Iron homeostasis in full-term, normal birthweight Gambian neonates over the first week of life

Human neonates elicit a profound hypoferremia which may protect against bacterial sepsis. We examined the transience of this hypoferremia by measuring iron and its chaperone proteins, inflammatory and haematological parameters over the first post-partum week. We prospectively studied term, normal weight Gambian newborns. Umbilical cord vein and artery, and serial venous blood samples up to day 7 were collected. Hepcidin, serum iron, transferrin, transferrin saturation, haptoglobin, c-reactive protein, alpha 1-acid-glycoprotein, soluble transferrin receptor, ferritin, unbound iron-binding capacity and full blood count were assayed. In 278 neonates we confirmed the profound early postnatal decrease in serum iron (22.77.0 mu mol/L at birth to 7.3 +/- 4.6 mu mol/L during the first 6-24 h after birth) and transferrin saturation (50.2 +/- 16.7% to 14.4 +/- 6.1%). Both variables increased steadily to reach 16.5 +/- 3.9 mu mol/L and 36.6 +/- 9.2% at day 7. Hepcidin increased rapidly during the first 24 h of life (19.4 +/- 14.4 ng/ml to 38.9 +/- 23.9 ng/ml) and then dipped (32.7 +/- 18.4 ng/ml) before rising again at one week after birth (45.2 +/- 19.1 ng/ml). Inflammatory markers increased during the first week of life. The acute postnatal hypoferremia in human neonates on the first day of life is highly reproducible but transient. The rise in serum iron during the first week of life occurs despite very high hepcidin levels indicating partial hepcidin resistance.

Automated summary

Newborns experience temporary hypoferremia on the first day of life, but the iron levels gradually increase during the first week. Inflammatory markers also increase during this time. Despite high levels of hepcidin, indicating partial hepcidin resistance, serum iron levels still rise.