Letters Section Editor: Stephen J. Lurie,
MD, PhD, Senior Editor.
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.
Combes V, Taylor TE, Juhan-Vague I, Mège J, Mwenechanya J, Tembo M, Grau GE, Molyneux ME. Circulating Endothelial Microparticles in Malawian Children With Severe Falciparum Malaria Complicated With Coma. JAMA. 2004;291(21):2542-2544. doi:10.1001/jama.291.21.2542-b