Implications of malaria on iron deficiency control strategies

Abstract

The populations in greatest need of iron supplementation are also those at greatest risk of malaria: pregnant women and young children. Iron supplementation has been shown to increase malaria risk in these groups in numerous studies, although this effect is likely diminished by factors such as host immunity, host iron status, and effective malaria surveillance and control. Conversely, the risk of anemia is increased by malaria infections and preventive measures against malaria decrease anemia prevalence in susceptible populations without iron supplementation. Studies have shown that subjects with malaria experience diminished absorption of orally administered iron, so that as a consequence, iron supplementation may have generally reduced efficacy in malarious populations. A possible mechanistic link between malaria, poor absorption of iron, and anemia is provided by recent research on hepcidin, the human iron control hormone. Our improved understanding of iron metabolism may contribute to the control of malaria and the treatment of anemia. Malaria surveillance and control are necessary components of programs to control iron deficiency and may enhance the efficacy of iron supplementation.

Figure 1

The role of hepcidin in iron metabolism. One milligram of iron is taken in daily from the diet; most of it is loaded onto transferrin in the plasma. Much of this iron is used for erythropoiesis. Aged red blood cells are phagocytized by macrophages, which then recycle their iron back onto transferrin. Iron export from both the duodenum and macrophages is dependent on ferroportin. Hepcidin causes ferroportin’s internalization and degradation, effectively blocking iron intake from the diet and restricting iron in the body to macrophages. Image adapted from Reference (75) with permission.