Ibarra H, Zapata C, Inostroza J, Mezzano S, Riedemann S
Blut. 1986 Jun;52(6):371-5. doi: 10.1007/BF00320784.
A 23-year-old man developed thrombocytopenic purpura at the end of the second week of the clinical evolution of hepatitis A confirmed by viral markers. The bone marrow of this patient showed megakaryocytic hyperplasia. Circulating in his serum immune complexes were demonstrated by solid phase conglutinin enzymo-immunoassay. Platelet-reactive serum factors were also detected by an indirect immunofluorescence test using fresh donor platelets as targets. The evolution of both the hepatitis and the purpura were benign with no therapy other than bedrest. Platelet count normalized within five weeks of the onset of purpura, and IgM antibodies against hepatitis A virus as well as circulating immune complexes dropped to normal levels. It is postulated that the thrombocytopenia of this case was caused by nonspecific deposition of immune complexes at the platelet surface.
一名23岁男性在甲型肝炎临床病程第二周结束时，经病毒标志物确诊为甲型肝炎，同时出现血小板减少性紫癜。该患者的骨髓显示巨核细胞增生。通过固相凝集素酶免疫测定法证实其血清中有循环免疫复合物。还使用新鲜供体血小板作为靶标，通过间接免疫荧光试验检测到血小板反应性血清因子。除卧床休息外未进行其他治疗，肝炎和紫癜的病程均呈良性。紫癜发作后五周内血小板计数恢复正常，抗甲型肝炎病毒IgM抗体以及循环免疫复合物降至正常水平。据推测，该病例的血小板减少是由免疫复合物非特异性沉积于血小板表面所致。
