Rose M, Wideman C S, Evatt B L, Haff E
Clin Lab Haematol. 1983;5(2):185-95. doi: 10.1111/j.1365-2257.1983.tb01351.x.
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.
抗凝血酶III（AT III）是血液凝固机制中凝血酶和其他丝氨酸蛋白酶最有效的生理性灭活剂。这种蛋白质的遗传性缺乏与始于青春期后期的复发性深静脉血栓形成有关。未经治疗，这种疾病可能因复发性大量肺栓塞导致早期死亡。由于缺乏检测方法的标准化以及无法比较不同AT III检测结果，试图确定因获得性AT III缺乏而最有可能发生血栓栓塞性疾病的患者群体的努力一直受挫。功能检测和免疫电泳测定所测量的并非同一成分。为了比较当前AT III检测方法在各种疾病状态下测定AT III水平的能力，我们使用免疫电泳、显色和可凝固检测法来测量先天性AT III缺乏患者以及可能存在获得性AT III缺乏患者的AT III。
