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血小板减少症患者体内的免疫复合物:是病因还是结果?

Immune complexes in thrombocytopenic patients: cause or effect?

作者信息

Trent R J, Clancy R L, Danis V, Basten A

出版信息

Br J Haematol. 1980 Apr;44(4):645-54. doi: 10.1111/j.1365-2141.1980.tb08719.x.

Abstract

Immune complexes (ICs) in the serum of 43 patients with chronic idiopathic thrombocytopenic purpura (ITP) were measured by the C1q deviation assay during the active and inactive phases of the disease. An inverse relationship between platelet count and levels of ICs was demonstrated in all but one patient. To test whether this phenomenon was specific for chronic ITP, ICs were assayed in sera from two groups of control patients with thrombocytopenia. Goup 1 had thrombocytopenia due to recognized immune mechanisms while group 2 had thrombocytopenia secondary to non-immune mechanisms. In both these groups the degree of thrombocytopenia proved to be inversely proportional to IC levels, which was similar to the pattern observed in chronic ITP. The specificity of the assay for detection of ICs was confirmed by demonstrating a positivity rate of 65% in sera of patients with systemic lupus erythematosus, a known IC disease. On analysis the ICs were shown to have molecular weights in excess of 500,000 daltons and contain variable immunoglobulin classes. The findings implicate ICs in immune destruction of platelets both in chronic ITP (as has been suggested previously) and also in thrombocytopenia secondary to known immune mechanisms. In addition the association of ICs with non-immune thrombocytopenias is consistent with the hypothesis that platelets play an important role in clearance of ICs from the circulation, thereby protecting the vascular endothelium from damage.

摘要

采用C1q偏离试验对43例慢性特发性血小板减少性紫癜(ITP)患者在疾病活动期和非活动期血清中的免疫复合物(ICs)进行了检测。除1例患者外,所有患者均显示血小板计数与ICs水平呈负相关。为了检验这种现象是否为慢性ITP所特有,对两组血小板减少症对照患者的血清进行了ICs检测。第1组血小板减少是由已知的免疫机制所致,而第2组血小板减少是继发于非免疫机制。在这两组中,血小板减少程度均与IC水平呈反比,这与慢性ITP中观察到的模式相似。通过显示系统性红斑狼疮(一种已知的IC疾病)患者血清中的阳性率为65%,证实了该检测方法检测ICs的特异性。经分析,ICs的分子量超过500,000道尔顿,且含有多种免疫球蛋白类别。这些发现表明,ICs在慢性ITP(如先前所提示的)以及继发于已知免疫机制的血小板减少症中均参与了血小板的免疫破坏。此外,ICs与非免疫性血小板减少症的关联与以下假设一致,即血小板在从循环中清除ICs方面发挥重要作用,从而保护血管内皮免受损伤。

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