at least 36 weeks(RR 0.30, 95% CI 0.03 to 2.67, five studies, study, 485 infants), but not those born before 24 hours(FWMD 557 infants). Cerebroventricular haemorrhage was significantly 46.52 grams, 95%CI- 94.26 to 187. 29 grams, two studies, 242 reduced in corticosteroid treated infants born before 28 weeks infants)and before 48 hours after the first dose(FWMD-590 (RR O34, 95%CI 0.14 to 0.86, one study, 62 infants), before 32 grams, 95% CI-13195 to 120.15 grams, one study, 373 infants weeks(RR O52, 95%CI 0. 28 to 0.99, one study, 277 infants)and No statistically significant differences between groups treated with before 34 weeks(RR 0.53, 95%CI 0. 29 to 0.95, one study, 515 antenatal corticosteroids and controls were seen for fetal deaths infants), but not in those born before 30 weeks(rR 0.56, 95% chorioamnionitis in the different subgroups of entry to delivery CI 0. 29 to 1.10, one study 150 infants), before 36 weeks(rr interval examined. 0.56, 95%CI 0.31 to 1.02, one study, 102 infants), at a gestation of at least 34 weeks(RR 1.13, 95%CI 0.07 to 17.92, one study, Antenatal corticosteroids versus placebo or no treatment(by 746 infants)and at a gestation of at least 36 weeks(no events presence or absence of rupture reported in 459 infants). No statistically significant differences Data were available by status of ruptured membranes for several of between groups treated with antenatal corticosteroids and controls the primary and secondary outcomes that relate to the mother and for fetal deaths, birthweight or chorioamnionitis in the fetus or neonate. No statistically significant differences were seen different subgroups of gestational age at delivery examined. for maternal death, chorioamnionitis or puerperal sepsis in moth- ers with rupture of membranes present at the time of first dose Antenatal corticosteroids versus placebo or no treatment(by with rupture of membranes for greater than 24 hours. Combined entry to delivery interval fetal and neonatal death was significantly reduced in corticosteroid Data were available by entry to delivery interval for several of the treated infants born following rupture of membranes present at primary outcomes that relate to the mother and fetus/neonate. time of first dose(RR 0.62, 95%CI 0.46 to 0.82, four studies Combined fetal and neonatal death was significantly reduced in 733 infants), but not following rupture of membranes for greater corticosteroid treated infants born before 24 hours(rro.60, 95% than 24(RRO.77, 95%CI0.51 to 1. 17, two studies, 508 infants) CI 0.39 to 0.94, three studies, 293 infants)and before 48 hours and greater than 48 hours(RR 0.93, 95%CI 0.57 to 1.51,one after the first dose(RR 0.59, 95%CI 0. 41 to 0.86, one study, 373 study, 255 infants). No statistically significant differences between infants), but not those born between one and seven days(RrO8l, groups exposed to antenatal corticosteroids and controls were 95%CI 0.60 to 1.09, three studies, 606 infants) and after seven for fetal deaths following rupture of membranes at first dose(rr days after the first dose(RR 1. 42, 95%CI 0.91 to 2.23, three 0.86, 95%CI 0.46 to 1.61, five studies, 790 infants), for greater studies,598 infants). Neonatal death was significantly reduced than 24(RR 1. 23, 95%CI 0.62 to 2.44, two studies, 508 infants) in corticosteroid treated infants born before 24 hours(RR 0.53, or greater than 48 hours(RR 1.10, 95% CI 0.52 to 2.32,one 95%CI 0. 29 to 0.96, four studies, 295 infants)and before 48 study, 255 infants). The reduction in combined fetal and neonatal hours after the first dose(rr 0.49, 95%CI 0.30 to 0.81, one death is due to a reduction in neonatal death in corticosteroid- study, 339 infants), but not those born between one and treated infants born following rupture of membranes present days(rr 0.74, 95% CI 0.51 to 1.07, three studies, 563 infants) time of first dose(RR 0.58, 95%CI 0.43 to 0.80, seven stud- d after seven days after the first dose(rr 1.45, 95%CI 0.75 to ies, 984 infants). RDS was significantly reduced in corticosteroid 2.80, three studies, 561 infants). RDS was significantly reduced treated infants born following rupture of membranes present at in corticosteroid-treated infants born before 48 hours(RR 0.63, first dose(RR 0.67, 95%CI 0.55 to 0.82, 11 studies, 1089 in- 95%CI 0.43 to 0.93, three studies, 374 infants) and between one fants)and for greater than 24 hours(RR 0.68, 95%CI 0.51to and seven days after the first dose(Rro. 46, 95%CI 0.35 to 0.60, 0.90, six studies, 626 infants), but not following rupture of mem- ne studies, 1110 infants), but not those born before 24 hours branes for greater than 48 hours(RR 0.71, 95%CI 0.36 to 1.4 (RR 0.87, 95%CI 0.66 to 1.15, nine studies, 517 infants)and two studies, 247 infants). Cerebroventricular haemorrhage was after seven days after the first dose( Rro. 82, 95%CI 0.53 to 1.28, significantly reduced in corticosteroid treated infants born follow. eight studies, 988 infants). Cerebroventricular haemorrhage was ing rupture of membranes present at time of first dose(rr 0.47, ignificantly reduced in corticosteroid treated infants born before 95% CI 0.28 to 0.79, five studies, 895 infants), but not follow- 48 hours after the first dose(RR 0.26, 95% CI 0.09 to 0.75, ing rupture of membranes for greater than 24(RR 0.55, 95% CI one study, 339 infants), but those born not before 24 hours(RR 0.16 to 1.84, two studies, 477 infants)and greater than 48 hours 0.54, 95%CI 0. 21 to 1.36, three studies, 264 infants), between (RR 0.87, 95%CI 0 18 to 4.22, one study, 230 infants). Birth- one and seven days(RR 0.51, 95%CI 0.23 to 1. 13, one study, weight was significantly reduced in corticosteroid treated infants 482 infants)and after seven days after the first dose(RR 2.01, born following rupture of membranes for greater than 24(FWMD 95%CI 0.37 to 10.86, one study, 453 infants). Birthweight was -196.46 grams, 95%CI-335 19 to-5773 grams, I study, 349 significantly reduced in infants born between one and seven days infants) and for greater than 48 hours(FWMD-20179 grams, (FWMD-10592 grams, 95%CI.52 to 0.68 grams, one 95%CI-36330 to. 28 grams, one study, 255 infants), but not study, 520 infants) and more than seven days after the first dose following prolonged rupture of membranes present at the time of (FWMD-14701 grams, 95%CI-29197 to.05 grams, one the first dose(FWMD-4268 grams, 95%CI-10891 to 23.55 Antenatal corticosteroids for accelerating fetal lung maturation for eterm birth( Review) Copyright @2006 The Cochrane Collaboration. Published by John wiley& Sons, Ltdat least 36 weeks (RR 0.30, 95% CI 0.03 to 2.67, five studies, 557 infants). Cerebroventricular haemorrhage was significantly reduced in corticosteroid treated infants born before 28 weeks (RR 0.34, 95% CI 0.14 to 0.86, one study, 62 infants), before 32 weeks (RR 0.52, 95% CI 0.28 to 0.99, onestudy, 277 infants) and before 34 weeks (RR 0.53, 95% CI 0.29 to 0.95, one study, 515 infants), but not in those born before 30 weeks (RR 0.56, 95% CI 0.29 to 1.10, one study, 150 infants), before 36 weeks (RR 0.56, 95% CI 0.31 to 1.02, one study, 102 infants), at a gestation of at least 34 weeks (RR 1.13, 95% CI 0.07 to 17.92, one study, 746 infants) and at a gestation of at least 36 weeks (no events reported in 459 infants). No statistically significant differences between groups treated with antenatalcorticosteroidsand controls were seen for fetal deaths, birthweight or chorioamnionitis in the different subgroups of gestational age at delivery examined. Antenatal corticosteroids versus placebo or no treatment (by entry to delivery interval) Data were available by entry to delivery interval for several of the primary outcomes that relate to the mother and fetus/neonate. Combined fetal and neonatal death was significantly reduced in corticosteroid treated infants born before 24 hours (RR 0.60, 95% CI 0.39 to 0.94, three studies, 293 infants) and before 48 hours after the first dose (RR 0.59, 95% CI 0.41 to 0.86, one study, 373 infants), but not those born between oneand seven days (RR 0.81, 95% CI 0.60 to 1.09, three studies, 606 infants) and after seven days after the first dose (RR 1.42, 95% CI 0.91 to 2.23, three studies, 598 infants). Neonatal death was significantly reduced in corticosteroid treated infants born before 24 hours (RR 0.53, 95% CI 0.29 to 0.96, four studies, 295 infants) and before 48 hours after the first dose (RR 0.49, 95% CI 0.30 to 0.81, one study, 339 infants), but not those born between one and seven days (RR 0.74, 95% CI 0.51 to 1.07, three studies, 563 infants) and after seven days after the first dose (RR 1.45, 95% CI 0.75 to 2.80, three studies, 561 infants). RDS was significantly reduced in corticosteroid-treated infants born before 48 hours (RR 0.63, 95% CI 0.43 to 0.93, three studies, 374 infants) and between one and seven days after the first dose (RR 0.46, 95% CI 0.35 to 0.60, nine studies, 1110 infants), but not those born before 24 hours (RR 0.87, 95% CI 0.66 to 1.15, nine studies, 517 infants) and after seven daysafter the first dose(RR 0.82, 95% CI 0.53 to 1.28, eight studies, 988 infants). Cerebroventricular haemorrhage was significantly reduced in corticosteroid treated infants born before 48 hours after the first dose (RR 0.26, 95% CI 0.09 to 0.75, one study, 339 infants), but those born not before 24 hours (RR 0.54, 95% CI 0.21 to 1.36, three studies, 264 infants), between one and seven days (RR 0.51, 95% CI 0.23 to 1.13, one study, 482 infants) and after seven days after the first dose (RR 2.01, 95% CI 0.37 to 10.86, one study, 453 infants). Birthweight was significantly reduced in infants born between one and seven days (FWMD -105.92 grams, 95% CI -212.52 to 0.68 grams, one study, 520 infants) and more than seven days after the first dose (FWMD -147.01 grams, 95% CI -291.97 to -2.05 grams, one study, 485 infants), but not those born before 24 hours (FWMD 46.52 grams, 95% CI -94.26 to 187.29 grams, two studies, 242 infants) and before 48 hours after the first dose (FWMD -5.90 grams, 95% CI -131.95 to 120.15 grams, one study, 373 infants). No statistically significant differences between groups treated with antenatal corticosteroids and controls were seen for fetal deaths or chorioamnionitis in the different subgroups of entry to delivery interval examined. Antenatal corticosteroids versus placebo or no treatment (by presence or absence of ruptured membranes) Data wereavailable by status of ruptured membranes for several of the primary and secondary outcomes that relateto the motherand fetus or neonate. No statistically significant differences were seen for maternal death, chorioamnionitis or puerperal sepsis in mothers with rupture of membranes present at the time of first dose or with rupture of membranes for greater than 24 hours. Combined fetaland neonatal death was significantly reduced in corticosteroid treated infants born following rupture of membranes present at time of first dose (RR 0.62, 95% CI 0.46 to 0.82, four studies, 733 infants), but not following rupture of membranes for greater than 24 (RR 0.77, 95% CI 0.51 to 1.17, two studies, 508 infants) and greater than 48 hours (RR 0.93, 95% CI 0.57 to 1.51, one study, 255 infants). No statistically significant differences between groups exposed to antenatalcorticosteroidsand controls wereseen for fetal deaths following rupture of membranes at first dose (RR 0.86, 95% CI 0.46 to 1.61, five studies, 790 infants), for greater than 24 (RR 1.23, 95% CI 0.62 to 2.44, two studies, 508 infants) or greater than 48 hours (RR 1.10, 95% CI 0.52 to 2.32, one study, 255 infants). Thereduction in combined fetaland neonatal death is due to a reduction in neonatal death in corticosteroidtreated infants born following rupture of membranes present at time of first dose (RR 0.58, 95% CI 0.43 to 0.80, seven studies, 984 infants). RDS was significantly reduced in corticosteroid treated infants born following rupture of membranes present at first dose (RR 0.67, 95% CI 0.55 to 0.82, 11 studies, 1089 infants) and for greater than 24 hours (RR 0.68, 95% CI 0.51 to 0.90, six studies, 626 infants), but not following rupture of membranes for greater than 48 hours (RR 0.71, 95% CI 0.36 to 1.41, two studies, 247 infants). Cerebroventricular haemorrhage was significantly reduced in corticosteroid treated infants born following rupture of membranes present at time of first dose (RR 0.47, 95% CI 0.28 to 0.79, five studies, 895 infants), but not following rupture of membranes for greater than 24 (RR 0.55, 95% CI 0.16 to 1.84, two studies, 477 infants) and greater than 48 hours (RR 0.87, 95% CI 0.18 to 4.22, one study, 230 infants). Birthweight was significantly reduced in corticosteroid treated infants born following rupture of membranesfor greaterthan 24 (FWMD -196.46 grams, 95% CI -335.19 to -57.73 grams, 1 study, 349 infants) and for greater than 48 hours (FWMD -201.79 grams, 95% CI -363.30 to -40.28 grams, one study, 255 infants), but not following prolonged rupture of membranes present at the time of the first dose (FWMD -42.68 grams, 95% CI -108.91 to 23.55 Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth (Review) 10 Copyright © 2006 The Cochrane Collaboration. Published by John Wiley & Sons, Ltd 第 104 页