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Do Extremely Low Gestational Age Neonates Regulate Iron Absorption via Hepcidin?

Kendell R German1, Bryan A Comstock2, Pratik Parikh3

  • 1Department of Pediatrics, University of Washington, Seattle, WA.

The Journal of Pediatrics
|October 9, 2021
PubMed
Summary

Extremely preterm infants appear to regulate iron status via hepcidin, as indicated by urine hepcidin levels correlating with iron markers. Treatment with erythropoietin affects these levels, suggesting active iron status regulation in neonates.

Keywords:
ferritinhepcidinironpretermzinc protoporphyrin-to-heme ratio

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Area of Science:

  • Neonatal physiology
  • Iron metabolism
  • Endocrinology

Background:

  • Extremely preterm infants often experience iron deficiency due to various factors.
  • Hepcidin is a key regulator of systemic iron homeostasis.
  • Understanding iron regulation in this vulnerable population is crucial for optimal growth and development.

Purpose of the Study:

  • To investigate whether extremely preterm neonates can regulate their iron status through hepcidin.
  • To assess the correlation between urine hepcidin levels and established serum iron markers.
  • To determine the impact of erythropoietin treatment on hepcidin regulation in preterm infants.

Main Methods:

  • Retrospective analysis of urine samples from the Preterm Epo Neuroprotection (PENUT) Trial.
  • Measurement of urine hepcidin normalized to creatinine (Uhep/UCr).
  • Correlation analysis between Uhep/UCr and serum ferritin, zinc protoporphyrin-to-heme ratio (ZnPP/H), and iron dose.

Main Results:

  • Uhep/UCr values showed significant correlations with serum ferritin and ZnPP/H levels at various time points.
  • Median Uhep/UCr concentrations varied over time in placebo-treated infants.
  • Erythropoietin treatment significantly affected Uhep/UCr values, particularly at 2 weeks.

Conclusions:

  • Urine hepcidin levels in extremely preterm infants correlate with serum iron markers, indicating a capacity for iron status regulation.
  • Hepcidin regulation is dynamic in this population and influenced by erythropoietin therapy.
  • Hepcidin appears suppressed in extremely preterm neonates, especially those receiving erythropoietin.