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      Iron Incorporation and Post-Malaria Anaemia

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          Abstract

          Background

          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.

          Methodology/Principal Findings

          We examined the red blood cell incorporation of oral administered stable isotopes of iron and compared incorporation between age matched 18 to 36 months 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.

          Conclusion/Significance

          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.

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          Most cited references26

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          Hepcidin, a putative mediator of anemia of inflammation, is a type II acute-phase protein.

          Hepcidin is a liver-made peptide proposed to be a central regulator of intestinal iron absorption and iron recycling by macrophages. In animal models, hepcidin is induced by inflammation and iron loading, but its regulation in humans has not been studied. We report that urinary excretion of hepcidin was greatly increased in patients with iron overload, infections, or inflammatory diseases. Hepcidin excretion correlated well with serum ferritin levels, which are regulated by similar pathologic stimuli. In vitro iron loading of primary human hepatocytes, however, unexpectedly down-regulated hepcidin mRNA, suggesting that in vivo regulation of hepcidin expression by iron stores involves complex indirect effects. Hepcidin mRNA was dramatically induced by interleukin-6 (IL-6) in vitro, but not by IL-1 or tumor necrosis factor alpha (TNF-alpha), demonstrating that human hepcidin is a type II acute-phase reactant. The linkage of hepcidin induction to inflammation in humans supports its proposed role as a key mediator of anemia of inflammation.
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            Iron deficiency anemia assessment prevention and control: a guide for program managers

            WHO WHO (2001)
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              Is Open Access

              Management of severe malnutrition: a manual for physicians and other senior health workers

              (1999)
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                Author and article information

                Contributors
                Role: Editor
                Journal
                PLoS ONE
                plos
                plosone
                PLoS ONE
                Public Library of Science (San Francisco, USA )
                1932-6203
                2008
                7 May 2008
                : 3
                : 5
                : e2133
                Affiliations
                [1 ]Nutrition Program, Keneba Field Station, Medical Research Council, Fajara, The Gambia
                [2 ]Medical Research Council International Nutrition Group, Nutrition & Public Health Intervention Research Unit, London School of Hygiene & Tropical Medicine, London, United Kingdom
                [3 ]Medical Research Council Human Nutrition Research, Elsie Widdowson Laboratory, Cambridge, United Kingdom
                [4 ]Department of Pediatrics, Baylor College of Medicine and Texas Children's Hospital, Houston, United States of America
                University of Oxford, United Kingdom
                Author notes

                Conceived and designed the experiments: AP AF SC CD SA DH. Performed the experiments: CD SA DH. Analyzed the data: AF CD. Contributed reagents/materials/analysis tools: SA SA DH. Wrote the paper: AP AF SC CD SA DH.

                Article
                07-PONE-RA-02503R1
                10.1371/journal.pone.0002133
                2330157
                18461143
                70fc229f-24e3-46c8-9231-05fa07c4cfb9
                Doherty et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
                History
                : 9 September 2007
                : 23 February 2008
                Page count
                Pages: 8
                Categories
                Research Article
                Pediatrics and Child Health
                Infectious Diseases/Tropical and Travel-Associated Diseases
                Nutrition/Deficiencies

                Uncategorized
                Uncategorized

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