Salama A, Mueller-Eckhardt C, Kiefel V
Lancet. 1983 Jul 23;2(8343):193-5. doi: 10.1016/s0140-6736(83)90175-7.
The rapid rise in platelet count after immunoglobulin treatment in acute and chronic forms of idiopathic thrombocytopenic purpura (ITP), autoimmune neutropenia, and post-transfusion purpura is well documented. It is suggested that the rise in platelet count is due to competitive inhibition of the macrophage binding of platelets by preferential sequestration of immunoglobulin-coated red blood cells. Measurement of haptoglobin levels, a sensitive indicator of haemolysis, suggests that clinically inapparent haemolysis occurs during immunoglobulin therapy of ITP patients. In-vitro experiments confirm that there is immunoglobulin coating of red blood cells. The hypothesis is further supported by the findings that immunoglobulin treatment in autoimmune haemolytic anaemia is ineffective, and that platelet counts rise in some ITP patients after induction of a mild haemolytic syndrome by injection of anti-Rho (D).
免疫球蛋白治疗急性和慢性特发性血小板减少性紫癜(ITP)、自身免疫性中性粒细胞减少症及输血后紫癜后血小板计数迅速上升,这已有充分文献记载。有观点认为,血小板计数上升是由于免疫球蛋白包被的红细胞被优先隔离,从而竞争性抑制巨噬细胞与血小板的结合。触珠蛋白水平是溶血的敏感指标,对其测量表明,ITP患者在接受免疫球蛋白治疗期间会发生临床上不明显的溶血。体外实验证实红细胞存在免疫球蛋白包被。自身免疫性溶血性贫血患者接受免疫球蛋白治疗无效,以及部分ITP患者注射抗Rho(D)诱导轻度溶血综合征后血小板计数上升,这些发现进一步支持了这一假说。