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Iron sufficiency is critical for rapidly developing fetal and neonatal organ systems. The majority of iron in the third trimester fetus and the neonate is found in the red cell mass (as hemoglobin), with lesser amounts in the tissues as storage iron (e.g. ferritin) or functional iron (e.g. myoglobin, cytochromes). Iron is prioritized to hemoglobin synthesis in red cells when iron supply does not meet iron demand. Thus, non‐heme tissues such as the skeletal muscle, heart and brain will become iron deficient before signs of iron‐deficiency anemia. Gestational conditions that result in lower newborn iron stores include severe maternal iron deficiency, maternal hypertension with intrauterine growth retardation and maternal diabetes mellitus. Stable, very low birthweight premature infants are also at risk for early postnatal iron deficiency because they accrete less iron during gestation, grow more rapidly postnatally, are typically undertreated with enteral iron and receive fewer red cell transfusions. Conversely, iron overload remains a significant concern in multiply transfused sick preterm infants because they have low levels of iron‐binding proteins and immature antioxidant systems.
Conclusion: The highly variable iron status of preterm infants combined with their risk for iron deficiency and toxicity warrants careful monitoring and support in the newborn and postdischarge periods.
Summary
Iron metabolism undergoes major changes during the last trimester and early postnatal period, at a time when the infant is particularly sensitive to both iron deficiency and iron overload. Various prenatal conditions affect the iron load at birth, including maternal iron deficiency, maternal hypertension with fetal growth restriction, maternal diabetes mellitus and preterm delivery. Since iron is prioritized to red cells in the fetus and neonate, other organs such as the liver, heart and brain can potentially suffer from iron deficiency when iron supply does not meet iron demand. In the postnatal period, the premature infant is placed at earlier risk of iron deficiency because of rapid growth rates, uncompensated iron losses from phlebotomy and low nascent iron stores. Conversely, the immature antioxidant systems and low total iron‐binding capacity of the preterm infant increase the risk of potential toxicity from iron.