High iron status in very low birth weight infants is associated with an increased risk of retinopathy of prematurity,☆☆,

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Abstract

To explore the hypothesis that excessive iron loads may increase the formation of free radicals and the development of retinopathy of prematurity in preterm infants, we carried out a prospective observational study of the association between transfusion volume, iron status, and retinopathy. (J Pediatr 1997;131:541-4)

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Methods

VLBW infants admitted within 48 hours of birth to the regional level III neonatal unit in either Christchurch or Dunedin, New Zealand, from October 1993 through October 1994 were eligible for the study after their parents had signed informed consent forms.

All infants in the study were treated in accordance with standard protocols in the neonatal unit. Parenterally fed infants received supplementary trace elements in the form of Ped-El (Kabi Pharmacia, Stockholm, Sweden), 4 ml/kg per day (iron,

Results

Seventy-one infants were enrolled in the study, 59 in Christchurch and 12 in Dunedin: 91% of all eligible VLBW infants born during the study period. Two infants died.

Of the 69 surviving infants, 56 met the criteria for retinopathy screening, and of these infants, 16 were identified with ROP; the highest stage in either eye was stage 1 in four infants, stage 2 in eight infants, stage 3 in two infants, and stage 4 in two infants. Three infants underwent cryotherapy during the study period.

Discussion

We have demonstrated that high erythrocyte transfusion volumes in the first week of life in the VLBW infant are associated with an elevation in serum iron status, which in turn is associated with an increased risk of ROP, independent of gestational age, use of postnatal steroids, days of oxygen therapy, and the CRIB score as a marker of severity of illness. At 7 days of age, elevated values of serum iron and transferrin saturation were correlated with the subsequent development of retinopathy.

Acknowledgements

We are grateful for the assistance received during the study from Mr. David Peart with ophthalmologic examinations and for the skilled advice of Prof. Christine Winterbourn.

References (12)

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    As suggested by Kaplan et al. [6], hemolytic hyperbilirubinemia is closely associated with bilirubin-induced neurological dysfunction in newborns. Premature infants have a high risk of iron and bilirubin neurotoxicity caused by the shortened lifespan of RBCs, reduced reutilization of iron, weakened defense system, insufficient capacity of iron-binding proteins, and immature conjugative system for bilirubin in the liver [7,8]. Neonatal brain is susceptible to oxidative damage by free radicals due to the high content of polyunsaturated fatty acids (PUFAs) in membranes, insufficient activity of antioxidants (e.g., glutathione peroxidase 4 [GPx4]), and increased supply of redox-active iron [9,10].

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Supported by the Health Research Council of New Zealand.

☆☆

Reprint requests: B. A. Darlow, MD, FRACP, Department of Paediatrics, Christchurch School of Medicine, Christchurch Hospital, Private Bag, Christchurch, New Zealand.

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