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Perinatal Factors Affecting Serum Hepcidin Levels in Low-Birth-Weight Infants
Kenji Ichinomiya1, Kenichi Maruyama, Takahiro Inoue
1Department of Neonatology, Gunma Children's Medical Center, Gunma, Japan.
Insights
Gestational age, interleukin-6, erythropoietin, and soluble transferrin receptor influence hepcidin levels in low-birth-weight infants. These factors highlight the impact of prematurity, inflammation, and hypoxia on iron regulation in vulnerable newborns.
Area of Science:
- Neonatal Medicine
- Iron Metabolism
- Endocrinology
Background:
- Hepcidin is a key hormone regulating iron balance and preventing iron overload.
- Low-birth-weight (LBW) infants are susceptible to iron imbalances.
- Limited research exists on hepcidin regulation in LBW infants.
Purpose of the Study:
- To identify perinatal factors associated with serum hepcidin levels in LBW infants.
- To understand the regulation of iron metabolism in premature infants.
Main Methods:
- Prospective enrollment of 92 LBW infants (median GA 32.6 weeks, birth weight 1,587 g).
- Measurement of serum hepcidin-25 (Hep25) from umbilical cord blood via LC-MS/MS.
- Evaluation of Hep25 levels in relation to prematurity and other regulatory factors.
Main Results:
- Serum Hep25 levels correlated with birth weight, IL-6, erythropoietin, transferrin saturation, soluble transferrin receptor, and ferritin.
- Hep25 levels were higher in infants with chorioamnionitis and born vaginally.
- Hep25 levels were lower in infants born to mothers with pregnancy-induced hypertension.
- Multiple regression confirmed associations between Hep25 and GA, IL-6, erythropoietin, and soluble transferrin receptor.
Conclusions:
- Gestational age, IL-6, erythropoietin, and soluble transferrin receptor are significant perinatal factors affecting Hep25 levels in LBW infants.
- Prematurity, inflammation, hypoxia, and erythropoietic activity are crucial in modulating hepcidin levels during the perinatal period.
- Findings provide insights into iron regulation challenges in LBW infants.
Background:
Hepcidin, an iron-regulatory hormone, plays a key role in preventing iron overload. Few studies have investigated the regulation of hepcidin in low-birth-weight (LBW) infants who are vulnerable to iron imbalance.
Objectives:
To identify perinatal factors associated with serum hepcidin levels in LBW infants.
Methods:
Ninety-two LBW infants with a median gestational age (GA) of 32.6 weeks and birth weight of 1,587 g were prospectively enrolled. Serum hepcidin-25 (Hep25) levels were measured from umbilical cord blood using liquid chromatography-tandem mass spectrometry. The relationship between Hep25 levels and prematurity or other possible hepcidin-regulatory factors was evaluated.
Results:
The median Hep25 level was 7.3 ng/mL (interquartile range: 2.85-16.38). log(Hep25) correlated with birth weight (r = 0.229, p = 0.028), log(interleukin-6 [IL-6]) (r = 0.408, p < 0.001), log(erythropoietin) (r = -0.302, p = 0.004), transferrin saturation (r = 0.29, p = 0.005), soluble transferrin receptor (r = -0.500, p < 0.001), and log(ferritin) (r = 0.696, p < 0.001). Serum iron and hemoglobin levels did not correlate with log(Hep25). Hep25 levels were higher among infants with chorioamnionitis and infants born vaginally and lower among infants born to mothers with pregnancy-induced hypertension than among infants without the respective characteristics. Stepwise multiple linear regression analysis confirmed the significant association of log(Hep25) with GA, log(IL-6), log(erythropoietin), and soluble transferrin receptor.
Conclusions:
Among LBW infants, GA, IL-6, erythropoietin, and soluble transferrin receptor were associated with Hep25 levels. Therefore, prematurity, inflammation, hypoxia, and erythropoietic activity may be important perinatal factors that affect hepcidin levels.
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