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Letters
June 2, 2004

Circulating Endothelial Microparticles in Malawian Children With Severe Falciparum Malaria Complicated With Coma

Author Affiliations
 

Letters Section Editor: Stephen J. Lurie, MD, PhD, Senior Editor.

JAMA. 2004;291(21):2542-2544. doi:10.1001/jama.291.21.2542-b

To the Editor: Malaria remains a major problem of public health in developing countries and is responsible for more than 1 million deaths each year.1 Life-threatening malaria is predominantly a result of Plasmodium falciparum infection, and central nervous system involvement, ie, "cerebral malaria," is observed in approximately 1% of P falciparum infections and is a major cause of death. In P falciparum malaria, parasitized erythrocytes sequester in capillary beds through adhesion to vascular endothelium, a process that occurs predominantly in deep tissues not amenable to direct examination.2 Activation of microvascular endothelium in a variety of disease states causes the release of endothelial microparticles (EMPs) into the circulation.3 Plasma concentrations of tumor necrosis factor (TNF) are increased in patients with malaria,2 and TNF can induce the release of procoagulant and proadhesive microparticles from cultured endothelial cells in vitro.3 Numbers of EMPs in peripheral blood may therefore serve as a marker of endothelial activation in deep tissues. Although increased numbers of EMPs are found in patients with inflammatory disease and severe sepsis,4 EMPs have not previously been studied in human malaria.

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