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疟疾中的血液和骨髓变化。

Blood and bone marrow changes in malaria.

作者信息

Wickramasinghe S N, Abdalla S H

机构信息

Department of Haematology, Imperial College School of Medicine, St Mary's Campus, London, W2 1PG, UK.

出版信息

Baillieres Best Pract Res Clin Haematol. 2000 Jun;13(2):277-99. doi: 10.1053/beha.1999.0072.

Abstract

A variety of abnormalities in the number, morphology and function of blood and bone marrow cells may be found in Plasmodium falciparum and P. vivax malaria. In a non-immune individual, the nature of such abnormalities depends on the time after infection. In others it is determined by the pattern and intensity of malaria transmission in the area and the extent of host immunity. Severe anaemia may occur in children with chronic falciparum malaria and low parasitaemia as well as in patients with complicated acute falciparum malaria with high parasitaemia. However, the mechanisms underlying the anaemia in these two situations appear to be different. The possible roles of parasite products, T-cell-derived cytokines produced in response to the infection, macrophage activation and hyperplasia, macrophage-derived factors such as tumour necrosis factor-alpha, and macrophage dysfunction in the pathogenesis of the haematological abnormalities are discussed.

摘要

在恶性疟原虫和间日疟原虫疟疾中,可能会发现血液和骨髓细胞的数量、形态及功能存在多种异常。在非免疫个体中,此类异常的性质取决于感染后的时间。在其他个体中,则由该地区疟疾传播的模式和强度以及宿主免疫程度决定。重度贫血可能发生在慢性恶性疟且疟原虫血症水平低的儿童中,也可能出现在急性复杂性恶性疟且疟原虫血症水平高的患者中。然而,这两种情况下贫血的潜在机制似乎有所不同。本文讨论了寄生虫产物、感染后产生的T细胞源性细胞因子、巨噬细胞活化与增生、巨噬细胞源性因子如肿瘤坏死因子-α以及巨噬细胞功能障碍在血液学异常发病机制中的可能作用。

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