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Implications of malaria on iron deficiency control strategies.

Spottiswoode N, Fried M, Drakesmith H, Duffy PE - Adv Nutr (2012)

Bottom Line: The populations in greatest need of iron supplementation are also those at greatest risk of malaria: pregnant women and young children.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.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Malaria Immunology and Vaccinology, NIAID, National Institutes of Health, Bethesda, MD, USA.

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.

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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.
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fig1: 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.

Mentions: Hepcidin, first described just over a decade ago, is the only known human iron control hormone and the primary controller of iron uptake and recycling (42, 43) (Fig. 1). Hepcidin serves to maintain iron homeostasis by decreasing the amount of biologically available iron (44, 45). Elegant studies by Nemeth et al. (46) revealed that hepcidin acts by binding to the only known iron export protein, ferroportin, causing its internalization and degradation. Iron is absorbed from the diet by transportation into duodenal enterocytes and is then exported from enterocytes via ferroportin (47–49). Ferroportin is also expressed on the surfaces of macrophages and is responsible for exporting the iron recycled during macrophage phagocytosis of RBC (47). The effect of hepcidin is therefore to simultaneously block iron absorption from the diet and prevent iron recycling from senescent RBC. When hepcidin levels are high, the physiological effect is a restriction of iron availability to the erythron; when hepcidin levels are low, iron is absorbed successfully from the diet and recycled efficiently via macrophages.


Implications of malaria on iron deficiency control strategies.

Spottiswoode N, Fried M, Drakesmith H, Duffy PE - Adv Nutr (2012)

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.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3649728&req=5

fig1: 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.
Mentions: Hepcidin, first described just over a decade ago, is the only known human iron control hormone and the primary controller of iron uptake and recycling (42, 43) (Fig. 1). Hepcidin serves to maintain iron homeostasis by decreasing the amount of biologically available iron (44, 45). Elegant studies by Nemeth et al. (46) revealed that hepcidin acts by binding to the only known iron export protein, ferroportin, causing its internalization and degradation. Iron is absorbed from the diet by transportation into duodenal enterocytes and is then exported from enterocytes via ferroportin (47–49). Ferroportin is also expressed on the surfaces of macrophages and is responsible for exporting the iron recycled during macrophage phagocytosis of RBC (47). The effect of hepcidin is therefore to simultaneously block iron absorption from the diet and prevent iron recycling from senescent RBC. When hepcidin levels are high, the physiological effect is a restriction of iron availability to the erythron; when hepcidin levels are low, iron is absorbed successfully from the diet and recycled efficiently via macrophages.

Bottom Line: The populations in greatest need of iron supplementation are also those at greatest risk of malaria: pregnant women and young children.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.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Malaria Immunology and Vaccinology, NIAID, National Institutes of Health, Bethesda, MD, USA.

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.

Show MeSH
Related in: MedlinePlus