bowel obstruction required surgical intervention, and antithrombin III concentrate, recently available in the United States as an investigational new drug (I.N.D.), was administered with no postoperative thrombotic complications. He was subsequently asymptomatic while on warfarin prophylaxis but twice developed venous thrombosis when he failed to take warfarin. The addition of danazol therapy led to a sustained rise in the antithrombin III level. Each of these therapeutic approaches is discussed and the literature reviewed with emphasis on the newer agents--streptokinase, antithrombin III concentrate, and danazol.

Adult↗
PubMed1995

Catastrophic secondary antiphospholipid syndrome with concomitant antithrombin III deficiency.

The association between thrombotic events and primary or secondary antiphospholipid/anticardiolipin syndrome is now well recognized. A spectrum of renal involvement ranging from glomerular thrombosis to renal infarction has been described. A case of systemic lupus erythematosus with immunoglobulin G and M antiphospholipid/anticardiolipin antibodies is reported. The patient developed catastrophic thrombosis in multiple organs, and glomerular thrombosis was documented by renal biopsy. The patient had an acquired antithrombin III deficiency, and the combination of secondary antiphospholipid syndrome with accompanying antithrombin III deficiency predisposed to thrombosis. Several mechanisms by which antiphospholipid/anticardiolipin antibodies cause thrombosis have been proposed and are briefly reviewed.

Adult↗