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Increased serum hepcidin and alterations in blood iron parameters associated with asymptomatic P. falciparum and P. vivax malaria

¹ Department of General Internal Medicine, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands
² Eijkman Institute for Molecular Biology, Jakarta, Indonesia
³ Karitas Hospital, Weetebula, Sumba Barat, Nusa Tenggara Timur, Indonesia
⁴ Department of Laboratory Medicine, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands

Correspondence: Quirijn de Mast, Department of Internal Medicine, Radboud University Medical Center PO Box 9101, 6500 HB, Nijmegen, the Netherlands. Phone: international +31.24.3619610 Fax: international +31.24.3566336. E-mail: q.demast{at}aig.umcn.nl

ABSTRACT

Background: Asymptomatic Plasmodium spp. infections and anemia are highly prevalent conditions in tropical regions. We studied whether asymptomatic parasitemia induces hepcidin- and/or cytokine-mediated iron maldistribution and anemia.

Design and methods: 1197 Indonesian schoolchildren, aged 5–15 years, were screened by microscopy for the presence of parasitemia. Concentrations of hemoglobin, serum hepcidin and parameters for iron status and inflammation were determined at baseline and 4 weeks after antimalarial treatment.

Results: Asymptomatic P. falciparum and P. vivax parasitemia were detected in 73 (6.1%) and 18 (1.5%) children, respectively, of whom 84% and 83% had a C-reactive protein concentration below 5mg/L. Children with P. falciparum or P. vivax parasitemia had significantly lower hemoglobin concentrations than 17 aparasitemic controls (12.6 and 12.2 g/dL vs. 14.4 g/dL; p<0.01), together with significantly higher serum hepcidin concentrations (5.2 and 5.6 nM vs. 3.1 nM; p <0.05). The latter was associated with signs of iron maldistribution with higher ferritin concentrations and lower values of serum iron concentration, transferrin saturation and erythrocyte mean cell volume. Concentrations of growth differentiation factor 15 were similar across groups. Antimalarial treatment partly reversed these abnormalities and lead to a significant increase in hemoglobin concentration.

Conclusions: Asymptomatic parasitemia is associated with increased hepcidin concentrations and anemia, in the absence of a manifest acute phase response. Prolonged iron maldistribution may be an underestimated cause of anemia. Screening for parasitemia should be performed before start of iron supplements, as iron therapy may be less effective and even hazardous in these circumstances.