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Blood transfusion and chronic lung disease in preterm infants
R W Cooke1, J A Drury, C W Yoxall
1Department of Child Health, University of Liverpool, Liverpool Women's Hospital, UK.
Insights
Frequent blood transfusions in preterm infants may alter iron status, but do not appear to cause oxidative injury linked to chronic lung disease (CLD) development. This suggests transfusion-related oxidative stress is not a primary risk factor for CLD.
Area of Science:
- Neonatal Medicine
- Pediatric Hematology
- Biochemistry
Background:
- Frequent blood transfusions are common in very preterm infants, particularly those developing chronic lung disease (CLD).
- Iron status changes and potential oxidative injury from transfusions are concerns in this vulnerable population.
Purpose of the Study:
- To investigate the relationship between blood transfusions, iron status, and oxidative stress markers in very preterm infants.
- To determine if transfusion-induced oxidative injury contributes to the development of CLD.
Main Methods:
- Weekly monitoring of iron status (serum iron, transferrin, ferritin, etc.) and oxidative stress markers (BDI, TBARS) in 73 very preterm infants over 28 days.
- Comparison of iron status and oxidative markers between infants who developed CLD and those who did not.
Main Results:
- Infants who developed CLD received more transfusions and had higher ferritin and caeruloplasmin levels.
- Higher ferritin levels correlated with the number of transfusions and the presence of bleomycin-detectable iron (BDI).
- Increased BDI was not associated with increased lipid peroxidation (TBARS).
Conclusions:
- Oxidative injury from oxygen-derived free radicals (ODFRs) induced by blood transfusions is unlikely to be a significant factor in the development of CLD in preterm infants.
- While transfusions affect iron status and can lead to detectable free iron, this does not translate to increased oxidative damage contributing to CLD.
Unlabelled:
Frequent blood transfusions may produce changes in iron status which can give rise to oxygen-derived free-radical (ODFR) generation and oxidative injury. Preterm infants developing chronic lung disease (CLD) receive significantly more transfusions. A total of 73 very preterm infants had weekly estimations of serum iron, transferrin, transferrin saturation, ferritin, caeruloplasmin, bleomycin detectable ('free') iron (BDI), and thiobarbituric acid reacting substances (TBARS) made over the first 28 days. Thirty infants remained oxygen dependent at 36 weeks postmenstrual age and were termed as having CLD. They were significantly lighter and less mature at birth and received more than twice as many transfusions during the 1st month. They had significantly lower transferrin levels initially but similar total iron and transferrin saturations as non-CLD infants. Ferritin and caeruloplasmin levels rose to significantly higher levels over the 1st month in CLD infants, and ferritin levels were significantly related to the number of transfusions given. Infants with higher ferritin levels were more likely to show BDI, although this was not associated with increased lipid peroxidation as evidenced by higher TBARS.
Conclusion:
It is unlikely that oxidative injury from ODFRs induced by blood transfusion contributes to the risk of developing CLD in preterm infants.