***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: To determine whether prenatal corticosteroid therapy would reduce the incidence of neonatal necrotizing enterocolitis ( NEC ) , we assigned a total of 466 women admitted in premature labor either to receive placebo  ( group A , n = 256 ) , if delivery was expected to occur within 24 hours of admission , or to receive betamethasone ( group B , n = 210 ) if delivery was expected to take place more than 24 hours after admission . All women were free of severe medical complications or drug therapy ; cases of intrauterine growth retardation or premature rupture of the membranes were excluded . Their newborn infants , excluding malformed , congenitally infected , and growth-retarded infants , were enrolled in the study unless they had died before the age of 10 postnatal days . Babies born to group A mothers ( n = 248 ) were further assigned to a treatment group ( group A1 , n = 130 ) receiving dexamethasone , 2 mg/kg/day by intravenous injection during the first 7 days of life , or to a control group ( group A2 , n = 118 ) receiving 10 % dextrose solution placebo .  Group B infants ( prenatal betamethasone , n = 205 ) received neither treatment nor placebo . The incidence of NEC in group A1 was 6.9 % ( 9/130 ) , and in group A2 it was 14.4 % ( 17/118 ) ( p less than 0.05 ) . In group B the incidence was 3.4 % ( 7/205 ) ; this was much lower than in group A2 ( p less than 0.01 ) and lower than in group A combined ( 10.4 % ) ( p less than 0.01 ) . There was no death from NEC and no surgical intervention among group B patients . The mortality rate for group A1 ( 11 % ) was lower than for group A2 ( 56 % ) ( p less than 0.02 ) . There were fewer indications for surgical intervention for NEC in group A1 than in group A2 . Histologic studies confirmed bowel ischemia in all specimens analyzed . These data support the hypothesis that the incidence of NEC is significantly reduced after prenatal steroid treatment . Although postnatal therapy with steroids does not decrease the incidence as effectively as prenatal therapy , it improves clinical outcome of NEC Early postnatal use of dexamethasone has recently been shown to be effective in improving the pulmonary status in premature infants with respiratory distress syndrome ( RDS ) . To study the effect of dexamethasone on pulmonary inflammatory responses , we studied ten infants treated with dexamethasone and ten infants without this treatment . Serial tracheal aspirates were obtained for cell counts , neutrophil counts , total protein concentrations , and leukotriene B4 ( LTB4 ) and 6-keto prostagl and in (PG)F(1 alpha ) levels before and after starting the study . Infants in the dexamethasone-treated group required significantly lower mean airway pressures for ventilation and had lower PaCO2 values from day 3 to day 14 than infants in the control group , suggesting better pulmonary function . For infants in the dexamethasone group , the tracheal aspirates showed significantly lower cell and neutrophil counts , protein concentrations , and 6-keto-PGF(1 alpha ) and LTB4 levels than in the control group . We conclude that early postnatal dexamethasone therapy may lessen lung inflammation and improve pulmonary function in infants with RDS Dexamethasone was compared with placebo in a double-blind , crossover , r and omised study of infants with severe bronchopulmonary dysplasia who had required mechanical ventilation for at least four weeks , despite treatment with diuretics , methylxanthines , bronchodilators , fluid restriction , nutritional supplementation , and ligation of the patent ductus arteriosus when indicated . Gestational age ranged from 27 to 33 weeks and birth weight from 800 to 1730 g. Patients received dexamethasone ( 0 . 5 mg/kg/day ) or normal saline for the first 3 days , then treatment was crossed over for the next 3 days . The study was terminated when sequential analysis showed that all six patients had improved during dexamethasone therapy . Significant improvements were seen in ventilator-determined respiratory rate , peak inspiratory pressure , fractional inspired oxygen concentration , and alveolar arterial oxygen gradients ( p less than 0 . 05 ) . Although dexamethasone hastened weaning from mechanical ventilation , infection occurred in a substantial proportion of patients Background . Although several trials of early dexamethasone therapy have been completed to determine if such therapy would reduce mortality and chronic lung disease ( CLD ) in infants with respiratory distress , optimal duration and side effects of such therapy remain unknown . Purpose . The purpose of this study was : 1 ) to determine if a 3-day course of early dexamethasone therapy would reduce CLD and increase survival without CLD in neonates who received surfactant therapy for respiratory distress syndrome and 2 ) to determine adverse effects associated with such therapy . Design . This was a prospect i ve multicenter r and omized trial comparing a 3-day course of dexamethasone therapy beginning at 24 to 48 hours of life to placebo therapy .  Two hundred forty-one neonates ( dexamethasone n = 118 , placebon = 123 ) , who weighed between 500 g and 1500 g , received surfactant therapy , and were at significant risk for CLD or death using a model to predict CLD or death at 24 hours of life , were enrolled in the trial . Infants r and omized to receive early dexamethasone  were given 6 doses of dexamethasone at 12-hour intervals beginning at 24 to 48 hours of life . The primary outcomes compared were survival without CLD and CLD . CLD was defined by the need for supplemental oxygen at the gestational age of 36 weeks . Complication rates and adverse effects of study drug therapy were also compared . Results . Neonates r and omized to early dexamethasone treatment were more likely to survive without CLD ( RR : 1.3 ; 95 % CI : 1.03 , 1.7 ) and were less likely to develop CLD ( RR : 0.6 ; CI : 0.3 , 0.98 ) . Mortality rates were not significantly different . Subsequent dexamethasone therapy use was less in early dexamethasone-treated neonates ( RR : 0.8 ; CI : 0.7 , 0.96 ) . Very early ( ≤7 days of life ) intestinal perforations were more common among dexamethasone-treated neonates ( 8 % vs 1 % ) . Conclusion . We conclude that an early 3-day course of dexamethasone therapy increases survival without CLD , reduces CLD , and reduces  late dexamethasone therapy in high-risk , low birth weight infants who receive surfactant therapy for respiratory distress syndrome . Potential benefits of early dexamethasone therapy at the dosing schedule used in this trial need to be weighed against the risk for early intestinal perforation BACKGROUND Early administration of high doses of dexamethasone may reduce the risk of  chronic lung disease in premature infants but can cause complications . Whether moderate doses would be as effective but safer is not known . METHODS We r and omly assigned 220 infants with a birth weight of 501 to 1000 g who were treated with mechanical ventilation within 12 hours after birth to receive dexamethasone or placebo with either routine ventilatory support or permissive hypercapnia . The dexamethasone was administered within 24 hours after birth at a dose of 0.15 mg per kilogram of body weight per day for three days , followed by a tapering of the dose over a period of seven days . The primary outcome was death or chronic lung disease at 36 weeks ' postmenstrual age . RESULTS The relative risk of death or chronic lung disease in the dexamethasone-treated infants , as compared with those who received placebo , was 0.9 ( 95 percent confidence interval , 0.8 to 1.1 ) . Since the effect of dexamethasone treatment did not vary according to the ventilatory approach , the two dexamethasone groups and the two placebo groups were combined . The infants in the dexamethasone group were less likely than those in the placebo group to be receiving oxygen supplementation 28 days after birth ( P=0.004 ) or open-label dexamethasone ( P=0.01 ) , were more likely to have hypertension ( P<0.001 ) , and were more likely to be receiving insulin treatment for hyperglycemia ( P=0.02 ) . During the first 14 days , spontaneous gastrointestinal perforation occurred in a larger proportion of infants in the dexamethasone group ( 13 percent , vs. 4 percent in the placebo group ; P=0.02 ) . The dexamethasone-treated infants had a lower weight ( P=0.02 ) and a smaller head circumference ( P=0.04 ) at 36 weeks ' postmenstrual age . CONCLUSIONS In preterm infants , early administration of dexamethasone at a moderate dose has no effect on death or chronic lung disease and is associated with gastrointestinal perforation and decreased growth 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 
    Output:
    
There were no differences in the rates of neonatal mortality , infection , severe ROP , severe IVH , PVL , NEC and pulmonary haemorrhage .
Gastrointestinal bleeding and intestinal perforation were important adverse effects and the risks of hyperglycaemia and hypertension were also increased .
In the two trials which have reported late outcomes , several adverse neurological effects were found at follow-up examinations of survivors treated with early steroids : abnormal neurological examination , cerebral palsy and developmental delay .
REVIEW ER 'S CONCLUSIONS The benefits of early postnatal corticosteroid treatment ( < 96 hours ) may not outweigh the known or potential adverse effects of this treatment .