Blood transfusion increases radical promoting non-transferrin bound iron in preterm infants
K Hirano, T Morinobu, H Kim, M Hiroi, R Ban, S Ogawa, H Ogihara, H Tamai, T Ogihara
Department of
Pediatrics, Division of Neonatology, Osaka Medical College, Osaka,
Japan
Correspondence to: Dr Ogihara, Department of Pediatrics, Osaka Medical College, 2-7, Daigaku-machi, Takatsuki, Osaka 569-8686, Japan ped025{at}poh.osaka-med.ac.jp
Accepted 20 December
2000
BACKGROUND
Blood
transfusion has been recognised as a risk factor for the development of
retinopathy of prematurity (ROP) or chronic lung disease (CLD) in
preterm infants, but the precise mechanism involved is not understood.
AIMTo investigate the
level of non-transferrin bound "free" iron, which has the potential
to promote the generation of reactive oxygen species, and its redox
status in the plasma of preterm infants immediately before and after
blood transfusion.
METHODSTwenty one
preterm infants with a median gestational age and birth weight of 27 weeks and 1021 g respectively were prospectively enrolled in the study.
Sixteen of the 21 infants developed ROP and/or CLD. The infants were
transfused with concentrated red blood cells at a median age of 32 days. The plasma concentration of total bleomycin detectable iron (BDI)
was measured and also the ferrous iron (Fe2+) activity by
bleomycin-iron complex dependent degradation of DNA.
RESULTSEven before
blood transfusion, BDI was detectable in one third of the blood
samples, and all but one sample had ferrous iron activity. After
transfusion, both BDI and ferrous iron activity were significantly
increased, in contrast with the situation in full term infants. Plasma
ascorbic acid (AA) concentration was significantly decreased after
blood transfusion, whereas the level of its oxidation product,
dehydroascorbic acid (DHAA), and the DHAA/AA ratio were significantly
increased compared with before the transfusion. The activity of plasma
ferroxidase, which converts iron from the ferrous to the ferric state,
was appreciably decreased in preterm infants, as expected from their
very low plasma caeruloplasmin concentration.
CONCLUSIONSPlasma
non-transferrin bound iron was significantly increased in preterm
infants after blood transfusion and existed partly in the ferrous form,
because of the low ferroxidase activity and the reduction of ferric
iron (Fe3+) by ascorbic acid. This finding was specific to
preterm infants and was not observed in full term infants after blood
transfusion. Non-transferrin bound "free" iron may catalyse the
generation of reactive oxygen species, which may be responsible for the
clinical association of blood transfusion with ROP and CLD.
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Key messages
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Keywords: retinopathy of prematurity; chronic lung disease; iron; ascorbic acid; blood transfusion; preterm
© 2001 by Archives of Disease in Childhood
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