Iron is an essential micronutrient that plays a significant role in critical cellular functions in all organ systems in all species. Iron is particularly vital for early brain growth and function in humans since it supports neuronal and glial energy metabolism, neurotransmitter synthesis and myelination \[1-5\]. The need to establish standard curves for cord serum ferritin concentrations throughout the third trimester of pregnancy is based on the risk of developing brain iron deficiency as storage iron pools become depleted in certain gestational conditions \[6-8\]. Iron deficiency during the fetal or postnatal periods can alter brain structure, neurochemistry and cognitive functioning, and lead to long-term cognitive and motor impairment that cannot be corrected by iron supplementation \[9-11\]. Newborn infants with the lowest quartile of cord ferritin concentrations (\<76 μg/l) have impaired mental and psychomotor function at school age \[12\]. Iron-deficient infants of diabetic mothers (IDM) with low neonatal ferritin concentrations (\<35 μg/l) have impaired auditory recognition memory processing at birth compared with iron-sufficient IDM (ferritin \>35 μg/l) \[13\]. Pre-term infants with low serum ferritin concentrations (\<75 μg/l) at 37 weeks post-conception have abnormal neurologic reflexes \[14\].

Direct measurement of brain iron in newborn infants is not currently feasible.Total body iron and iron storage estimates are based on measurements of serum markers, such as hemoglobin (Hgb) and ferritin concentrations \[15\]. Serumferritin concentration has been used as a standard measurement of iron stores ininfants, children and adults \[16-19\]. The relationships between ferritin concentrations and total body storage iron in these populations are well established. In adults, 1 μg/l of serum ferritin is equivalent to 8-10 mg ofstorage iron \[20\]. In newborn infants, the ratio of serum ferritin to liver nonheme iron concentration is closer to 1:2.7 \[21\]. In spite of the wide availability of serum ferritin as a screening test, normative data at birth, as a function of specific gestational ages from 23 to 41 weeks,

Low serum ferritin concentrations are seen only in iron deficiency. Elevated ferritin concentrations in the newborn can be a consequence of neonatal hemochromatosis, excessiveiron administration or RBC transfusions. Serum ferritin concentrations are also elevated during periods of infection,inflammation and neoplasia. Under these conditions, serum ferritin behaves as an acute-phase reactant that can mask the diagnosis of iron deficiency \[22\]. Iron requirements in women are significantly higher in the pregnant state than in the nonpregnant state. The total iron requirement of a full-term pregnancy is approximately 1,000 mg \[23\]. Iron requirements for pregnant women increase significantly in the second and third trimesters, with the expansion of maternal blood volume and fetal red cell mass \[23\]. The fetus accumulates iron at a rate of 1.35 mg/kg of fetal weight in the third trimester, maintaining an average iron content of 75 mg/kg of body weight during the last trimester \[24.25\]. At term, 70-80% of fetal iron is present in RBCs as Hgb, 10% in tissues as myoglobin and cytochromes, and the remaining 10-15% stored in reticuloendothelial and parenchymal tissues as ferritin and hemosiderin \[24\]. The placenta serves as the regulatable conduit for maternal-fetal iron transport. The amount of iron passing through the placenta increases with gestation. Iron is transferred against a concentration gradient from the placenta to the fetus, especially during the later stages of pregnancy. The placenta can also serve as a storage organ for iron during pregnancy.

Factors that influence neonatal ferritin concentration at birth include duration of gestation, fetal sex, maternal iron status and conditions altering maternal-fetal iron exchange.. At- or near-term female newborn infants have higher cord serum ferritin concentrations than male