Abstract
Iron is an essential micronutrient for early development, being involved in several cellular processes and playing a significant role in neurodevelopment. Prematurity may impact on iron homeostasis in different ways. On the one hand, more than half of preterm infants develop iron deficiency (ID)/ID anemia (IDA), due to the shorter duration of pregnancy, early postnatal growth, insufficient erythropoiesis, and phlebotomy losses. On the other hand, the sickest patients are exposed to erythrocytes transfusions, increasing the risk of iron overload under conditions of impaired antioxidant capacity. Prevention of iron shortage through placental transfusion, blood-sparing practices for laboratory assessments, and iron supplementation is the first frontier in the management of anemia in preterm infants. The American Academy of Pediatrics recommends the administration of 2 mg/kg/day of oral elemental iron to human milk-fed preterm infants from one month of age to prevent ID. To date, there is no consensus on the type of iron preparations, dosages, or starting time of administration to meet optimal cost-efficacy and safety measures. We will identify the main determinants of iron homeostasis in premature infants, elaborate on iron-mediated redox unbalance, and highlight areas for further research to tailor the management of iron metabolism.
Highlights
Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, Neonatal Intensive Care Unit (NICU), 20122 Milano, Italy; Department of Clinical Sciences and Community Health, Università degli Studi di Milano, 20122 Milano, Italy
The sickest premature neonates are prone to develop complications that may share the same etiology, grouped under the expression coined by Saugstad, “the oxygen radical disease of neonatology” [24]: bronchopulmonary dysplasia (BPD), retinopathy of prematurity (ROP), necrotizing enterocolitis (NEC), intraventricular hemorrhage (IVH), periventricular leukomalacia (PVL), and punctate white matter lesions (PWM) [1,21,25]
Many preventive measures have already been implemented in clinical practice to tackle iron deficiency (ID), and iron supplementation is recommended for all preterm neonates
Summary
Iron is an essential micronutrient that plays a pivotal role in early development, being involved in hemoglobin synthesis, oxygen delivery, electron transfer, energy metabolism, and cell differentiation [1]. In the event of high iron levels or inflammation, hepatic hepcidin release is increased and ferroportin expression is downregulated. Iron deficiency (ID) is a relevant public health problem and is the most common single-element deficiency worldwide, affecting around 2 billion people globally [1,8] Both pre-existing anemia and increased iron requirements during pregnancy make pregnant women vulnerable to develop iron deficiency anemia (IDA) [2]. NTBI can derive from high doses of oral or parental iron supplementation and recurrent erythrocyte transfusions [14] The latter is relevant if we consider that around 40% of very low birth weight (VLBW) and more than 90% of extremely low birth weight (ELBW) infants receive at least one blood transfusion during hospitalization [21]. The sickest premature neonates are prone to develop complications that may share the same etiology, grouped under the expression coined by Saugstad, “the oxygen radical disease of neonatology” [24]: bronchopulmonary dysplasia (BPD), retinopathy of prematurity (ROP), necrotizing enterocolitis (NEC), intraventricular hemorrhage (IVH), periventricular leukomalacia (PVL), and punctate white matter lesions (PWM) [1,21,25]
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