Hepcidin, Serum Iron, and Transferrin Saturation in Full-Term and Premature Infants during the First Month of Life: A State-of-the-Art Review of Existing Evidence in Humans

Abstract

Neonates regulate iron at birth and in early postnatal life. We reviewed literature from PubMed and Ovid Medline containing data on umbilical cord and venous blood concentrations of hepcidin, iron and transferrin saturation (TSAT) in human neonates from 0–1 month of age. Data from 59 studies were used to create reference ranges for hepcidin, iron and TSAT for full-term neonates over the first month of life. In full-term neonates, venous hepcidin increases 2–3-fold over the first month of life (to reach 61.1 ng/mL; CI: 20.1–102.0 ng/mL) compared to umbilical cord blood (29.7 ng/mL; CI: 21.1–38.3 ng/mL). Cord blood has high levels of serum iron (28.5 μmol/L; CI: 26.0–31.1 μmol/L) and TSAT (51.7%; CI: 46.5–56.9%). Following a short-lived immediate postnatal hypoferremia, iron and TSAT rebounded to approximately half the levels in the cord by the end of the first month. There was insufficient data to formulate reference ranges for preterm neonates.

Bioinformatics analyses and experimental validation of ferroptosis-related genes in bronchopulmonary dysplasia pathogenesis

“…There existed a decrease in the number of cells in the model group with variable changes in cell morphology during the construction of a hyperoxic BPD cell model, and also detected a decrease in GPX4 mRNA expression and an upregulation of PTGS2 expression in the model group, which has not been reported before. In addition, Cross et al (18, 19) reported that free iron concentrations in cord blood were significantly higher in preterm infants than in full-term infants and adults. Patel et al (20) reported that increased cumulative iron supplementation in very low birth weight infants is an independent risk factor for BPD.…”

Iron deficiency in infancy: current insights

“…Contrary to this, Dewan et al [14] concluded that serum hepcidin is not useful to detect IDA in infants but instead suggested that the predictive value for IDA was higher from urinary Hepcidin. Reference ranges for Hepcidin at different ages have been suggested but there is a lack of standardized laboratory methods and the ranges diverge [8 & , [15][16][17][18]. Another more recently suggested biomarker is reticulocyte Hb (Chr).…”

Early Human Iron Equilibrium: A Review

“…Ferroportin transports iron out of the placenta while ceruloplasmin, zyklopen and hephaestin endow the fetal circulation with iron by transendothelial transfer [47]. Hepcidin may also be important in feto-placental iron regulation , as when increased fetal iron transport occurs in the last trimester of pregnancy, the fetus synthesizes hepcidin, influencing placental iron equilibrium [47].…”

“…A significant fall in hemoglobin during the first 6 weeks of life due to RBC hemolysis [30,32], inkeeping with the oxygen rich extrauterine environment, and a fall in plasma erythropoietin levels occur [48].In the term infant, hepcidin , the key iron regulator, increases significantly in early life , leading to a short period of hypoferremia , perhaps as a defense against sepsis by iron utilising microbes, but this is followed by increases in iron and transferrin saturation by the end of the first month [47].There is a 'physiologic anemia' , recognised as normal, at around 3 months of age , in the term infant, when the fullterm healthy infant is observed to have a body iron content proportionate to weight [49].Whereas, premature infants experience a lower nadir of hematocrit with a normocytic, normochromic anemia coincident with low reticulocyte counts and Epo levels [50].…”