Malarial anemia leads to adequately increased erythropoiesis in asymptomatic Kenyan children.

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 x 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.