Anaemia is a public health problem affecting one quarter of the global population with significant health consequences as well as an adverse impact on social and economic development. In malaria endemic areas, Plasmodium infection remains the major cause of anaemia. The ferroportin Q248H mutation has been described to protect red blood cells against oxidative stress and malaria infection. The objective of this study was to describe the main mechanisms causing anaemia and the role of ferroportin Q248H mutation in relation with anaemia and malaria in childhood in a Bantu population living in the volcanic region of South Kivu. 1088 healthy children aged under five years were randomly selected in the health zone of Miti Murhesa in South Kivu/Democratic Republic of Congo. Almost 40% of children under five years were anaemic, submicroscopic Plasmodium infection was as high as 22.3%. The prevalence of ferroportin Q248H mutation was 11.4%. No difference was observed in the frequencies of malaria or anaemia between ferroportin mutated compared to ferroportin wild type children. The prevalence of iron deficiency was found to be high (49.1%) when free erythrocyte protoporphyrin (FEP) was used to assess iron status. We found zinc deficiency in 17.6% of children. The prevalence of anaemia in South Kivu remains high, children with low parasitemia detected by loop mediated-isothermal amplification assay (LAMP) but not by microscopy showed a significantly increased prevalence of anaemia. Ferritin, an acute phase protein of infection is less suited to assess iron status in endemic areas of Plasmodium infection.
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