Febrile malaria and asymptomatic malaria parasitemia substantially decrease ironabsorption in single-meal, stable isotope studies in women and children, but todate there is no evidence of decreased efficacy of iron-fortified foods inmalaria-endemic regions. Without inadequate malarial surveillance or health care,giving iron supplements to children in areas of high transmission could increasemorbidity and mortality. The most likely explanation is the appearance ofnon-transferrin-bound iron (NTBI) in the plasma. NTBI forms when the rate of ironinflux into the plasma exceeds the rate of iron binding to transferrin. Twostudies in women have reported substantially increased NTBI with the ingestion ofiron supplements. Our studies confirm this, but found no significant increase inNTBI on consumption of iron-fortified food. It seems likely that the malarialparasite in hepatocytes can utilize NTBI, but it cannot do so in infectederythrocytes. NTBI however may increase the sequestration of parasite-infectederythrocytes in capillaries. Bacteremia is common in children with severe malariaand sequestration in villi capillaries could lead to a breaching of theintestinal barrier, allowing the passage of pathogenic bacteria into the systemiccirculation. This is especially important as frequent high iron doses increasethe number of pathogens in the intestine at the expense of the barrier bacteria.
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