Acquired antithrombin III deficiency and systemic lupus erythematosus.
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appropriate evaluation of synovial fluid be carried out in all such patients.Keywords:
Antithrombin III deficiency
Systemic lupus
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.
Antithrombin III deficiency
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Antithrombin III deficiency
Pathophysiology
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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 IIIdeficiency are described, and the use of antithrombotic drugs and human antithrombin III concentrates in this deficiency is discus
Antithrombin III deficiency
Inheritance
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The pregnancy and the serum antithrombin III levels during the antenatal and postpartum period of two patients with hereditary antithrombin III deficiency is described. Both antithrombin III antigen and activity levels dropped to their lowest levels immediately after delivery. A review of the literature emphasizes the high risk for thromboembolism in patients with hereditary antithrombin III deficiency. Important considerations for the obstetrician concerning hereditary antithrombin III deficiency are discussed, including: 1) the need to therapeutically anticoagulate these patients postpartum, 2) the need to consider prophylactic anticoagulation throughout pregnancy especially in patients with a history of thrombosis, 3) the practical aspects of assaying antithrombin III in plasma rather than serum, 4) the normally low antithrombin III levels in normal newborns, and 5) the need to provide prepregnancy counseling, including information about the autosomal dominant inheritance of hereditary antithrombin III deficiency.
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S ummary . A family including four members with decreased antithrombin III (ATIII) measured by a biological and an immunological method is described. Immunologically measured levels of other coagulation inhibitors were normal. In the antithrombin III deficient family members there was a history of thrombotic disease. Turnover of 125 I‐antithrombin III in a deficient individual showed the lower plasma levels probably to be due to a deficiency in the rate of synthesis rather than to an increased catabolic rate.
Antithrombin III deficiency
Catabolism
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SummaryThis paper describes two Belgian families in which congenital plasma antithrombin III deficiency was found. Both propositi presented with recurrent iliac vein thrombosis. These patients strikingly illustrate known features of antithrombin III deficiency: the occurrence of thrombosis in association with the intake of oestrogen or with pregnancy and delivery; the relative resistance to the anticoagulant effect of heparin; the rebound hypercoagulability following interruption of heparin administration, due to a more pronounced decrease of the antithrombin III level. The relevant literature is reviewed.
Antithrombin III deficiency
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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.
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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.
Antithrombin III deficiency
Anticoagulant Therapy
Protein S deficiency
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Evidence linking familial thrombosis with a defective antithrombin III gene in two British kindreds.
Using DNA probes in a structural study of the antithrombin III gene locus we found no evidence of gene deletion in two British kindreds with inherited antithrombin III deficiency. However, linkage analysis between a common DNA polymorphism and the antithrombin III deficiency trait showed that the defect lies at or close to the antithrombin III structural gene. The lod score for linkage within the larger Scottish kindred was 3.1 (theta = 0). These results are consistent with previously published data suggesting that mutation of the antithrombin III structural gene is the cause of inherited antithrombin III deficiency in some families.
Antithrombin III deficiency
Genetic linkage
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Antithrombin III deficiency
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