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Results for “Antithrombin III Deficiency”

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At least 19 recordsLinked to original sources
PubMed1993

Obstetrical analgesia in a parturient with antithrombin III deficiency.

Antithrombin III (AT III) deficiency is a rare inherited disorder which predisposes patients to thrombotic complications. Anticoagulation is necessary to prevent recurrent thrombosis and high doses of heparin are often required. Anticoagulation complicates analgesia in parturients with the condition. We describe such a patient, in pre-term labour, who was successfully managed during labour with intravenous nalbuphine and inhaled nitrous oxide (N2O).

Administration, Inhalation↗
PubMed1981

Surgical implications of antithrombin III deficiency.

Antithrombin III is a potent coagulant inhibitor in plasma. Congenital deficiency of antithrombin III may predispose to thrombotic events and may complicate surgical management. We describe a patient with congenital antithrombin III deficiency who developed superior mesenteric vein thrombosis after the cessation of warfarin therapy which resulted in venous gangrene of the small intestine. Initial treatment of this deficiency with fresh frozen plasma and subsequent long-term management with warfarin therapy has been effective in avoiding further thrombotic events.

Adult↗
PubMed1987

Prophylactic use of antithrombin III concentrate following surgery in congenital antithrombin III deficiency.

Antithrombin III is the major physiological inhibitor of thrombin, and congenital deficiency of antithrombin III is associated with increased risk of venous thrombosis either spontaneously or following trauma, surgery or pregnancy. The successful use of antithrombin III concentrate during and following surgery to prevent venous thrombosis is described in a previously asymptomatic man with familial antithrombin III deficiency.

Antithrombin III↗
PubMed1980

A South African family with antithrombin III deficiency.

Antithrombin III is the most important natural inhibitor of coagulation. Reduced levels of antithrombin III are a well-documented cause of hypercoagulability. Several families have been described with hereditary antithrombin III deficiency, including one from South Africa. We report a second South African family with this defect.

Antithrombin III↗
PubMed1982

Familial antithrombin III deficiency.

Antithrombin III is the major physiological inhibitor of the coagulation mechanism and a deficiency of this protein results in a marked predisposition to venous thromboembolic disease. Three Scottish families with a deficiency of this protein are described and other reported families are reviewed. The properties, functions and methods of assay of antithrombin III are outlined; the molecular abnormalities, inheritance, clinical and laboratory characteristics of antithrombin III deficiency are described, and the use of antithrombotic drugs and human antithrombin III concentrates in this deficiency is discussed.

Adolescent↗
PubMed1990

Premature arterial disease associated with familial antithrombin III deficiency.

Antithrombin III (ATIII) deficiency is one of the few known abnormalities of the coagulation system known to predispose to venous thromboembolism but its relation to arterial disease is not established. We describe two related patients with this disorder, both of whom suffered arterial thrombotic events, at an early age. Both patients had other potential risk factors, though these would normally be considered unlikely to lead to such catastrophic events at such an age. Thrombosis due to ATIII deficiency is potentially preventable, and this diagnosis should be sought more frequently in patients with arterial thromboembolism, particularly if occurring at a young age. In addition, in patients with known ATIII deficiency, other risk factors for arterial disease should be eliminated, if possible. In particular, these patients should be counselled against smoking.

Adult↗
PubMed1987

[Antithrombin III determination in horses. Reference values and acquired antithrombin III deficiency].

Antithrombin III (AT III) determinations were done in healthy and sick horses using the chromogenic substrate Chromozym TH. Reference values for adult horses at 25 degrees C were 18-25 IU AT III per ml plasma and 84-118% AT III activity of normal horse plasma, respectively. Precision and accuracy were good (intra assay coefficient of variation less than 2%, accuracy 10%). Surgical operations on healthy horses led to a biphasic decrease in AT III activity touching the lower border of the reference values on the second postoperative day. Other reasons for acquired AT III deficiencies included disseminated intravascular coagulation (DIC), liver disease and glomerulonephritis. Using follow-up studies, differences in the dynamics of acquired AT III deficiency and coagulation promoting factors were demonstrated. 12 of 35 horses with decreased AT III values suffered from phlebothrombosis of the jugular veins. It was presumed that acquired AT III deficiencies promote development and progression of phlebothrombosis/thrombophlebitis in horses.

Animals↗
PubMed1976

Hereditary antithrombin III deficiency. Effect of antithrombin III deficiency on platelet function.

Antithrombin III (AT III) is the main physiologic inhibitor of thrombin, and activated factors X and IX as well. Normal levels of AT III appear to be necessary to maintain blood fluidity and to prevent thrombosis. Four families with AT III deficiency and recurrent venous thromboembolism have been reported on. We present an additional family with AT III deficiency and a high incidence of thromboembolism. AT III levels were determined by both a functional and an immunologic assay. Results of platelet function tests, not previously reported in persons with AT III deficiency, were found to be normal. Following gel filtration, the platelets were very sensitive to thrombin. Thrombin-induced platelet aggregation appears to be dependent on a balance between the amount of thrombin and AT III present.

Adolescent↗
PubMed1999

Plasma antithrombin III deficiency in ischaemic stroke in the young.

A deficiency of plasma antithrombin III has been identified as a potential risk factor for thrombosis. In a pilot study of 56 patients aged less than 40 years who presented with ischaemic stroke of unknown etiology, we detected only one case of plasma antithrombin III deficiency. Antithrombin III activity was estimated by a chromogenic assay. Hence, antithrombin III deficiency, though rare, should be considered while evaluating young patients with stroke of unknown etiology.

Adult↗
PubMed1992

[Acquired antithrombin III deficiency].

Acquired antithrombin III (AT III) deficiency is based on either decreased activity or synthesis, increased loss or increased consumption. The activity of AT III is decreased in metabolic acidosis, hyperlipoproteinemias and by lipid peroxides. Chronic liver diseases especially liver cirrhosis are associated with very low levels of AT III due to insufficient hepatic synthesis, reduced transcapillary flux ratios, diffuse intravascular coagulation and loss in the ascites. Gastrointestinal loss of AT III may occur in patients with active inflammatory bowel diseases. AT III deficiency is observed in nephrotic syndrome when urinary loss of protein exceeds 5 g/d. During hemodialysis we have not found low AT III levels. Disseminated intravascular coagulation is characterized by activation of the coagulation system and increased consumption of AT III. AT III complexes with activated coagulation factors are subsequently cleared by the reticuloendothelial system.

Antithrombin III↗
PubMed1993

Acquired antithrombin III deficiency: replacement with antithrombin III concentrates in a patient with protein S deficiency accelerates response to therapy.

A 33-year-old man with inherited protein S deficiency and a 20-year history of deep and superficial venous thrombosis was admitted for treatment of extensive, acute, superficial venous thrombosis of the left lower extremity. Clinical response to intravenous heparin was very slow. After discovery of acquired antithrombin III deficiency superimposed on the protein S deficiency, he was given antithrombin III concentrates with the intravenous heparin. His response to therapy was accelerated. The development of acquired antithrombin III deficiency in patients with venous thrombosis may slow the response to standard anticoagulant therapy. Therapy of the thrombosis may be improved with administration of antithrombin III concentrates.

Adult↗
PubMed1992

The pregnant antithrombin III deficient patient: management without antithrombin III concentrate.

Pregnant patients with antithrombin III (AT III) deficiency have an unacceptably high risk of venous thromboembolism (VTE). Antithrombotic therapy is therefore recommended. The reported clinical experience of such prophylaxis is limited. Some authors have recommended the use of AT III concentrate in addition to heparin in the management of these patients. We report successful management with heparin alone during pregnancy and the postpartum period in two patients with AT III deficiency. Both patients had experienced VTE during a prior pregnancy; one also experienced VTE during the reported pregnancy. Both patients were therefore at particularly high risk of further VTE. Based on the good results in these two patients, and a review of previously reported cases, we propose that heparin alone, in a dose to maintain the APTT in a therapeutic range, provides adequate prophylaxis and treatment for VTE during pregnancy and delivery in many AT III deficient subjects.

Adult↗
PubMed1993

Overtight nappy precipitating thrombosis in antithrombin III deficiency.

An antithrombin III deficient infant presented with iliac vein thrombosis, apparently precipitated by an overtight nappy. Venous thrombosis is unusual, both in normal and in antithrombin III deficient children, but children with venous thrombosis should have their natural anticoagulants assayed and obvious risk factors avoided.

Antithrombin III Deficiency↗
PubMed1991

[Clinical and genetic aspects of antithrombin III deficiency and abnormal antithrombin III].

Antithrombin III (AT III) has been confirmed to play an important role as a serine protease inhibitor in the mechanism of blood coagulation, and its deficiency or abnormality is found to cause thromboembolic disorders by reducing the anticoagulant activity. In this paper AT III gene of patient with congenital AT III deficiency, which was suggested to have qualitative abnormality by isoelectric focusing, was investigated. Analysis of the genomic structure by Southern blot hybridization with a cDNA probe (pAT6) revealed no detectable changes indicating any deletions, rearrangements and translocations. Therefore, we focused to analyze the sequence of exon 6 of AT III gene by polymerase chain reaction (PCR) methods followed by direct sequencing analysis. Nucleotide sequencing of exon 6 of AT III gene showed a G to T transitional mutation resulting in the conversion of arginine-406 to methionine coexisted with normal allele which encodes arginine. The mutation is located near the reactive center of AT III molecule, which region has been proved to be highly conserved during the evolution of serine protease inhibitor (serpin) family. From these results, it is concluded that the new type of mutation at amino acid site 407, which is similar to AT III Utah, is important for maintaining the structural and biological function of this inhibitor.

Antithrombin III↗
PubMed1993

Venous thrombosis: antithrombin III deficiency.

Antithrombin (ATIII) is believed to be one of the body's most powerful natural anticoagulants, so individuals with a deficiency of this protein exhibit a marked propensity to venous thrombosis. This article will focus on the pathophysiology of this disorder, including clinical presentation, diagnosis, and treatment.

Adult↗
PubMed1983

Molecular heterogeneity of inherited antithrombin III deficiency.

Inherited antithrombin III deficiency is associated with an increased risk of thromboembolism. Using recombinant-DNA techniques, we isolated a molecular probe for the antithrombin III structural gene and identified a common DNA polymorphism within the gene. We found that there is genetic heterogeneity in this disorder. In one family, the antithrombin III gene was deleted in affected members, whereas in another no deletion occurred. Use of the DNA polymorphism should allow identification and further characterization of abnormal antithrombin III genes.

Adolescent↗
PubMed1993

Congenital antithrombin III deficient neonate treated with antithrombin III concentrates.

A patient with antithrombin III deficiency developed deep vein thrombosis during her first pregnancy. Her pregnancy and delivery were successfully treated with simultaneous administration of antithrombin III concentrates and low molecular weight heparin. She delivered a 2,412g girl at 39 weeks' gestation. The baby was administered with antithrombin III concentrates as prophylaxis for neonatal arterial and venous thrombosis because the antithrombin III level was extremely low to be 2%. Her second pregnancy was uneventful at 38 weeks' gestation, and she was treated with administration of antithrombin III concentrates prophylactically. She delivered a 3,256g boy at 42 weeks' gestation without any complications. The antithrombin III level of the second baby was normal. These results showed that in a neonate with congenital antithrombin III deficiency the antithrombin III concentrates would be administered to prevent neonatal arterial and venous thrombosis.

Adult↗