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Prepublished online as a Blood First Edition Paper on July 25, 2002; DOI 10.1182/blood-2001-12-0228.
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Blood, 15 November 2002, Vol. 100, No. 10, pp. 3489-3494
HEMATOPOIESIS
Malarial anemia leads to adequately increased erythropoiesis
in asymptomatic Kenyan children
Hans Verhoef,
Clive E. West,
Rob Kraaijenhagen,
Silas M. Nzyuko,
Rose King,
Mary M. Mbandi,
Susanne van Laatum,
Roos Hogervorst,
Carla Schep, and
Frans J. Kok
From the Division of Human Nutrition and Epidemiology,
Wageningen University, The Netherlands; the African
Medical and Research Foundation, Nairobi, Kenya; the
Department of Gastroenterology, Nijmegen University Medical Centre, The
Netherlands; and the Clinical-Chemical Laboratory, Eemland
Hospital, Amersfoort, The Netherlands.
Malarial anemia is associated with a shift in iron
distribution from functional to storage compartments. This suggests a
relative deficit in erythropoietin production or action similar to that observed in other infections. Our study in Kenyan children with asymptomatic malaria aimed at investigating whether malaria causes increased erythropoiesis, and whether the erythropoietic response appeared appropriate for the degree of resulting anemia. Longitudinal and baseline data were used from a trial with a 2 × 2 factorial design, in which 328 anemic Kenyan children were randomly assigned to
receive either iron or placebo, and sulfadoxine-pyrimethamine or
placebo. Erythropoiesis was evaluated by serum concentrations of
erythropoietin and soluble transferrin receptor. Prospectively collected data showed that malarial infection resulted in decreased hemoglobin concentrations, and increased serum concentrations of
erythropoietin and transferrin receptor. Conversely, disappearance of
malarial antigenemia resulted in increased hemoglobin concentrations, and decreased concentrations of these serum indicators. Additionally, our baseline data showed that current or recent malarial infection is
associated with increased serum concentrations of erythropoietin and
transferrin receptor, and that these were as high as or perhaps even
higher than values of children without malarial infection and without
inflammation. Our findings indicate that in asymptomatic malaria, the
erythropoietic response is adequate for the degree of anemia, and that
inflammation probably plays no or only a minor role in the pathogenesis
of the resulting anemia. Further research is needed to demonstrate the
role of deficient erythropoietin production or action in the
pathogenesis of the anemia of symptomatic malaria.
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