Antithrombin III, Antifactor Xa and Heparin

Biggs, Rosemary; Denson, K. W. E.; Akman, N; Borrett, R.; Hadden, M. Kyle

doi:10.1111/j.1365-2141.1970.tb01627.x

Cited by 218 publications

(75 citation statements)

References 7 publications

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“…Fibrino gen-fibrin degradation products (FDP) were mea sured by the latex aggregation method (Teikokuzoki Pharm., Tokyo). Antithrombin III was determined by two methods, i.e., activity according to Biggs et al [2] and immunological levels according to an M-Partigen single radial immunodiffusion plate (Behringwerke). a r Antitrypsin, a2-macroglobulin and C|-INH were also determined by the single radial im munodiffusion method.…”

Section: Methodsmentioning

confidence: 99%

Factor XIII Deficiency Associated with Klippel-Weber Disease, Platelet Dysfunction and Cryofibrinogenemia

et al. 1983

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A 23-year-old woman with factor XIII deficiency was presented. The patient had no consanguinity, but familial traits were present. A bleeding tendency and poor wound healing had been noted in the patient since birth. She had hemangiomas in the leg and vulva (Klippel-Weber disease). Hematologic studies revealed platelet dysfunction, cryofibrinogenemia and mild chronic disseminated intravascular coagulation with prolonged PT and PTT, hypofibrinogenemia, a high turnover rate of ¹²⁵I-fibrinogen and mild elevation of fibrinogen-fibrin degradation products, β-thromboglobulin and platelet factor 4. A decrease in clot retraction and a marked reduction in maximal amplitude of thrombelastogram were also found. The assay of the factor XIII level was 10% by the antiserum inhibition method, and the assay of subunits A and S were 16 and 29%, respectively, by the electroimmunoassay method. Transamidase activity of factor XIII was 26%. The level of factor XIII of her sister was low, similar to that of the patient. The concentration of cold-insoluble globulin in EDTA-plasma was 36.5 mg/dl.

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Section: Methodsmentioning

confidence: 99%

Factor XIII Deficiency Associated with Klippel-Weber Disease, Platelet Dysfunction and Cryofibrinogenemia

et al. 1983

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“…presence of low heparin concentrations and ATIII is probably identical with the agent formerly known as plasma heparin cofactor. [8][9][10] A predisposition to venous thrombosis, such as is acquired during oestrogen treatment and surgery, has been associated with reduced ATIII concentrations.8 11-13 A clearer. association of venous thrombosis with reduced concentrations of this coagulation inhibitor occurs in the rare hereditary deficiency of ATIII.14 We describe here a large family in which major thromboembolic disease was associated with ATIII deficiency.…”

Section: Introductionmentioning

confidence: 99%

Familial thrombosis: inherited deficiency of antithrombin III.

Mackie¹,

Bennett²,

Ogston³

et al. 1978

BMJ

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“…However, only a fraction of all heparin molecules has high affinity for antithrombin III and these high affinity-heparin molecules account for most of the anticoagulant activity (14). The antithrombin-heparin system also inactivates several other factors in the coagulation cascade such as IXa, Xa, XIa and XIIa (15)(16)(17)(18). Under the optimally comparable conditions, the synthetic inhibitors exhibited a more potent antithrombotic effect than heparin in our highly thrombogenic venous graft model.…”

Section: Discussionmentioning

confidence: 99%