An abnormal plasma antithrombin with no apparent afflnity for heparin
Laboratoire de Biochimie - Faculté de Médecine - F-37032 TOURS Cedex, FranceThrombosis Research (Impact Factor: 2.45). 06/1984; 34(4):297-302. DOI: 10.1016/0049-3848(84)90386-4
Congenital antithrombin abnormality was found in several members of a French family. No history of thrombotic episodes was associated with this abnormality. Plasma antithrombin concentration as well as the rate of thrombin inactivation by defibrinated plasma in the absence of heparin were normal. However, the heparin cofactor activity was decreased by about 50% in plasma of affected patients. Accordingly, about half the amount of plasma antithrombin did not bind to gel bound heparin. Moreover the crossed immunoelectrophoretic pattern in the presence of heparin demonstrated two peaks of antithrombin, the slower one migrating as normal antithrombin when heparin was omitted from the first agarose gel. It was concluded that molecular alteration of the antithrombin molecule seemed to affect only the heparin binding site thus preventing from any rate enhancement of thrombin inactivation.
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ABSTRACT: An antithrombin III (AT III) functional defect (AT III Charleville) was discovered in a patient presenting with recurrent venous thrombosis. Both anti-activated factor X (anti Xa) and antithrombin activity were decreased, in the absence and in the presence of heparin, while protein concentration was normal in an immunological assay. The abnormal AT III copurified with functional AT III using insolubilized heparin affinity chromatography. Polyacrylamide gel electrophoresis (PAGE) and high pressure liquid chromatography (HPLC) on a TSK column suggest that AT III Charleville forms unstable complexes with thrombin from which a modified protein is rapidly released.Thrombosis Research 10/1985; 39(5):559-70. DOI:10.1016/0049-3848(85)90236-1 · 2.45 Impact Factor
- Nucleic Acids Research 04/1986; 14(5):2408. DOI:10.1093/nar/14.5.2408 · 9.11 Impact Factor
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ABSTRACT: The biochemical and biological properties of antithrombin III (AT III) and the clinical consequences of a deficiency of this inhibitor are described. Therapy with concentrates of purified AT III has been carried out for about 10 years and the present experience is reviewed. In a relatively small number of patients with congenital AT III deficiency it is necessary, under certain condition to substitute AT III. A considerably more frequent use of AT III concentrates has been made in acquired AT III deficiency, especially in shock and diffuse intravascular coagulation (DIC). This therapy was shown to be promising since the duration of DIC could be considerably shortened and the frequency of fatal events could be significantly diminished. No undesirable side effects of substitution with virus-sterilized AT III concentrates have been hitherto observed.Vox Sanguinis 02/1987; 53(4):193-8. · 2.80 Impact Factor
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