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Fetal Effects Of Maternal Iron Deficiency

Deepak Chawla
Published 2015 · Medicine
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Iron is one of the most important element in the human body. It is needed for tissue oxygenation, intracellular energy metabolism, DNA replication, neurotransmitter synthesis, myelination, and hormone synthesis. Rapidly dividing cells need higher supply of iron due to latter’s role in DNA replication. In children and adults, hematological, neurological and other effects of iron deficiency have been well studied. Apart from anemia, these effects include cognitive impairment, cardiomyopathy, skeletal muscle weakness, fatigue and intestinal dysmotility [1]. However, literature is sparse on the adverse effects of iron deficiency on various organ systems of fetus and neonate. An efficient iron uptake mechanism in placenta ensures delivery of adequate iron to the developing fetus. Transferrin receptors present on the apical membrane of syncytiotrophoblast cells uptake iron from the maternal circulation and release it into the fetal circulation. Although transfer of iron frommother to the fetus is an active process, previously held view that adequate fetal iron accretion occurs even in presence of iron deficiency in mother has been rejected over last few years. Cord blood ferritin levels, which reflect fetal iron stores are lower in neonates born to mothers with hemoglobin less than 10 g/dl. Severe anemia in third trimester has been associated with low birth weight, prematurity and increased perinatal mortality [2]. In low-resource settings, iron and folic acid supplementation has been associated with significant reduction in early-neonatal, neonatal, infant and child mortality. Greatest protective effect has been observed if iron supplementation is started early in pregnancy. Neonates with low cord blood ferritin levels have been observed to have significantly prolonged inter-peak latencies in auditory brainstem response indicating that in utero iron deficiency may be associated with abnormal neural myelination [3]. In a micronutrient supplementation trial among pregnant women, infants born to non-iron supplemented mothers had lower mental development index at 12, 18 and 24 mo of age [4]. In an animal model, iron deficiency in early gestation altered the synaptic proteome in hippocampus [5]. This adverse effect was present despite correction of iron-deficient status later in pregnancy. Altered hippocampal synaptic function may be responsible for cognitive dysfunction and neurobehavioral disorders observed in iron deficiency. Coupled with lack of adequate iron supplementation during infancy, iron deficiency during this critical period of brain development can have irreversible adverse effect on cognitive development. With 30–45 % prevalence of iron deficiency anemia among pregnant women in developing countries, potential population-level reduction in intellect could have major public health and socio-economic implications [6]. In this issue of the Journal Basu et al. present their investigation on effect of maternal iron deficiency on neonatal platelet indices [7]. Platelet count was lower in cord blood of neonates whose mothers had severe anemia. This effect persisted when subgroup analysis was done according to low birth weight status of the neonates born to iron-deficient mothers. However, presence of other confounding variables effecting platelet counts cannot be ruled out. Iron deficiency is often accompanied by deficiency of other micro-nutrients especially folic acid and vitamin B12. Unless these variables are measured and accounted for, cause-and-effect relationship between iron-deficiency and thrombocytopenia cannot be established with a cross-sectional study. Iron deficiency has been associated with thrombophilia in children and adults. This effect is due to increased erythropoietin levels in fetuses with iron deficiency [8]. Decreased platelet count if caused by iron deficiency may be due to effect of iron deficiency on * Deepak Chawla
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