Serum hepcidin in infants born after 32 to 37 wk of gestational age

Uijterschout, Lieke; Domellöf, Magnus; Berglund, Staffan; Abbink, M; Vos, Paul; Rövekamp, Lyanne W; Boersma, Bart; Lagerqvist, Carina; Hudig, Cisca; Goudoever, Johannes B. van; Brus, F

doi:10.1038/pr.2015.258

Cited by 11 publications

(6 citation statements)

References 34 publications

(41 reference statements)

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“…TSAT alterations were largely driven by alterations in serum iron rather than by changes to the chaperone protein transferrin, as total iron binding capacity (TIBC) remained relatively constant, though showing a slight fall by 72–96 h of age. Geometric mean hepcidin levels in cord blood (43.8 ng/ml, CI 36.8–52.3 ng/ml) were within the expected reference range for healthy older children 12–14 , and had almost doubled by the first post-natal blood draw at a median time of 6 h post-partum (79.4 ng/ml, CI 68.1–92.4). This was followed by a decline at the subsequent sampling point at 24–48 h (45 ng/ml, CI 36.5–57.8) and a rise again by 72–96 h (87.1 ng/ml, CI 73.8–102.7).…”

Section: Resultsmentioning

confidence: 64%

Hepcidin mediates hypoferremia and reduces the growth potential of bacteria in the immediate post-natal period in human neonates

Prentice

Jallow

Sinjanka

et al. 2019

Sci Rep

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Septicemia is a leading cause of death among neonates in low-income settings, a situation that is deteriorating due to high levels of antimicrobial resistance. Novel interventions are urgently needed. Iron stimulates the growth of most bacteria and hypoferremia induced by the acute phase response is a key element of innate immunity. Cord blood, which has high levels of hemoglobin, iron and transferrin saturation, has hitherto been used as a proxy for the iron status of neonates. We investigated hepcidin-mediated redistribution of iron in the immediate post-natal period and tested the effect of the observed hypoferremia on the growth of pathogens frequently associated with neonatal sepsis. Healthy, vaginally delivered neonates were enrolled in a cohort study at a single center in rural Gambia (N = 120). Cord blood and two further blood samples up to 96 hours of age were analyzed for markers of iron metabolism. Samples pooled by transferrin saturation were used to conduct ex-vivo growth assays with Staphylococcus aureus, Streptococcus agalactiae, Escherichia coli and Klebsiella pneumonia. A profound reduction in transferrin saturation occurred within the first 12 h of life, from high mean levels in cord blood (47.6% (95% CI 43.7–51.5%)) to levels at the lower end of the normal reference range by 24 h of age (24.4% (21.2–27.6%)). These levels remained suppressed to 48 h of age with some recovery by 96 h. Reductions in serum iron were associated with high hepcidin and IL-6 levels. Ex-vivo growth of all sentinel pathogens was strongly associated with serum transferrin saturation. These results suggest the possibility that the hypoferremia could be augmented (e.g. by mini-hepcidins) as a novel therapeutic option that would not be vulnerable to antimicrobial resistance. Trial registration: The original trial in which this study was nested is registered at ISRCTN, number 93854442.

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Section: Resultsmentioning

confidence: 64%

Hepcidin mediates hypoferremia and reduces the growth potential of bacteria in the immediate post-natal period in human neonates

Prentice

Jallow

Sinjanka

et al. 2019

Sci Rep

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“…(A) Full-term neonates: α shows the weighted mean (95% CI) for all studies seen in Supplemental Figure 1A; β, χ, and ε show Prentice et al ( 99 ); δ shows Kulik-Rechberger et al ( 46 ). (B) Preterm neonates: α shows the weighted mean (95% CI) for all studies seen in Supplemental Figure 1B; β shows Uijterschout et al ( 100 ).…”

Section: Resultsmentioning

confidence: 99%

Hepcidin, Serum Iron, and Transferrin Saturation in Full-Term and Premature Infants during the First Month of Life: A State-of-the-Art Review of Existing Evidence in Humans

Cross

Prentice

Cerami

2020

Current Developments in Nutrition

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Neonates regulate iron at birth and in early postnatal life. We reviewed literature from PubMed and Ovid Medline containing data on umbilical cord and venous blood concentrations of hepcidin, iron and transferrin saturation (TSAT) in human neonates from 0–1 month of age. Data from 59 studies were used to create reference ranges for hepcidin, iron and TSAT for full-term neonates over the first month of life. In full-term neonates, venous hepcidin increases 2–3-fold over the first month of life (to reach 61.1 ng/mL; CI: 20.1–102.0 ng/mL) compared to umbilical cord blood (29.7 ng/mL; CI: 21.1–38.3 ng/mL). Cord blood has high levels of serum iron (28.5 μmol/L; CI: 26.0–31.1 μmol/L) and TSAT (51.7%; CI: 46.5–56.9%). Following a short-lived immediate postnatal hypoferremia, iron and TSAT rebounded to approximately half the levels in the cord by the end of the first month. There was insufficient data to formulate reference ranges for preterm neonates.

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“…Lower hepatic expression of hepcidin was also reported in naturally fed piglets compared with those fed iron-supplemented formula [19]. A study in former preterm infants at 4 months of age observed lower serum hepcidin levels in those fed breast milk compared with those predominantly fed formula [20].…”

Section: Discussionmentioning

confidence: 96%

Hepcidin Status at 2 Months in Infants Fed Breast Milk Compared with Formula

et al. 2020

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Introduction: The basis for the superior absorption of iron from breast milk compared with infant formulas is unclear. The hormone hepcidin downregulates dietary iron absorption. Hepcidin production increases with increased body iron status (reflected in serum ferritin levels). We hypothesized that serum hepcidin levels are suppressed relative to iron status in infants fed breast milk compared with formula. Methods: Subjects were healthy infants presenting for routine 2-month clinic visit and strictly fed either breast milk or standard infant formula. Urinary hepcidin and ferritin levels (reflective of serum levels) were analyzed and compared across the breast milk- and formula-fed groups. The relationship between urinary hepcidin and ferritin levels within each group was analyzed by linear regression. Results: Twenty-four subjects were enrolled in each group. The median urinary hepcidin level in the group fed breast milk was lower than in formula (130 vs. 359 ng hepcidin/mg creatinine, p < 0.05). However, the median ferritin levels were similar (2.1 vs. 1.9 ng/mL). Within each group, urinary hepcidin correlated with urinary ferritin (r = 0.5, p < 0.05 for each group); however, the slope of the regression line was lower in the group fed breast milk compared with formula (p < 0.005). Conclusion: Despite similar urinary ferritin levels, urinary hepcidin levels are lower at 2 months in infants fed breast milk compared with infants fed formula. Hepcidin levels correlate with iron status in each group; however, this relationship is relatively dampened in infants fed breast milk. We speculate that relatively lower infant hepcidin contributes to the superior efficiency of iron absorption from breast milk.

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Serum hepcidin in infants born after 32 to 37 wk of gestational age

Cited by 11 publications

References 34 publications

Hepcidin mediates hypoferremia and reduces the growth potential of bacteria in the immediate post-natal period in human neonates

Hepcidin mediates hypoferremia and reduces the growth potential of bacteria in the immediate post-natal period in human neonates

Hepcidin, Serum Iron, and Transferrin Saturation in Full-Term and Premature Infants during the First Month of Life: A State-of-the-Art Review of Existing Evidence in Humans

Hepcidin Status at 2 Months in Infants Fed Breast Milk Compared with Formula

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