Article Text

DOES EARLY DEXAMETHASONE TREATMENT AFFECT THE SEVERITY OF NEONATAL HYPERBILIRUBINAEMIA IN PRETERM INFANTS?
  1. C V Hulzebos1,
  2. A F Bos1,
  3. H J Verkade2
  1. 1Division of Neonatology, Department of Pediatrics, University Medical Center Groningen, Groningen, The Netherlands
  2. 2Division of Pediatric Gastroenterology, Department of Pediatrics, University Medical Center Groningen, Groningen, The Netherlands

Abstract

Background/Objective Neonatal hyperbilirubinaemia is caused by high bilirubin production in relation to limited conjugation capacity. Expression of UDP-glucuronosyltransferase 1A1, responsible for bilirubin glucuronidation, is positively regulated by corticosteroids. It is unclear whether postnatal corticosteroid treatment affects neonatal hyperbilirubinaemia. We determined whether early corticosteroid treatment affects the severity of neonatal hyperbilirubinaemia in preterm infants.

Methods Our centre participated in a randomised controlled trial aimed to assess the effects of early dexamethasone treatment on bronchopulmonary dysplasia (Antilla et al, Eur J Pediatr 2005). Infants were treated with dexamethasone (0.25 mg/kg twice daily at postnatal days 1 and 2) or with placebo. In the 26 infants (12 dexamethasone, 14 placebo) who were enrolled in our hospital, we analysed total serum bilirubin (TSB) concentrations during 7 postnatal days.

Statistics Student’s t test, significance p<0.05.

Results Main results are shown in the table. Mean birth weights and gestational ages were similar, as were the mean and maximum TSB levels. The TSB concentrations in the dexamethasone group reached their maximum earlier than those in the placebo group, but the difference was not statistically significant (p = 0.10).

Hulzebos et al Demographic and total serum bilirubin data of dexamethasone and placebo-treated infants

Conclusions Early dexamethasone treatment does not affect the severity of neonatal hyperbilirubinaemia. Present data do not support the hypothesis that early dexamethasone treatment sufficiently increases the (UDPGT1A1) bilirubin conjugation capacity to accommodate the increased UCB production in preterm infants.

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