Umbilical Cord Hepcidin as a Predictive Biomarker for Neonatal Iron Deficiency

For many physiological processes, iron is a vital micronutrient., particularly in fetal growth and neurodevelopment. In the course of pregnancy, maternal iron needs increase significantly to assist expanding red cell mass, placental function, and fetal demands. Impairment in iron homeostasis may result in fetal and iron deficit in newborns,a condition linked to adverse cognitive, motor, and behavioral outcomes in later life. Hepcidin, a peptide hormone produced by the liver, functions as the principal overseer of systemic iron metabolism. This mechanism governs the absorption and release of iron via the interaction with the iron exporter ferroportin, leading to its internalization and eventual degradation.In recent years, umbilical cord hepcidin has garnered attention as a potential biomarker for assessing iron status in neonates. This review synthesizes current evidence on iron metabolism during pregnancy, The intricate mechanisms underlying fetal iron deficiency and the pivotal function of hepcidin in modulating the transfer of iron between mother and fetus. Furthermore, it explores the utility of measuring umbilical cord hepcidin levels to identify neonates at risk for iron deficiency anemia and discusses the clinical implications and challenges related to assay variability, interpretation, and implementation in different populations. Understanding the regulatory mechanisms of hepcidin in fetal and neonatal contexts may lead to improved screening strategies, targeted supplementation, and ultimately better neurodevelopmental outcomes.