Читать книгу Neonatal Haematology - Barbara J. Bain, Irene Roberts - Страница 21

Although stores of iron are adequate at birth in term babies born to well‐nourished mothers, this is not always the case in preterm neonates. This is because the majority of fetal total body iron is stored during the third trimester. Estimates have shown that total body iron increases from 35–40 mg at 24 weeks’ gestation to 225 mg at term, with the result that preterm neonates, especially those with IUGR, are born with lower iron stores than term neonates.^47,48 These amounts of iron are equivalent to 6 months iron store for a term neonate⁴⁹ but only around 2 months for extremely preterm neonates unless they are given supplementary iron. In addition, preterm neonates have an increased requirement for iron both because of their rapid growth rate and because of frequent phlebotomy.^50,51 Therefore, preterm neonates generally develop iron deficiency after 2–4 months if the recommended daily intakes are not maintained.⁵² Administration of iron supplements to preterm babies leads to a slightly higher haemoglobin concentration (Hb) and improved iron stores, thereby reducing the risk of subsequent iron deficiency anaemia.⁵³ The recommended iron intake of preterm infants with a birthweight of 1500–2000 g is 2 mg/kg/day from 2 to 4 weeks of life using iron‐containing human milk fortifier or preterm formula milk and/or iron supplements until at least 6 months of age.⁵⁴ For very low birthweight neonates, a higher daily iron intake (2–3 mg/kg/day) is usually recommended, starting at 2 weeks of age.⁵⁴

The regulation of iron status in the neonate, even in those who are born extremely preterm, has recently been shown to depend on the action of hepcidin, erythroferrone (ERFE), ferroportin and EPO, as in adults.^55,56 Thus, hepcidin falls when iron deficiency develops, facilitating increased iron absorption, while hepcidin is upregulated when iron stores are sufficient, triggering degradation of the iron exporter ferroportin, which results in inhibition of iron absorption and mobilisation.⁵⁷ Like serum ferritin, hepcidin levels increase with gestational age and in parallel with the increasing iron stores.⁵⁸ Hepcidin and pro‐hepcidin levels in term and preterm infants vary in response to inflammation, infection and red blood cell transfusion.^59–61 ERFE, an erythroid hormone, acts as a direct suppressor of hepcidin expression in the liver in response to EPO. Little is known about the role of ERFE in regulating iron metabolism in neonates but some preliminary data suggest that although the components of the EPO–ERFE–hepcidin–ferroportin axis are present in neonates,⁵⁵ ERFE‐mediated suppression of hepcidin is impaired, at least in preterm neonates.⁶²