TREATMENT OF REFRACTORY IMMUNE THROMBOCYTOPENIC PURPURA WITH AN ANTI-FC-GAMMA-RECEPTOR ANTIBODY
TREATMENT OF REFRACTORY IMMUNE THROMBOCYTOPENIC PURPURA WITH AN ANTI-FC-GAMMA-RECEPTOR ANTIBODY
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DOI：
10.1056/nejm198605083141907
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发表时间：
1986-05-08
影响因子：
158.5
通讯作者：
UNKELESS, JC
中科院分区：
文献类型：
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作者：
CLARKSON, SB;BUSSEL, JB;UNKELESS, JC
抗血小板抗体的产生和单核巨噬细胞系统对包被免疫球蛋白的血小板的清除在免疫性血小板减少性紫癜的发病机制中起重要作用。包被免疫球蛋白的血小板导致免疫球蛋白在脾和肝脏中的去除，推测是通过免疫球蛋白Fc片段(Fcγ)的受体。1，2脾切除后，Fcγ受体介导的调理红细胞清除的延长1，3和静脉注射大剂量丙种球蛋白，4，5结合这些治疗的良好的临床反应，支持这一假说。然而，一些患者对这些治疗或其他不太特异的免疫抑制形式，如……都没有反应。
THE production of antiplatelet antibodies and removal of IgG-coated platelets by the mononuclear phagocyte system play an important part in the pathogenesis of immune thrombocytopenic purpura. The coating of platelets with immunoglobulin results in their removal in the spleen and liver, presumably by receptors for the Fc fragment of IgG (Fcγ).1,2Prolongation of Fcγ-receptor-mediated clearance of opsonized red cells after splenectomy1,3and infusions of high doses of intravenous gamma globulin,4,5in conjunction with favorable clinical responses to these therapies, support this hypothesis. Some patients, however, respond to neither of these treatments nor to other, less specific forms of immunosuppression, such . . .