Oral iron supplements for children in malaria-endemic areas
Iron supplements for children living in malaria-endemic countries
Joseph U Okebe2, Dafna Yahav3, Rana Shbita3, Mical Paul1,*
1 Sackler Faculty of Medicine, Infectious Diseases Unit, Tel Aviv, Israel
2 Medical Research Council Unit, Banjul, Gambia
3 Beilinson Hospital, Rabin Medical Center, Department of Medicine E, Petah Tikva, Israel
Okebe JU, Yahav D, Shbita R, Paul M. Oral iron supplements for children in malaria-endemic areas. Cochrane Database of Systematic Reviews 2011, Issue 10. Art. No.: CD006589.
To read the full review please follow this link: DOI: 10.1002/14651858.CD006589.pub3.
Children commonly develop anaemia (low haemoglobin) after birth. Anaemia is associated with several ill effects, including hindering motor development and learning skills, and impaired immunity. Children are therefore commonly given iron supplements to prevent or treat anaemia. In countries where malaria is prevalent, it has been suggested that iron supplementation increases the risk of malaria and death. The high dose of iron which is given as medicine may result in free iron circulating in the blood and is made available to the malaria parasite, promoting its growth. We aimed to assess the effects of oral iron supplementation in children living in countries where malaria is prevalent.
Iron did not increase the risk of malaria, indicated by fever and the presence of parasites in the blood. There was no increased risk of death among children treated with iron. Although it is hypothesized that iron supplementation might harm children who do not have anaemia because of the iron overload, we did not find an increased risk for malaria among non-anaemic children. When iron was administered with folic acid (a vitamin necessary for DNA synthesis) one large trial suggested there was an increased risk of severe (lethal) malaria. When iron was administered in settings of poor malaria management there was an increased risk for malaria. Iron supplementation increased haemoglobin by about 1 g/dL in areas where malaria is highly prevalent. At the end of follow-up, which varied between two weeks and six months after the end of iron supplementation, the haemoglobin gain was smaller but still present at 0.4 g/dL. Iron did not increase the risk of respiratory infections or other infections. Children given iron visited medical clinics less than children given placebo, but the rate of hospitalization was similar. The children's weight and height at the end of treatment were similar. Iron did not adversely affect the rates of cure when it was given together with antimalarial treatment in the three trials that examined this issue.
Our conclusions are that iron supplementation (without folic acid) does not adversely affect children living in malaria-endemic areas. The evidence shown in our review is limited by the lack of trials examining the relevant outcomes and the limited information available, so that we were unable to fully analyse factors that could affect our results, such as the children's baseline level of haemoglobin. Based on our review, routine iron supplementation should not be withheld from children living in countries where malaria is prevalent.