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Blood, Vol. 95 No. 4 (February 15), 2000:
pp. 1481-1486
Red cell surface changes and erythrophagocytosis in children with
severe Plasmodium falciparum anemia
John N. Waitumbi,
Malachi O. Opollo,
Richard O. Muga,
Ambrose O. Misore, and
José A. Stoute
US Army Medical Research Unit, Kenya; the Kenya Medical Research
Institute, Nairobi, Kenya; the Nyanza Provincial General Hospital,
Kisumu, Kenya; Department of Medicine, Uniformed Services University of
Health Sciences, Bethesda, MD; and the Kenyan Ministry of Health.
Severe anemia is one of the most lethal complications in
children infected with Plasmodium falciparum. The pathogenesis
of this anemia is not completely understood. Experimental data from malaria-infected humans and animal models suggest that uninfected red
cells have a shortened life span. This study looked for changes in the
red cell surfaces of children with severe malarial anemia that could
explain this accelerated destruction. A prospective case-control study
was conducted of children with severe P falciparum anemia
(hemoglobin of 5 g/dL or lower) admitted to a large general hospital in
western Kenya. Children with severe anemia were compared with children
who had symptoms of uncomplicated malaria and with asymptomatic
children. Cytofluorometry was used to quantify in vitro
erythrophagocytosis and to measure red cell surface immunoglobulin G
(IgG) and the complement regulatory proteins CR1, CD55, and CD59. Red
cells from patients with severe anemia were more susceptible to
phagocytosis and also showed increased surface IgG and deficiencies in
CR1 and CD55 compared with controls. Red cell surface CD59 was
elevated in cases of severe anemia compared with asymptomatic controls
but not as compared with symptomatic controls. The surface of red cells
of children with severe P falciparum anemia is modified by the
deposition of IgG and alterations in the levels of complement regulatory proteins. These changes could contribute to the accelerated destruction of red cells in these patients by mechanisms such as
phagocytosis or complement-mediated lysis.
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