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ARS Home » Plains Area » Houston, Texas » Children's Nutrition Research Center » Research » Publications at this Location » Publication #227175

Title: Iron incorporation and post-malaria anaemia

Author
item Doherty, Conor
item Cox, Sharon
item Fulford, Antony
item Austin, Steven
item Hilmers, David
item Abrams, Steven
item Prentice, Andrew

Submitted to: PLoS One
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/23/2008
Publication Date: 5/7/2008
Citation: Doherty, C.P., Cox, S.E., Fulford, A.J., Austin, S., Hilmers, D.C., Abrams, S.A., Prentice, A.M. 2008. Iron incorporation and post-malaria anaemia. PLoS One [serial online]. 3(5):e2133.

Interpretive Summary: Extra iron supplementation is given to children after they recover from malaria to fight the anemia that comes after malaria infections. Malaria is believed to cause a decrease in the absorption of iron, but it isn't known for how long or how much absorption is stopped. In this study, conducted in the nation of The Gambia, a small country in Western Africa with a very high incidence of malaria, we examined how iron was absorbed in children who were 18 to 36 months of age who either had malaria or had iron deficiency anemia without malaria. All children were given 2mg/kg of elemental iron. Iron absorption was significantly reduced in the malaria vs. non-malaria groups both right after they had malaria and several weeks later. There was a significantly greater haemoglobin response in the malaria group. We concluded that the anemia that occurs post-malaria is associated with a better hemoglobin recovery despite a significant depressant effect of malaria on oral iron incorporation. This may mean that early iron needed after malaria infection is met by iron recycling rather than oral iron. Supplemental iron administration is of questionable benefit within 2 weeks of clinical malaria in children with mild or moderate anaemia.

Technical Abstract: Iron supplementation is employed to treat post-malarial anaemia in environments where iron deficiency is common. Malaria induces an intense inflammatory reaction that stalls reticulo-endothelial macrophagal iron recycling from haemolysed red blood cells and inhibits oral iron absorption, but the magnitude and duration of these effects are unclear. We examined the red blood cell incorporation of oral administered stable isotopes of iron and compared incorporation between age matched 18- to 36-month-old children with either anaemia post-malaria (n = 37) or presumed iron deficiency anaemia alone (n = 36). All children were supplemented for 30 days with 2 mg/kg elemental iron as liquid iron sulphate and administered 57Fe and 58Fe on days 1 and 15 of supplementation respectively. 57Fe and 58Fe incorporation were significantly reduced (8% vs. 28%: p<0.001 and 14% vs. 26%: p = 0.045) in the malaria vs. non-malaria groups. There was a significantly greater haemoglobin response in the malaria group at both day 15 (p = 0.001) and 30 (p<0.000) with a regression analysis estimated greater change in haemoglobin of 7.2 g/l (s.e. 2.0) and 10.1 g/l (s.e. 2.5) respectively. Post-malaria anaemia is associated with a better haemoglobin recovery despite a significant depressant effect on oral iron incorporation which may indicate that early erythropoetic iron need is met by iron recycling rather than oral iron. Supplemental iron administration is of questionable utility within 2 weeks of clinical malaria in children with mild or moderate anaemia.