Key Points Hepcidin rises more dramatically in mild malaria than in severe malaria. Hepcidin levels are linked to inflammation, not anemia, in severe malarial anemia and cerebral malaria.

Malaria remains an important public heath concern in Nigeria because of its impact on child and maternal health, but the contribution of severe malaria to morbidity among Nigerian children was scantly reported. This study was undertaking to document the hospital-burden of severe malaria among children in Ibadan in order to reflect on the impacts and health implications of the current malaria control strategies. A review of 6-year case records of all children admitted to the emergency ward of the University College Hospital Ibadan was carried out. Cases of severe malaria were defined as those children in whom parasitaemia were confirmed with blood film microscopy and any of the WHO case definitions for severe malaria was documented. Severe malaria cases constituted 11.3% of 16 031 admissions (2000-05) with 89.1% being children <5 years old. Cerebral malaria accounted for about one-fifth (19.7%) of all severe malaria cases. The yearly proportional morbidity rate from severe malaria ranged from 8.7% to 13.2% with significant increase from 2000 to 2004 (X2 = 48.49; df = 5; P < 0.001). Severe malaria accounted for 12.4% of all paediatric deaths with an estimated overall case fatality rate of 9.6%. Deaths from malaria were significantly associated with wasting (Z-score for weight-for-height

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Systemic inflammation and sequestration of parasitized erythrocytes are central processes in the pathophysiology of severe Plasmodium falciparum childhood malaria. However, it is still not understood why some children are more at risks to develop malaria complications than others. To identify human proteins in plasma related to childhood malaria syndromes, multiplex antibody suspension bead arrays were employed. Out of the 1,015 proteins analyzed in plasma from more than 700 children, 41 differed between malaria infected children and community controls, whereas 13 discriminated uncomplicated malaria from severe malaria syndromes. Markers of oxidative stress were found related to severe malaria anemia while markers of endothelial activation, platelet adhesion and muscular damage were identified in relation to children with cerebral malaria. These findings suggest the presence of generalized vascular inflammation, vascular wall modulations, activation of endothelium and unbalanced glucose metabolism in severe malaria. The increased levels of specific muscle proteins in plasma implicate potential muscle damage and microvasculature lesions during the course of cerebral malaria.