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Anemia, Hepcidin, and Vitamin D in Healthy Preterm Infants: A Pilot Study
Yael Koren1, Ronit Lubetzky2, Dror Mandel1
1Department of Neonatology, Dana Dwek Children's Hospital, Tel Aviv Sourasky Medical Center, affiliated to the Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
Insights
Anemia in premature infants is linked to higher hepcidin levels, a key regulator of iron metabolism. Further research is needed to understand the role of vitamin D in this condition.
Area of Science:
- Neonatal Medicine
- Pediatric Hematology
- Endocrinology
Background:
- Anemia in premature neonates is multifactorial, potentially involving inflammation-mediated hepcidin.
- Hepcidin expression is known to be suppressed by vitamin D.
Purpose of the Study:
- To investigate the interrelationship between hepcidin, anemia, and vitamin D status in preterm infants.
- To compare hepcidin, ferritin, iron, 25-hydroxyvitamin D [25(OH)D], and C-reactive protein (CRP) levels between anemic and nonanemic preterm infants.
Main Methods:
- Prospective recruitment of 47 preterm infants (1-5 weeks old) in a neonatal intensive care unit.
- Measurement of blood counts and serum levels of hepcidin, ferritin, iron, 25(OH)D, and CRP.
- Comparison of these parameters between anemic and nonanemic infants.
Main Results:
- Anemic preterm infants had significantly higher hepcidin levels compared to nonanemic infants (55.3 vs. 30.1 ng/mL).
- No significant differences in iron, ferritin, 25(OH)D, or CRP levels were observed between the groups.
- A positive correlation was found between hepcidin and ferritin (R² = 0.247, p = 0.02).
- A negative correlation was found between 25(OH)D and CRP (R² = 0.1, p = 0.04).
Conclusions:
- Anemia of prematurity is associated with elevated serum hepcidin levels.
- The precise mechanisms driving anemia in preterm infants and the specific role of vitamin D require further investigation.
Objective:
The etiology of anemia in premature neonates is multifactorial and may involve anemia of inflammation mediated by hepcidin. Hepcidin expression is suppressed by vitamin D. We aimed to investigate the interrelationship between hepcidin, anemia, and vitamin D status in preterm infants.
Study Design:
Preterm infants aged 1 to 5 weeks were prospectively recruited at the neonatal intensive care unit of the Dana Dwek Children Hospital. Blood counts and serum levels of hepcidin, ferritin, iron, 25-hydroxyvitamin D [25(OH)D] and C-reactive protein (CRP) were measured and compared between anemic and nonanemic preterm infants.
Results:
Forty-seven preterm infants (mean ± standard deviation gestational age at birth 32.8 ± 1.1 weeks, 66% males) were recruited. In total, 36% of the preterm infants were vitamin D deficient [25(OH)D < 20 ng/mL] and 15% were anemic. Hepcidin levels were significantly higher in anemic premature infants than in the nonanemic group (55.3 ± 23.9 ng/mL vs. 30.1 ± 16.3 ng/mL, respectively, p < 0.05). No differences were found in iron, ferritin, 25(OH)D, and CRP levels between anemic and nonanemic premature newborn infants. A positive correlation was found between hepcidin and ferritin (R 2 = 0.247, p = 0.02) and a negative correlation was found between 25(OH)D and CRP (R 2 = 0.1, p = 0.04). No significant correlations were found between 25(OH)D and hepcidin, iron, ferritin, or CRP.
Conclusion:
Anemia of prematurity was associated with high hepcidin serum levels. The exact mechanisms leading to anemia and the role of vitamin D warrant further investigation.
Key Points:
· Hepcidin levels were significantly higher in anemic premature infants.. · A positive correlation was found between hepcidin and ferritin.. · Negative correlation was found between 25(OH)D and CRP..
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