Hepcidin Levels and Iron Homeostasis During Early Infancy

Document Type : Original Article

Authors

1 Department of Pediatrics, Batnan Medical Center, Lybia

2 Department of Physiology , Faculty of Medicine, Tanta University

3 Department of Pediatric, faculty of Medicine, Tanta University

Abstract

Background: Iron status is usually assessed in children and adults through the
measurement of the concentrations of serum ferritin (SF) and serum soluble
transferrin receptor (sTfR), which reflect storage iron and cellular iron needs,
respectively. However SF and sTfR are difficult to interpret in infants. Hepcidinliver
hormone- is a negative regulator of iron absorption and mobilization. Objective:
We aimed in this study to characterize changes in hepcidin levels in healthy breast fed
infants in correlation to the dynamic change in iron status in this young age.
Patients and methods: 106 healthy breast fed infant were included in the study and
followed from 4 to 9 mo. Iron supplementation was given to infants with iron
deficiency (ID) at 6 mo till the age of 9 mo. Blood samples at 4, 6, and 9 months of
age were analyzed for hemoglobin (Hb), mean cell volume (MCV), zinc
protoporphyrin (ZPP), plasma ferritin, and transferrin receptors (TfR). Urinary
hepcidin was measure at 4, 6 and 9 mo. Results: In unsupplemented infants, Hb,
MCV and ferritin means decreased, whereas ZPP and sTfR means increased from 4
to 6 mo. Urinary hepcidin levels were decreasing with age between 4 and 6 months.
We found significant urinary hepcidin deficiency in ID group at 6mo. Changes of Hb
levels after iron supplementation were correlated significantly to urinary hepcidin at
the age of 6 mo (r=-0.756), less significantly correlated to sTfR(r=394) and serum
ferritin (r= 32). Conclusions: Iron deficiency in healthy full term infants is less
common at 4 mo but iron deficiency increased after that. Not all ID infants will
manifest by anemia and not all anemic infants are iron deficient. Urinary hepcidin
could help to early diagnose infants with true iron deficiency.