grams, five studies, 835 infants) nificant differences between groups treated with antenatal corti- costeroids and controls in fetal death, birthweight or chorioam- No statistically significant differences between groups treated with nionitis were seen in subgroups treated with dexamethasone or antenatal corticosteroids and controls were seen for postnatal fever betamethasone separately. However, dexamethasone significantly RR1.00, 95%CI 0.36 to 2.75, one study, 204 women)or fever increased the incidence of puerperal sepsis(RR 1.74, 95%CI 1.04 ter trial entry requiring the use of antibiotics(RR O25, 95%CI to 2.89 four studies, 536 women)while betamethasone did not 03 to 2.06, one study, 44 women)in women with prolonged rup- (RR 1.00,95% CI 0 58 to 1.72, four studies, 467 women) of membranes at first dose. Infants whose mothers were treated with corticosteroids following rupture of membranes present at Antenatal corticosteroids versus placebo or no treatment(by he time of the first dose had significantly reduced chronic lung decade of recruitment to study) disease(Rr 0.50, 95%CI 0.33 to 0.76, one study, 165 infants), Data were available by decade of recruitment for several of the necrotising enterocolitis(RR 0.39, 95% CI 0 18 to 0.86, four primary outcomes that relate to the mother and fetus or neonate studies,583 infants)and duration of mechanical ventilation or RDS(1970s RR 0.55, 95%CI 0.43 to 0.70, six studies, 1847 in- CPAP(FWMD-3.50 days, 95% CI-512 to-1.88 grams, one fants:: 1980s RR 0.71, 95%CI 0.58 to 0.87, six studies, 1127 in- study,165 infants). No statistically significant differences between fants; 1990s RRO.69, 95%CI 0.59 to0.81, nine studies, 1064in groups treated with antenatal corticosteroids and controls were fants)and cerebroventricular haemorrhage(1970s RR O50,95% seen for neonatal infection(RR 1.26, 95% CI 0.86 to 1.85, seven CI 0. 29 to 0.85, four studies, 1646 infants; 1980s RR O61,95% studies, 796 infants), systemic infection in the first 48 hours of CI0.39 to 0.94, two studies, 238 infants: 1990s RR O53,95% life(RR.96,95% CI 0.44 to 2.12, two studies, 249 infants)or CI 0.38 to 0.74, seven studies, 988 infants) were significantly re- need for mechanical ventilation or CPAP(RR 0.90, 95%CI 0.47 duced in infants treated with corticosteroids in all three decades to 1.73, one study, 206 infants) in infants following prolonged of recruitment. Combined fetal and neonatal death, and neonatal pture of membranes at first dose death alone(1970s RR 0.73, 95% CI 0.56 to 0.93, six studies, 1876 infants: 1980s RR 0.98, 95% CI 0.69 to 1. 40, five stud- Antenatal corticosteroids versus placebo or no treatment(by the ies, 1056 infants: 1990s RR 0.50, 95% CI 0.38 to 0.66, seven presence or absence of hypertension syndromes in pregnancy) studies, 1024 infants ), were significantly reduced in infants treated Data were available by presence or absence of hypertension syn- with corticosteroids in the 1970s and 1990s, but not the 1980s. dromes in pregnancy for several of the primary outcomes that re. No statistically significant differences between groups treated with late to the mother and fetus/neonate. Infants born to pregnan- antenatal corticosteroids and controls were seen for fetal death cies complicated by hypertension syndromes treated with corticos- birthweight, puerperal sepsis or chorioamnionitis for any of the teroids had significantly reduced risk of neonatal death(rr 0.50, individual decades of recruitment subgroups 95%CI 0.29 to 0.87, two studies, 278 infants), RDS(RR 0.50, 95%CI 0.35 to 0.72, five studies, 382 infants) and cerebroven- 3. Post hoc analysis ricular haemorrhage(RR 0.38, 95% CI 0.17 to 0.87, two stud. Antenatal corticosteroids versus placebo or no treatment(by ies, 278 infants). No statistically significant differences between gestational age at entry to rial) groups treated with antenatal corticosteroids and controls were Data were available by gestational age at entry seen for combined fetal and neonatal death (RR 0.83, 95%CI the primary outcomes that relate to the mother and fetus or 0.57 to 1.20, two studies, 313 infants), fetal death(RR 1.73.95% neonate Chorioamnionitis was significantly reduced in corticos- CI0.91 to 3.28, three studies, 331 infants), birthweight(FWMD teroid-treated women entering a trial from 30 to 32+6weeks(RR 131.72 grams, 95%CI-319 68 to 56.24 grams, one study, 95 0 19,95%CI 0.04 to 0.86, one study, 194 women),but not from infants, chorioamnionitis(RR2.36, 95%CI 0.36 to 15.73, two less than 26 weeks(RR 2.18, 95% CI 0.62 to 7.69, one study, studies,311 women)or puerperal sepsis(RR 0.68, 95%CI 0.30 women), 26 to 29 +6 weeks(RR 1.06, 95%CI 0.55 to 2.06, to 1.52, one study, 218 women)in pregnancies complicated by one study, 242 women), 33 to 34+6 weeks(RR 0.47, 95%CI 0 12 to 1. 80, one study, 333 women), 35 to 36+6 weeks(Rr 0.18, 95% CI 0.01 to 3.36, one study, 181 women)and Antenatal corticosteroids versus placebo or no treatment (by than 36 weeks(no events in 40 women). Neonatal death was sig- ype of corticosteroid) nificantly reduced in corticosteroid treated infants entering a trial Data were available by type of corticosteroid used for several of the from 26 to 29+6 weeks(RR 0.67, 95%CI 0.45 to 0.99, one primary outcomes that relate to the mother and fetus or neonate. study, 227 infants), but not from less than 26 weeks(RR 1.87, Both dexamethasone and betamethasone significantly reduced 95% CI 0.61 to 5.72, one study, 27 infants), 30 to 32+6 weeks ombined fetal and neonatal death, neonatal death, RDS and cere-(RR 0.51,95%CI 0.23 to 1.1l, one study, 195 infants), 33 to 34 broventricular haemorrhage. Betamethasone treatment(RR 0.56, +6 weeks(RR 1.11, 95%CI 0.49 to 2.48, one study, 339 infants 5%CI 0.48 to 0.65, 14 studies, 2563 infants)resulted in a greater 35 to 36+6 weeks(RR 0.62, 95%CI 0.06 to 6.76, one study reduction in RDS than dexamethasone treatment(RR 0.80, 95% 191 infants)and greater than 36 weeks(RR 9.21, 95%CI 0.51 CI 0.68 to 0.93, six studies, 1457 infants). No statistically sig. to 167. 82, one study, 42 infants). RDS was significantly reduced Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth( Review) Copyright @2006 The Cochrane Collaboration. Published by John wiley& Sons, Ltdgrams, five studies, 835 infants). No statistically significant differences between groups treated with antenatal corticosteroidsand controls wereseen for postnatal fever (RR 1.00, 95% CI 0.36 to 2.75, one study, 204 women) or fever after trial entry requiring the use of antibiotics (RR 0.25, 95% CI 0.03 to 2.06, onestudy, 44women) inwomenwith prolonged rup￾ture ofmembranesat first dose.Infantswhosemothersweretreated with corticosteroids following rupture of membranes present at the time of the first dose had significantly reduced chronic lung disease (RR 0.50, 95% CI 0.33 to 0.76, one study, 165 infants), necrotising enterocolitis (RR 0.39, 95% CI 0.18 to 0.86, four studies, 583 infants) and duration of mechanical ventilation or CPAP (FWMD -3.50 days, 95% CI -5.12 to -1.88 grams, one study, 165 infants). No statistically significant differences between groups treated with antenatal corticosteroids and controls were seen for neonatal infection (RR 1.26, 95% CI 0.86 to 1.85, seven studies, 796 infants), systemic infection in the first 48 hours of life (RR 0.96, 95% CI 0.44 to 2.12, two studies, 249 infants) or need for mechanical ventilation or CPAP (RR 0.90, 95% CI 0.47 to 1.73, one study, 206 infants) in infants following prolonged rupture of membranes at first dose. Antenatalcorticosteroids versus placebo or no treatment (by the presence or absence of hypertension syndromes in pregnancy) Data were available by presence or absence of hypertension syn￾dromes in pregnancy for several of the primary outcomes that re￾late to the mother and fetus/neonate. Infants born to pregnan￾ciescomplicated by hypertension syndromestreatedwith corticos￾teroids had significantly reduced risk of neonatal death (RR 0.50, 95% CI 0.29 to 0.87, two studies, 278 infants), RDS (RR 0.50, 95% CI 0.35 to 0.72, five studies, 382 infants) and cerebroven￾tricular haemorrhage (RR 0.38, 95% CI 0.17 to 0.87, two stud￾ies, 278 infants). No statistically significant differences between groups treated with antenatal corticosteroids and controls were seen for combined fetal and neonatal death (RR 0.83, 95% CI 0.57 to 1.20, two studies, 313 infants), fetal death (RR 1.73, 95% CI 0.91 to 3.28, three studies, 331 infants), birthweight (FWMD -131.72 grams, 95% CI -319.68 to 56.24 grams, one study, 95 infants), chorioamnionitis (RR 2.36, 95% CI 0.36 to 15.73, two studies, 311 women) or puerperal sepsis (RR 0.68, 95% CI 0.30 to 1.52, one study, 218 women) in pregnancies complicated by hypertension syndromes. Antenatal corticosteroids versus placebo or no treatment (by type of corticosteroid) Data wereavailable by type ofcorticosteroid used for several of the primary outcomes that relate to the mother and fetus or neonate. Both dexamethasone and betamethasone significantly reduced combined fetaland neonatal death, neonatal death, RDS and cere￾broventricular haemorrhage. Betamethasone treatment (RR 0.56, 95% CI 0.48 to 0.65, 14 studies, 2563 infants)resulted in a greater reduction in RDS than dexamethasone treatment (RR 0.80, 95% CI 0.68 to 0.93, six studies, 1457 infants) . No statistically sig￾nificant differences between groups treated with antenatal corti￾costeroids and controls in fetal death, birthweight or chorioam￾nionitis were seen in subgroups treated with dexamethasone or betamethasone separately . However, dexamethasone significantly increased theincidence of puerperal sepsis (RR 1.74, 95% CI 1.04 to 2.89, four studies, 536 women) while betamethasone did not (RR 1.00, 95% CI 0.58 to 1.72, four studies, 467 women). Antenatal corticosteroids versus placebo or no treatment (by decade of recruitment to study) Data were available by decade of recruitment for several of the primary outcomes that relate to the mother and fetus or neonate. RDS (1970s RR 0.55, 95% CI 0.43 to 0.70, six studies, 1847 in￾fants; 1980s RR 0.71, 95% CI 0.58 to 0.87, six studies, 1127 in￾fants; 1990s RR 0.69, 95% CI 0.59 to 0.81, ninestudies, 1064 in￾fants) and cerebroventricular haemorrhage (1970s RR 0.50, 95% CI 0.29 to 0.85, four studies, 1646 infants; 1980s RR 0.61, 95% CI 0.39 to 0.94, two studies, 238 infants; 1990s RR 0.53, 95% CI 0.38 to 0.74, seven studies, 988 infants) were significantly re￾duced in infants treated with corticosteroids in all three decades of recruitment. Combined fetal and neonatal death, and neonatal death alone (1970s RR 0.73, 95% CI 0.56 to 0.93, six studies, 1876 infants; 1980s RR 0.98, 95% CI 0.69 to 1.40, five stud￾ies, 1056 infants; 1990s RR 0.50, 95% CI 0.38 to 0.66, seven studies, 1024 infants), weresignificantly reduced in infants treated with corticosteroids in the 1970s and 1990s, but not the 1980s. No statistically significant differences between groups treated with antenatal corticosteroids and controls were seen for fetal death, birthweight, puerperal sepsis or chorioamnionitis for any of the individual decades of recruitment subgroups. 3. Post hoc analysis Antenatal corticosteroids versus placebo or no treatment (by gestational age at entry to trial) Data were available by gestational age at entry for several of the primary outcomes that relate to the mother and fetus or neonate. Chorioamnionitis was significantly reduced in corticos￾teroid-treated women entering atrial from 30 to 32 + 6 weeks (RR 0.19, 95% CI 0.04 to 0.86, one study, 194 women), but not from less than 26 weeks (RR 2.18, 95% CI 0.62 to 7.69, one study, 46 women), 26 to 29 + 6 weeks (RR 1.06, 95% CI 0.55 to 2.06, one study, 242 women), 33 to 34 + 6 weeks (RR 0.47, 95% CI 0.12 to 1.80, one study, 333 women), 35 to 36 + 6 weeks (RR 0.18, 95% CI 0.01 to 3.36, one study, 181 women) and greater than 36 weeks (no events in 40 women). Neonatal death was sig￾nificantly reduced in corticosteroid treated infants entering a trial from 26 to 29 + 6 weeks (RR 0.67, 95% CI 0.45 to 0.99, one study, 227 infants), but not from less than 26 weeks (RR 1.87, 95% CI 0.61 to 5.72, one study, 27 infants), 30 to 32 + 6 weeks (RR 0.51, 95% CI 0.23 to 1.11, one study, 195 infants), 33 to 34 + 6 weeks (RR 1.11, 95% CI 0.49 to 2.48, onestudy, 339 infants), 35 to 36 + 6 weeks (RR 0.62, 95% CI 0.06 to 6.76, one study, 191 infants) and greater than 36 weeks (RR 9.21, 95% CI 0.51 to 167.82, one study, 42 infants). RDS was significantly reduced Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth (Review) 11 Copyright © 2006 The Cochrane Collaboration. Published by John Wiley & Sons, Ltd 第 105 页