Howard M A, Firkin B G
Thromb Haemost. 1983 Dec 30;50(4):775-9.
Plasmas from ten patients with a lupus or lupus-like inhibitor were investigated. In each case the partial thromboplastin time with kaolin (PTTK) was prolonged and failed to correct on the addition of an equal volume of normal plasma. Activated control platelets corrected the inhibitory effect in the PTTK or thrombin generation time (TGT) in every instance. Activated autologous platelets were as effective as control platelets and may thus explain why bleeding is rarely associated with the lupus inhibitor. Experiments using platelets or plasma from patients congenitally deficient in a single clotting factor or normal washed platelets resuspended in deficient plasma indicated that the inhibitor by-passing activity is platelet and not plasma derived. Platelet fractionation studies suggested that this activity is localised at the platelet membrane.
对10例患有狼疮或狼疮样抑制剂的患者的血浆进行了研究。在每种情况下，高岭土部分凝血活酶时间（PTTK）均延长，加入等量正常血浆后仍未纠正。活化的对照血小板在每种情况下均能纠正PTTK或凝血酶生成时间（TGT）中的抑制作用。活化的自体血小板与对照血小板一样有效，因此可以解释为什么出血很少与狼疮抑制剂相关。使用先天性缺乏单一凝血因子的患者的血小板或血浆，或悬浮在缺乏血浆中的正常洗涤血小板进行的实验表明，抑制剂旁路活性源自血小板而非血浆。血小板分级分离研究表明，这种活性定位于血小板膜。
