Comparing a group of infants treated with recombinant erythropoietin and iron supplementation to a group of control infants, no difference was observed concerning the transfusion need. The incidence of retinopathy of prematurity was significantly higher in the treated group. These data need to be confirmed in randomized controlled studies.

Objective: To assess the effect of moderately early postnatal dexamethasone treatment on growth and neurodevelopmental outcome in preterm infants. Methods: Thirty preterm infants enrolled in a randomised clinical trial to investigate the effectiveness of moderately early dexamethasone administration in the treatment of chronic lung disease were routinely followed up. Fifteen babies received a total dose of 4.75 mg/kg over 14 days from the 10th day of life, and 15 babies were untreated. Five infants in each group received open label steroids to facilitate extubation later in their clinical course. Growth and neurodevelopmental outcome are reported. Results: The mean body weight, height, and head circumference as well as the number of babies with anthropometric measurements within normal range were similar in treated and untreated babies. There was no significant difference between treated and control groups with respect to incidence of cerebral palsy, major neurosensory impairment, mean intelligence quotient scores, and behavioural abnormalities. Conclusions: Postnatal dexamethasone treatment with the schedule used in this study did not impair growth and neurodevelopmental outcome in preterm infants. Data from larger trials have raised major concern that postnatal steroid treatment may increase neurodevelopmental impairment. The full extent of the risk will only be known when more trials have reported follow up data. P ostnatal dexamethasone has been widely used in the treatment of chronic lung disease (CLD) in preterm infants, and several randomised trials have shown that it rapidly reduces requirements for oxygen and ventilation. However, the long term consequences on mortality and morbidity are less clear, and recent reports have raised concerns that postnatal steroids may cause neurodevelopmental impairment in preterm infants. [1][2][3] In animal models, corticosteroids significantly impair cell multiplication in the central nervous system and lung. 4 Murphy et al, 5 using advanced magnetic resonance imaging techniques, documented a reduction in the volume of cortical grey matter in preterm infants exposed to postnatal dexamethasone treatment, and this finding is consistent with clinical trials reporting a reduction in head growth and an increase in the rates of cerebral palsy among children who received steroids as compared with controls. The recent systematic review performed by Barrington,6 which included eight randomised controlled trials enrolling 679 infants, showed a relative risk for neurodevelopmental impairment among surviving, followed up, treated infants of 1.34 (95% confidence interval (CI) 1.09 to 1.64) and a relative risk for cerebral palsy of 2.02 (95% CI 1.51 to 2.71).In this study we describe the follow up findings at three years of adjusted age for 30 surviving infants at high risk for CLD who participated in a randomised clinical trial on the moderately early postnatal use of dexamethasone. MATERIALS AND METHODSThe original randomised clinical trial was carried out in our neonatal intensiv...

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The changes induced on respiratory mechanics and on tracheobronchial aspirate fluid (TAF) cytology by dexamethasone courses started at two different postnatal ages in preterm infants at risk of chronic lung disease (CLD) were reported in this clinical trial designed in two phases. The first phase of the study included 20 neonates with birth weight ≤1,250 g and gestational age ≤32 weeks, who were oxygen and ventilator dependent on the 10th day of life. They were randomly assigned to the moderately early dexamethasone (MED) group or to the control group. The second phase of the study included 20 neonates with the same characteristics, oxygen and ventilator dependent on the 4th day of life, randomly assigned to the early dexamethasone (ED) group or to the control group. Both treated groups received dexamethasone intravenously for 7 days (0.5 mg/kg/day for the first 3 days, 0.25 mg/kg/day for the next 3 days, and 0.125 mg/kg/day for the last day of treatment). The control groups received no steroid treatment. A significantly lower absolute cell count and percentage of neutrophils (PMN) in the TAF and significantly higher dynamic lung compliance (Cdyn) values were observed in both the MED treated compared to the untreated infants and the ED treated infants compared to the control group. Moreover these changes were more precocious in the ED Group compared to the MED Group. Our study suggests that dexamethasone could be more efficacious in reducing effects of ventilator-induced lung injury in preterm infants at high risk of CLD when started earlier.

At 2 years, 8 infants had normal motor outcome and 8 had cerebral palsy. The presence and severity of cerebral palsy or neurodevelopmental delay was not always related to the magnitude or symmetry of the ventricular dilatation per se. The presence of associated lesions was a negative prognostic marker. The early development of epilepsy was also associated with an abnormal outcome.