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  • Title: A comparison of antithrombin III procedures.
    Author: Rose M, Wideman CS, Evatt BL, Haff E.
    Journal: Clin Lab Haematol; 1983; 5(2):185-95. PubMed ID: 6883970.
    Abstract:
    Antithrombin III (AT III) is the most potent physiologic inactivator of thrombin and other serine proteases in the blood clotting mechanism. Hereditary deficiency of this protein is associated with recurrent deep-vein thrombosis that begins in late adolescence. Untreated, this disease may lead to early death from recurrent and massive pulmonary emboli. Attempts to identify groups of patients who are the most likely to develop thromboembolic disease because of an acquired deficiency of AT III have been frustrated by the lack of standardization of the assays and the inability to compare results of the different AT III assays. The functional assays and immunoelectrophoretic determinations do not measure the same component. In order to compare the ability of current AT III procedures to determine levels of AT III in various disease states, we used immunoelectrophoretic, chromogenic, and clottable assays to measure the AT III of patients with congenital AT III deficiency and of patients with possible acquired AT III deficiency. Antithrombin 3 (AT 3) is the most potent physiologic inactivator of thrombin and other serine proteases in the blood clotting mechanism. Hereditary deficiency of this protein is associated with recurrent deep vein thrombosis that begins in late adolescence. Untreated, this disease may lead to early death from recurrent and massive pulmonary emboli. Attempts to identify groups of patients most likely to develop thromboembolic disease because of an acquired deficiency of AT 3 have been frustrated by the lack of standardization of the assays and the inability to compare results of different AT 3 assays. The functional assays and immunoelectrophoretic determinations do not measure the same component. In order to compare the ability of current AT 3 procedures to determine levels of AT 3 in various disease states, we used immunoelectrophoretic, chromogenic, and clottable assays to measure AT 3 in patients with congenital AT 3 deficiency and with possible acquired AT 3 deficiency.
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