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HIV感染患者血小板减少的机制。

The mechanism of thrombocytopenia in patients with HIV infection.

作者信息

Najean Y, Rain J D

机构信息

Department of Nuclear Medicine, Saint-Louis Hospital 1, Paris, France.

出版信息

J Lab Clin Med. 1994 Mar;123(3):415-20.

PMID:8133154
Abstract

From a retrospective analysis of 85 patients with thrombocytopenia and HIV infection, in whom platelet production and destruction were studied by isotopic methods, the following conclusions are drawn. In most recently infected patients thrombocytopenia is due to accelerated platelet destruction; in these patients the platelet sequestration is predominantly splenic, and splenectomy is usually effective. The same pattern is seen in approximately one third of patients with more advanced disease (i.e., those with AIDS-related complex or frank AIDS). In most patients with AIDS-related complex or AIDS, the thrombocytopenia is due chiefly to a platelet production defect; splenectomy is less likely to help and is thus generally inadvisable. When the patients who were receiving zidovudine were examined separately, they were found to have a lesser rate of platelet destruction but also to have a more prominent defect in platelet production defect. This suggests that the drug may help blunt platelet destruction but may do so at a price in marrow response to the thrombocytolysis.

摘要

通过对85例血小板减少症合并HIV感染患者进行回顾性分析,采用同位素方法研究血小板生成和破坏情况,得出以下结论。在近期感染的大多数患者中,血小板减少是由于血小板破坏加速;在这些患者中,血小板的扣押主要在脾脏,脾切除术通常有效。在约三分之一病情较严重的患者(即患有艾滋病相关综合征或典型艾滋病的患者)中也观察到相同模式。在大多数患有艾滋病相关综合征或艾滋病的患者中,血小板减少主要是由于血小板生成缺陷;脾切除术帮助不大,因此一般不建议进行。当单独检查接受齐多夫定治疗的患者时,发现他们的血小板破坏率较低,但血小板生成缺陷更为突出。这表明该药物可能有助于减轻血小板破坏,但可能是以骨髓对血小板溶解反应为代价的。

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