***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: OBJECTIVES To study whether early postnatal ( < 12 hours ) dexamethasone therapy reduces the incidence of chronic lung disease in preterm infants with respiratory distress syndrome . MATERIAL S AND METHODS A multicenter r and omized , double-blind clinical trial was undertaken on 262 ( saline placebo , 130 ; dexamethasone , 132 ) preterm infants ( < 2000 g ) who had respiratory distress syndrome and required mechanical ventilation shortly after birth . The sample size was calculated based on the 50 % reduction in the incidence of chronic lung disease when early dexamethasone is used , allowing a 5 % chance of a type I error and a 10 % chance of a type II error . For infants who received dexamethasone , the dosing schedules were : 0.25 mg/kg/dose every 12 hours intravenously on days 1 through 7 ; 0.12 mg/kg/dose every 12 hours intravenously on days 8 through 14 ; 0.05 mg/kg/dose every 12 hours intravenously on days 15 through 21 ; and 0 . 02 mg/kg/dose every 12 hours intravenously on days 22 through 28 . A st and ard protocol for respiratory care was followed by the participating hospitals . The protocol emphasized the criteria of initiation and weaning from mechanical ventilation . The diagnosis of chronic lung disease based on oxygen dependence and abnormal chest roentgenogram was made at 28 days of age . To assess the effect of dexamethasone on pulmonary inflammatory response , serial tracheal aspirates were assayed for cell counts , protein , leukotriene B4 , and 6-keto prostagl and in F1alpha . All infants were observed for possible side effects , including hypertension , hyperglycemia , sepsis , intraventricular hemorrhage , retinopathy of prematurity , cardiomyopathy , and alterations in calcium homeostasis , protein metabolism , and somatic growth . RESULTS Infants in the dexamethasone group had a significantly lower incidence of chronic lung disease than infants in the placebo group either judged at 28 postnatal days ( 21/132 vs 40/130 ) or at 36 postconceptional weeks ( 20/132 vs 37/130 ) . More infants in the dexamethasone group than in the placebo group were extubated during the study . There was no difference between the groups in mortality ( 39/130 vs 44/132 ) ; however , a higher proportion of infants in the dexamethasone group died in the late study period , probably attributable to infection or sepsis . There was no difference between the groups in duration of oxygen therapy and hospitalization . Early postnatal use of dexamethasone was associated with a significant decrease in tracheal aspirate cell counts , protein , leukotriene B4 , and 6-keto prostagl and in F1alpha , suggesting a suppression of pulmonary inflammatory response . Significantly more infants in the dexamethasone group than in the placebo group had either bacteremia or clinical sepsis ( 43/132 vs 27/130 ) . Other immediate , but transient , side effects observed in the dexamethasone group are : an increase in blood glucose and blood pressure , cardiac hypertrophy , hyperparathyroidism , and a transient delay in the rate of growth . CONCLUSIONS In preterm infants with severe respiratory distress syndrome requiring assisted ventilation shortly after birth , early postnatal dexamethasone therapy reduces the incidence of chronic lung disease , probably on the basis of decreasing the pulmonary inflammatory process during the early neonatal period . Infection or sepsis is the major side effect that may affect the immediate outcome . Other observable side effects are transient . In view of the significant side effects and the lack of overall improvement in outcome and mortality , and the lack of long term follow-up data , the routine use of early dexamethasone therapy is not yet recommended A r and omized trial was conducted of dexamethasone therapy in infants with bronchopulmonary dysplasia who were dependent on respirators and were not progressing clinical ly despite conventional treatment . Babies were admitted to the study if they had a roentgenogram and clinical diagnosis of bronchopulmonary dysplasia , were 2 to 6 weeks in age , weighed less than 1,500 g , had made no progress in weaning for the preceding five days , and were free of sepsis , patent ductus arteriosus , and congenital heart disease , and had had no intravenous fat for at least 24 hours . After parental consent was obtained , infants were r and omly assigned to control or treatment groups . The study hypothesis was that with steroid treatment , babies could be weaned from the respirator within 72 hours and would show a significant improvement in lung compliance within that time . Sequential analysis exceeded criterion ( P less than .05 ) when seven consecutive untied pairs showed weaning with dexamethasone and failure to wean in control infants . Pulmonary compliance improved by 64 % in the treated group and 5 % in the control group ( P less than .01 ) . No significant intergroup differences were noted in mortality , length of hospital stay , sepsis , hypertension , hyperglycemia , or electrolyte abnormalities . Study design permits the conclusion that dexamethasone can produce substantial short-term improvement in lung function , often permitting rapid weaning from the respirator , but long-term efficacy and safety must be demonstrated by further investigations OBJECTIVE To test the hypothesis that early postnatal dexamethasone will reduce the incidence of death or chronic lung disease ( CLD )  in ventilated extremely low birth weight premature infants . DESIGN Multicenter r and omized double-blinded controlled clinical trial . SETTING A total of 42 neonatal intensive care units in the Vermont Oxford Network . PARTICIPANTS Infants weighing 501 to 1000 g were eligible for enrollment at 12 hours of age if they needed assisted ventilation , had received surfactant replacement therapy , were physiologically stable , had no obvious life-threatening congenital anomaly , and had blood cultures obtained and antibiotic therapy initiated . INTERVENTION Infants were r and omly assigned to dexamethasone or saline placebo . Intravenous dexamethasone was administered for 12 days according to the following dosing schedule : 0.5 mg/kg/d for 3 days , 0.25 mg/kg/d for 3 days , 0.10 mg/kg/d for 3 days , 0.05 mg/kg/d for 3 days . Infants in either group could receive treatment with selective late postnatal steroids beginning on day 14 of life if they were on assisted ventilation with supplemental oxygen greater than 30 % . OUTCOME MEASUREMENTS The primary outcome measure was CLD or death at 36 weeks postmenstrual age . RESULTS The study was stopped before completion of sample size goals because of concern about serious side effects in the early steroid treatment group . A total of 542 infants were enrolled ( early treatment N = 273 , control N = 269 ) . The 2 groups had similar demographic characteristics . No differences were noted in the primary outcome of CLD or death at 36 weeks postmenstrual age ( early treatment 50 % vs control : 53 % , relative risk : 0.93 ; 95 % confidence interval [ CI ] : 0.79 - 1.09 ) . Fewer infants who received early steroid treatment had a patent ductus arteriosus ( relative risk : 0.78 ; 95 % CI : 0.63 - 0.96 ) , and fewer infants in the early steroid group received  indomethacin therapy ( relative risk : 0.74 ; 95 % CI : 0.64 - 0.86 ) or  late steroid  treatment ( relative risk : 0.69 ; 95 % CI : 0.58 - 0.81 ) . However , more infants who received early steroid treatment had complications associated with therapy including an increase in hyperglycemia ( relative risk : 1.29 ; 95 % CI : 1.13 - 1.46 ) and an increase in the use of insulin therapy ( relative risk : 1.62 ; 95 % CI : 1.36 - 1.94 ) . A trend toward increased gastrointestinal hemorrhage ( relative risk : 1.55 ; 95 % CI : 0.92 - 2.61 ) , gastrointestinal perforation ( relative risk : 1.53 ; 95 % CI : 0.89 - 2.61 ) , and an increased systolic blood pressure ( relative risk : 1.34 ; 95 % CI : 0.97 - 1.85 ) was noted . In infants receiving cranial ultrasound examinations , a marginal increase in periventricular leukomalacia was noted in the early steroid treatment group ( relative risk : 2.23 ; 95 % CI : 0.99 - 5.04 ) . Infants who received early steroid therapy had fewer days in supplemental oxygen but experienced poor weight gain . CONCLUSIONS A 12-day course of early postnatal steroid therapy given to extremely low birth weight infants did not decrease the risk of CLD or death at 36 weeks postmenstrual age and was associated with an increased risk of complications and poor weight gain OBJECTIVE To study the long term neurodevelopmental outcome of children who participated in a r and omised , double blind , placebo controlled study of early postnatal dexamethasone treatment for prevention of chronic lung disease . METHODS The original study compared a three day course of dexamethasone  ( n = 132 ) with a saline placebo ( n = 116 ) administered from before 12 hours of age in preterm infants , who were ventilated for respiratory distress syndrome and had received surfactant treatment .  Dexamethasone treatment was associated with an increased incidence of hypertension , hyperglycaemia , and gastrointestinal haemorrhage and no reduction in either the incidence or severity of chronic lung disease or mortality . A total of 195 infants survived to discharge and five died later . Follow up data were obtained on 159 of 190 survivors at a mean ( SD ) age of 53 ( 18 ) months . RESULTS No differences were found between the groups in terms of perinatal or neonatal course , antenatal steroid administration , severity of initial disease , or major neonatal morbidity .  Dexamethasone treated children had a significantly higher incidence of cerebral palsy than those receiving placebo ( 39/80 ( 49 % ) v 12/79 ( 15 % ) respectively ; odds ratio ( OR ) 4.62 , 95 % confidence interval ( 95 % CI ) 2.38 to 8.98 ) . The most common form of cerebral palsy was spastic diplegia ( incidence 22/80 ( 28 % ) v 5/79 ( 6 % ) in dexamethasone and placebo treated infants respectively ; OR 4.45 , 95 % CI 1.95 to 10.15 ) . Developmental delay was significantly more common in the dexamethasone treated group ( 44/80 ( 55 % ) ) than in the placebo treated group ( 23/79 ( 29 % ) ; OR 2.87 , 95 % CI 1.53 to 5.38 ) . Dexamethasone treated infants had more periventricular leucomalacia and less intraventricular haemorrhage in the neonatal period than those in the placebo group , although these differences were not statistically significant . Eleven children with cerebral palsy had normal ultrasound scans in the neonatal period ; all 11 had received dexamethasone . Logistic regression analysis showed both periventricular leucomalacia and drug assignment to dexamethasone to be highly significant predictors of abnormal neurological outcome . CONCLUSIONS A three day course of dexamethasone administered shortly after birth in preterm infants with respiratory distress syndrome is associated with a significantly increased incidence of cerebral palsy and developmental delay OBJECTIVE We compared the effects of a policy of neonatal steroid administration versus placebo for babies chronically dependent on supplemental oxygen in terms of long-term health and development , judged at 3 years of age . DESIGN Double-blind r and omized controlled trial . SETTING Thirty-one centers in the United Kingdom , Irel and , Belgium , Germany , Canada , and the United States . PATIENTS Babies who were chronically dependent on supplemental oxygen between 2 and 12 weeks of age were recruited to the trial between 1986 and 1989 . Sixty-two children were known to have died , 23 before discharge from the hospital and 10 afterward in the active group , compared with 25 and 4 , respectively , in the placebo group . Information was available for 209 of the 212 eligible for follow-up ( 99 % ) . INTERVENTIONS A 1-week course of active dexamethasone phosphate 0.6 mg/kg/d ( dexamethasone base 0.5 mg/kg/d ) or saline placebo was given intravenously ( or orally , if no intravenous line ) . There was an option to give a second tapering 9-day course 
    Output:
    
Results Postnatal steroid therapy is associated with an increase in cerebral palsy and neuro-developmental impairment .
The studies with less contamination show a greater effect of the steroids , consistent with a real direct toxic effect of steroids on the developing central nervous system .
Conclusions Postnatal pharmacologic steroid treatment for prevention or treatment of bronchopulmonary dysplasia is associated with dramatic increases in neuro-developmental impairment .