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原发性血小板减少性紫癜(ITP)的发病机制是由于抗血小板抗体引起血小板破坏过多所致。这种特异性的抗血小板抗体大部分是IgG型,产生血小板抗体的血小板相关抗原的性质,目前尚难肯定。我院1987年由苏州医学院血栓研究室提供抗血小板膜糖蛋白Ⅱb/Ⅲa(GPⅡ/Ⅲa)单克隆抗体测定35例ITP患者血浆中抗血小板膜GPⅡb/Ⅲa自身抗体(后简称抗GPⅡb/Ⅲa)含量,并同时测定30例正常人血浆进行比较。一、观察对象和方法1.对照组:30名健康献血员及本院职工,男12例,女18例,年龄20～42岁,无出
The pathogenesis of idiopathic thrombocytopenic purpura (ITP) is due to excessive platelet destruction caused by anti-platelet antibodies. The majority of this specific anti-platelet antibody is of the IgG type and the properties of platelet-associated antigens that produce platelet antibodies are not readily available. In our hospital, anti-platelet glycoprotein Ⅱb / Ⅲa (GPⅡ / Ⅲa) monoclonal antibody was obtained from the Thrombi Laboratory of Suzhou Medical College in 1987. Anti-platelet membrane GPⅡb / Ⅲa autoantibodies in plasma of 35 patients with ITP ) Content, and simultaneously measured 30 cases of normal plasma for comparison. First, the observed objects and methods 1. Control group: 30 healthy blood donors and hospital staff, 12 males and 18 females, aged 20 to 42 years, no