Iron

Research output: Chapter in Book/Report/Conference proceedingChapter

4 Citations (Scopus)

Abstract

Ironisaubiquitouselementrequiredby virtually all cells for normal growth and metabolism. Rapidly growing and differentiating cellshaveparticularly high ironrequirements.1Since preterm and term human infants have high growth rates (on a per-weight basis), it is not surprising that these infants also have high iron needs. Term infants typically acquire adequate iron stores during the last trimester of gestation, but preterm infants are relatively compromised in this respect.2This fact, combined with their higher postnatal growth rates in the first year, renders preterminfants at higher risk than their term counterparts for iron deficiency and iron-deficiency anemia.3, 4This increased risk could theoretically be avoidedby administering large doses of iron to the preterminfant, were it not for the concern of iron toxicity; iron plays an important catalytic role in the Fenton reaction, which creates radical oxygen species that peroxidate the lipids in cell membranes. The concern is relevant particularly in the premature infant whose plasma total iron-binding capacity (TIBC) is lowand whose antioxidant defense system is immature.5, 6Thus, ironcan be considereda highly necessaryelementwith a narrowtherapeutic window where both deficiency and overload contribute to significant morbidity. Iron balance in the fetus and neonate Iron is classically seen as an integral part of the hemoglobin molecule, and iron deficiency is thus frequently assumed to be synonymous with anemia.

Original languageEnglish (US)
Title of host publicationNeonatal Nutrition and Metabolism, Second Edition
PublisherCambridge University Press
Pages291-298
Number of pages8
ISBN (Electronic)9780511544712
ISBN (Print)0521824559, 9780521824552
DOIs
StatePublished - Jan 1 2006

Fingerprint

Iron
Premature Infants
Growth
Third Pregnancy Trimester
Membrane Lipids
Anemia
Reactive Oxygen Species
Hemoglobins
Fetus
Antioxidants
Newborn Infant
Morbidity
Weights and Measures
Pregnancy

Cite this

Georgieff, M. K. (2006). Iron. In Neonatal Nutrition and Metabolism, Second Edition (pp. 291-298). Cambridge University Press. https://doi.org/10.1017/CBO9780511544712.019

Iron. / Georgieff, Michael K.

Neonatal Nutrition and Metabolism, Second Edition. Cambridge University Press, 2006. p. 291-298.

Research output: Chapter in Book/Report/Conference proceedingChapter

Georgieff, MK 2006, Iron. in Neonatal Nutrition and Metabolism, Second Edition. Cambridge University Press, pp. 291-298. https://doi.org/10.1017/CBO9780511544712.019
Georgieff MK. Iron. In Neonatal Nutrition and Metabolism, Second Edition. Cambridge University Press. 2006. p. 291-298 https://doi.org/10.1017/CBO9780511544712.019
Georgieff, Michael K. / Iron. Neonatal Nutrition and Metabolism, Second Edition. Cambridge University Press, 2006. pp. 291-298
@inbook{195f2d9d158045c78725487f95f8a15f,
title = "Iron",
abstract = "Ironisaubiquitouselementrequiredby virtually all cells for normal growth and metabolism. Rapidly growing and differentiating cellshaveparticularly high ironrequirements.1Since preterm and term human infants have high growth rates (on a per-weight basis), it is not surprising that these infants also have high iron needs. Term infants typically acquire adequate iron stores during the last trimester of gestation, but preterm infants are relatively compromised in this respect.2This fact, combined with their higher postnatal growth rates in the first year, renders preterminfants at higher risk than their term counterparts for iron deficiency and iron-deficiency anemia.3, 4This increased risk could theoretically be avoidedby administering large doses of iron to the preterminfant, were it not for the concern of iron toxicity; iron plays an important catalytic role in the Fenton reaction, which creates radical oxygen species that peroxidate the lipids in cell membranes. The concern is relevant particularly in the premature infant whose plasma total iron-binding capacity (TIBC) is lowand whose antioxidant defense system is immature.5, 6Thus, ironcan be considereda highly necessaryelementwith a narrowtherapeutic window where both deficiency and overload contribute to significant morbidity. Iron balance in the fetus and neonate Iron is classically seen as an integral part of the hemoglobin molecule, and iron deficiency is thus frequently assumed to be synonymous with anemia.",
author = "Georgieff, {Michael K.}",
year = "2006",
month = "1",
day = "1",
doi = "10.1017/CBO9780511544712.019",
language = "English (US)",
isbn = "0521824559",
pages = "291--298",
booktitle = "Neonatal Nutrition and Metabolism, Second Edition",
publisher = "Cambridge University Press",

}

TY - CHAP

T1 - Iron

AU - Georgieff, Michael K.

PY - 2006/1/1

Y1 - 2006/1/1

N2 - Ironisaubiquitouselementrequiredby virtually all cells for normal growth and metabolism. Rapidly growing and differentiating cellshaveparticularly high ironrequirements.1Since preterm and term human infants have high growth rates (on a per-weight basis), it is not surprising that these infants also have high iron needs. Term infants typically acquire adequate iron stores during the last trimester of gestation, but preterm infants are relatively compromised in this respect.2This fact, combined with their higher postnatal growth rates in the first year, renders preterminfants at higher risk than their term counterparts for iron deficiency and iron-deficiency anemia.3, 4This increased risk could theoretically be avoidedby administering large doses of iron to the preterminfant, were it not for the concern of iron toxicity; iron plays an important catalytic role in the Fenton reaction, which creates radical oxygen species that peroxidate the lipids in cell membranes. The concern is relevant particularly in the premature infant whose plasma total iron-binding capacity (TIBC) is lowand whose antioxidant defense system is immature.5, 6Thus, ironcan be considereda highly necessaryelementwith a narrowtherapeutic window where both deficiency and overload contribute to significant morbidity. Iron balance in the fetus and neonate Iron is classically seen as an integral part of the hemoglobin molecule, and iron deficiency is thus frequently assumed to be synonymous with anemia.

AB - Ironisaubiquitouselementrequiredby virtually all cells for normal growth and metabolism. Rapidly growing and differentiating cellshaveparticularly high ironrequirements.1Since preterm and term human infants have high growth rates (on a per-weight basis), it is not surprising that these infants also have high iron needs. Term infants typically acquire adequate iron stores during the last trimester of gestation, but preterm infants are relatively compromised in this respect.2This fact, combined with their higher postnatal growth rates in the first year, renders preterminfants at higher risk than their term counterparts for iron deficiency and iron-deficiency anemia.3, 4This increased risk could theoretically be avoidedby administering large doses of iron to the preterminfant, were it not for the concern of iron toxicity; iron plays an important catalytic role in the Fenton reaction, which creates radical oxygen species that peroxidate the lipids in cell membranes. The concern is relevant particularly in the premature infant whose plasma total iron-binding capacity (TIBC) is lowand whose antioxidant defense system is immature.5, 6Thus, ironcan be considereda highly necessaryelementwith a narrowtherapeutic window where both deficiency and overload contribute to significant morbidity. Iron balance in the fetus and neonate Iron is classically seen as an integral part of the hemoglobin molecule, and iron deficiency is thus frequently assumed to be synonymous with anemia.

UR - http://www.scopus.com/inward/record.url?scp=84926954577&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84926954577&partnerID=8YFLogxK

U2 - 10.1017/CBO9780511544712.019

DO - 10.1017/CBO9780511544712.019

M3 - Chapter

AN - SCOPUS:84926954577

SN - 0521824559

SN - 9780521824552

SP - 291

EP - 298

BT - Neonatal Nutrition and Metabolism, Second Edition

PB - Cambridge University Press

ER -