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Published on: May 10, 2022
Hepcidin concentrations in serum and urine correlate with iron homeostasis in preterm infants
Katharina F Müller1, Laila Lorenz, Christian F Poets
1Department of Neonatology, University of Tuebingen, Germany.
Insights
Serum and urine hepcidin levels correlate with iron status, red blood cell production, and inflammation in preterm infants. Urine hepcidin shows promise for non-invasive monitoring of iron status in this population.
Area of Science:
- Neonatal Medicine
- Pediatric Hematology
- Biochemistry
Background:
- Hepcidin is a key regulator of iron metabolism.
- Understanding hepcidin's role in preterm infants is crucial for managing iron homeostasis and anemia.
- Preterm infants are at risk for iron deficiency and related complications.
Purpose of the Study:
- To investigate the correlation between serum (Hep((S))) and urine (Hep((U))) hepcidin concentrations and indicators of iron metabolism, erythropoiesis, and inflammation in preterm infants.
- To assess the potential of urinary hepcidin as a non-invasive biomarker in this vulnerable population.
Main Methods:
- A cohort of 31 preterm infants (23-32 weeks gestational age) was studied.
- Mature 25 amino-acid hepcidin was quantified using enzyme-linked immunosorbent assay in serum and urine.
- Blood counts, reticulocyte parameters, and iron status markers were analyzed.
Main Results:
- Serum hepcidin concentrations were highest in infants with systemic inflammation.
- Both serum and urine hepcidin showed strong positive correlations with ferritin levels and reticulocyte hemoglobin content.
- Hepcidin levels correlated negatively with the soluble transferrin receptor/ferritin ratio.
- Lower hemoglobin concentrations and higher reticulocyte counts were associated with lower serum hepcidin.
Conclusions:
- In sick preterm infants, the mature 25 amino-acid form of hepcidin is significantly associated with iron status, erythropoiesis, anemia, and inflammation.
- Urinary hepcidin warrants further investigation as a non-invasive tool for monitoring iron status in preterm infants.
Objectives:
To evaluate whether hepcidin concentrations in serum (Hep((S))) and urine (Hep((U))) correlate with iron metabolism, erythropoiesis, and inflammation in preterm infants.
Study Design:
Thirty-one preterm infants (23-32 weeks gestational age) were included. The concentration of the mature, 25 amino-acid form of hepcidin was determined by enzyme-linked immunosorbent assay in serum, urine, blood counts, reticulocytes, and iron measurements.
Results:
Median (IQR) Hep((S)) was 52.4 (27.9-91.9) ng/mL. The highest values were measured in patients with systemic inflammation. Hep((S)) and Hep((U)) correlated strongly (P = .0007). Hep((S)) and Hep((U)) also correlated positively with ferritin (P = .005 and P = .0002) and with reticulocyte hemoglobin content (P = .015 and P = .015). Hep((S)) and Hep((U)) correlated negatively with soluble transferrin receptor/ferritin-ratio (P = .005 and P = .003). Infants with lower hemoglobin concentrations and higher reticulocyte counts had lower Hep((S)) (P = .0016 and P = .0089).
Conclusion:
In sick preterm infants, iron status, erythropoiesis, anemia, and inflammation correlated with the mature 25 amino-acid form of hepcidin. Further evaluation of Hep((U)) for non-invasive monitoring of iron status in preterm infants appears justified.
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