childhood (FWMD 0.30 kg, 95% Data were available for several of the ry outcomes that relate CI-0.39 to 1.00 kg, two studies, 333 children), height( FWMd to the mother and fetus or neonate for pregnancies complicated by 1.02 cm, 95%CI -0 26 to 2.29 cm, two studies, 334 children), multiple birth. However most of these were from just two studies head circumference(FWMD 0 27 cm, 95%CI-008 to 0.63 cm, ( Collaborative 1981: Liggins 1972b). No statistically significant two studies, 328 children), lung function(vital capacity FWMd differences between groups treated with antenatal corticosteroids 1.68% predicted, 95%CI-512 to 1.75 predicted, two stud.(in women with multiple pregnancies)and controls were seen for ies, 150 children), systolic blood pressure(FWMD-1. 60 mmHg, chorioamnionitis(RR 0.48, 95% CI 0.04 to 4.49, one study, 74 95%CI-4.06 to 0.86 mmHg, one study, 223 children), visual women), fetal death(RR 0.53, 95%CI 0.20 to 1.40, two studies, impairment(RR 0.55, 95%CI 0. 24 to 1. 23, two studies, 166 252 infants), neonatal death(RR 0.79, 95%CI 0.39 to 1.61 children), hearing impairment(RR 0.64, 95% CI 0.04 to 9.87, two studies, 236 infants), RDS(RR 0.85, 95%CI 0.60 to 1.20, two studies, 166 children), behavioural/learning difficulties(rr four studies, 320 infants, cerebroventricular haemorrhage(RR 0.86,95%CI 0.35 to 2.09, one study, 90 children)or intellectual 0.39, 95%CI 0.07 to 2.06, one study, 137 infants)or birthweight impairment(RR 0.86, 95%CI 0.44 to 1.69, three studies, 778 (FWMD 82.36 grams, 95%Cl-14623 to 310.95 grams, one study, 150 infants), although the RRs were similar to those in For the the overall analysis, though small numbers meant the confidence One study(Liggins 1972b) showed increased insulin tervals were wide and crossed one (FWMD 0 16 log insulin units, 95% CI 0.04 to 0. 28 log insulin gestational age at deliery Dzas Placebo or no treatment(by minutes following a fasting 75 g oral glucose tolerance tes Antenatal corticosteroids units,one study, 412 adults)in 30 year olds who had been ex- Data were available by gestational age at delivery for several of the posed to antenatal corticosteroid. However, the study reported no primary outcomes that relate to the mother and fetus or neonate difference between those exposed to antenatal corticosteroids and Combined fetal and neonatal death was significantly reduced controls in the prevalence of diabetes. No statistically significant corticosteroid treated infants born before 32 weeks(RRO.71,95% differences between those exposed to antenatal corticosteroids and CI0.57 to 0.88, three studies, 453 infants), before 34 weeks(RR controls were seen for weight(FWMD 0.80 kg, 95%CI-2.02 to 0.73, 95%CI 0.58 to 0.91, one study, 598 infants)and before 36 3. 62 kg, two studies, 538 adults ), height(FWMD 0.91 cm,95% weeks(RR 0.75, 95%CI 0.61 to 0.94, two studies, 969 infants) CI-0.28 to 2.10 cm, two studies, 537 adults), head circumference but not in those born before 28 weeks(RR 0.81, 95%CI 0.65 (FWMD 0.03 cm, 95% CI -0.33 to 0.38 cm, two studies, 537 to 1.01, two studies, 129 infants), before 30 weeks(RR 0.86, adults),skinfold thickness(triceps FWMD-002 log units, 95% 95%CI 0.70 to 1.05,one study, 201 infants)and at a gestation CI-0.11 to 0.07 log units, one study, 456 adults ) systolic blood of at least 34 weeks(RR 1. 13,95%C1 0.66 to 1.96, one study pressure(FWMD-087 mmHg, 95%CI-2.81 to 1.07 mmHg, 770 infants). In infants born at a gestation of at least 36 weeks two studies, 545 adults), HPA axis function(Cortisol FWMD there was a non-significant trend towards an increase in combined 0.06 log units, 95% CI-002 to 0. 14 log units, one study, 444 fetal and neonatal death(Rr 3.25, 95% CI 0.99 to 10.66,two dults ), cholesterol(FWMD-O 11 mmol/L, 95%CI-0 28 to 0.06 studies, 498 infants). Neonatal death was significantly reduced mmol/L,one study, 445 adults), age at puberty(FWMD for fe- in corticosteroid treated infants born before 32 weeks(RR O59 males years, 95%CI-094 to 0.94 years, one study, 38 adults), 95% CI 0.43 to 0.80, three studies, 378 infants), before 34 weeks ducational attainment(RR0.94,95%C1 0.80 to 1.10, one study, (RR 0.69,95% CI 0.52 to 0. 92, two studies, 715 infants)and 534 adults), visual impairment(RR 0.91, 95%CI 0.53 to 1.55, before 36 weeks(RR O68, 95%CI 0.50 to 0.92, two studies, 869 one study, 192 adults), hearing impairment(RR 0.24, 95%CI infants), but not in those born before 28 weeks(RRO.79,95%CI 0.03 to 2.03, one study, 192 adults)or intellectual impairment 0.56 to 1. 12, two studies, 89 infants), before 30 weeks(RR 0.82, (RR 0.24, 95%CI 0.01 to 4.95, two studies, 273 adults) 95%CI 0.60 to 1.11, one study, 150 infants), at a gestation of at least 34 weeks(RR 1.58, 95% CI 0.71 to 3.50, two studies, 808 For the health services infants), and at a gestation of at least 36 weeks(rr 2.62, 95%CI No statistically significant differences between groups treated with 0.77 to 8.96, three studies, 514 infants) natal corticosteroids and controls were seen for length of ante natal hospitalisation for women(FWMD 0.50 days, 95%CI-1.40 RDS was significantly reduced in corticosteroid treated infants to 2. 40 days, one study, 218 women ), postnatal hospitalisation for born before 30 weeks(RRO. 67 95%C10. 52 to 0. 87, four studies, men(FWMD 0.00 days, 95%CI-1.72 to 1.72 days, one stuc 218 women)or neonatal hospitalisation for infants(FWMD 0.78 studies, 583 infants), before 34 weeks(RR0.58,95%CI0.47to days, 95%CI-2.43 to 3.99 days, three studies, 321 infants 0.72, five studies, 1177 infants) and before 36 weeks(RR 0.54 95%CI 0.41 to 0.72, three studies, 922 infants), but not in those 2. Subgroup analysis born before 28 weeks(rRo.79, 95%CI 0.53 to 1. 18, four studies, antenatal corticosteroids versus placebo or no treatment(by 102 infants), at a gestation of at least 34 weeks(RR 0.66,95% ingle or multiple pregnancy) CI 0.38 to 1.16, five studies, 1261 infants)and at a gestation of 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, Ltd
controls were seen for childhood weight (FWMD 0.30 kg, 95% CI -0.39 to 1.00 kg, two studies, 333 children), height (FWMD 1.02 cm, 95% CI -0.26 to 2.29 cm, two studies, 334 children), head circumference (FWMD 0.27 cm, 95% CI -0.08 to 0.63 cm, two studies, 328 children), lung function (vital capacity FWMD -1.68 % predicted, 95% CI -5.12 to 1.75 % predicted, two studies, 150 children), systolic blood pressure (FWMD -1.60 mmHg, 95% CI -4.06 to 0.86 mmHg, one study, 223 children), visual impairment (RR 0.55, 95% CI 0.24 to 1.23, two studies, 166 children), hearing impairment (RR 0.64, 95% CI 0.04 to 9.87, two studies, 166 children), behavioural/learning difficulties (RR 0.86, 95% CI 0.35 to 2.09, one study, 90 children) or intellectual impairment (RR 0.86, 95% CI 0.44 to 1.69, three studies, 778 children). For the child as adult One study (Liggins 1972b) showed increased insulin release 30 minutes following a fasting 75 g oral glucose tolerance test (FWMD 0.16 log insulin units, 95% CI 0.04 to 0.28 log insulin units, one study, 412 adults) in 30 year olds who had been exposed to antenatal corticosteroid. However, thestudy reported no difference between those exposed to antenatal corticosteroids and controls in the prevalence of diabetes. No statistically significant differences between thoseexposed to antenatal corticosteroidsand controls were seen for weight (FWMD 0.80 kg, 95% CI -2.02 to 3.62 kg, two studies, 538 adults), height (FWMD 0.91 cm, 95% CI -0.28 to 2.10 cm, two studies, 537 adults), head circumference (FWMD 0.03 cm, 95% CI -0.33 to 0.38 cm, two studies, 537 adults), skinfold thickness (triceps FWMD -0.02 log units, 95% CI -0.11 to 0.07 log units, one study, 456 adults), systolic blood pressure (FWMD -0.87 mmHg, 95% CI -2.81 to 1.07 mmHg, two studies, 545 adults), HPA axis function (Cortisol FWMD 0.06 log units, 95% CI -0.02 to 0.14 log units, one study, 444 adults),cholesterol (FWMD -0.11 mmol/L, 95% CI-0.28 to 0.06 mmol/L, one study, 445 adults), age at puberty (FWMD for females 0 years, 95% CI -0.94 to 0.94 years, one study, 38 adults), educationalattainment(RR0.94, 95% CI 0.80 to 1.10, onestudy, 534 adults), visual impairment (RR 0.91, 95% CI 0.53 to 1.55, one study, 192 adults), hearing impairment (RR 0.24, 95% CI 0.03 to 2.03, one study, 192 adults) or intellectual impairment (RR 0.24, 95% CI 0.01 to 4.95, two studies, 273 adults). For the health services No statistically significant differences between groups treated with antenatal corticosteroidsand controls wereseen for length ofantenatal hospitalisation forwomen (FWMD 0.50 days, 95% CI-1.40 to 2.40 days, onestudy, 218 women), postnatal hospitalisation for women (FWMD 0.00 days, 95% CI -1.72 to 1.72 days, onestudy, 218 women) or neonatal hospitalisation for infants (FWMD 0.78 days, 95% CI -2.43 to 3.99 days, three studies, 321 infants). 2. Subgroup analysis Antenatal corticosteroids versus placebo or no treatment (by single or multiple pregnancy) Data wereavailable for several of the primary outcomes that relate to the motherand fetus or neonatefor pregnanciescomplicated by multiple birth. However most of these were from just two studies (Collaborative 1981; Liggins 1972b). No statistically significant differences between groups treated with antenatal corticosteroids (in women with multiple pregnancies) and controls were seen for chorioamnionitis (RR 0.48, 95% CI 0.04 to 4.49, one study, 74 women), fetal death (RR 0.53, 95% CI 0.20 to 1.40, two studies, 252 infants), neonatal death (RR 0.79, 95% CI 0.39 to 1.61, two studies, 236 infants), RDS (RR 0.85, 95% CI 0.60 to 1.20, four studies, 320 infants), cerebroventricular haemorrhage (RR 0.39, 95% CI 0.07 to 2.06, onestudy, 137 infants) or birthweight (FWMD 82.36 grams, 95% CI -146.23 to 310.95 grams, one study, 150 infants), although the RRs were similar to those in the overall analysis, though small numbers meant the confidence intervals were wide and crossed one. Antenatal corticosteroids versus placebo or no treatment (by gestational age at delivery) Data were available by gestational age at delivery for several of the primary outcomes that relate to the mother and fetus or neonate. Combined fetal and neonatal death was significantly reduced in corticosteroid treated infants born before 32 weeks (RR 0.71, 95% CI 0.57 to 0.88, three studies, 453 infants), before 34 weeks (RR 0.73, 95% CI 0.58 to 0.91, one study, 598 infants) and before 36 weeks (RR 0.75, 95% CI 0.61 to 0.94, two studies, 969 infants), but not in those born before 28 weeks (RR 0.81, 95% CI 0.65 to 1.01, two studies, 129 infants), before 30 weeks (RR 0.86, 95% CI 0.70 to 1.05, one study, 201 infants) and at a gestation of at least 34 weeks (RR 1.13, 95% CI 0.66 to 1.96, one study, 770 infants). In infants born at a gestation of at least 36 weeks, there was a non-significant trend towards an increase in combined fetal and neonatal death (RR 3.25, 95% CI 0.99 to 10.66, two studies, 498 infants). Neonatal death was significantly reduced in corticosteroid treated infants born before 32 weeks (RR 0.59, 95% CI 0.43 to 0.80, three studies, 378 infants), before 34 weeks (RR 0.69, 95% CI 0.52 to 0.92, two studies, 715 infants) and before 36 weeks (RR 0.68, 95% CI 0.50 to 0.92, two studies, 869 infants), but not in those born before 28 weeks (RR 0.79, 95% CI 0.56 to 1.12, two studies, 89 infants), before 30 weeks (RR 0.82, 95% CI 0.60 to 1.11, one study, 150 infants), at a gestation of at least 34 weeks (RR 1.58, 95% CI 0.71 to 3.50, two studies, 808 infants), and at a gestation of at least 36 weeks (RR 2.62, 95% CI 0.77 to 8.96, three studies, 514 infants). RDS was significantly reduced in corticosteroid treated infants born before 30weeks(RR 0.67, 95% CI 0.52 to 0.87, fourstudies, 218 infants), before 32 weeks (RR 0.56, 95% CI 0.45 to 0.71, six studies, 583 infants), before 34 weeks (RR 0.58, 95% CI 0.47 to 0.72, five studies, 1177 infants) and before 36 weeks (RR 0.54, 95% CI 0.41 to 0.72, three studies, 922 infants), but not in those born before 28weeks(RR 0.79, 95% CI 0.53 to 1.18, fourstudies, 102 infants), at a gestation of at least 34 weeks (RR 0.66, 95% CI 0.38 to 1.16, five studies, 1261 infants) and at a gestation of Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth (Review) 9 Copyright © 2006 The Cochrane Collaboration. Published by John Wiley & Sons, Ltd 第 103 页
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, Ltd
at 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
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, Ltd
grams, 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 rupture 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 syndromes in pregnancy for several of the primary outcomes that relate to the mother and fetus/neonate. Infants born to pregnanciescomplicated by hypertension syndromestreatedwith corticosteroids 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 cerebroventricular haemorrhage (RR 0.38, 95% CI 0.17 to 0.87, two studies, 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 cerebroventricular 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 significant differences between groups treated with antenatal corticosteroids and controls in fetal death, birthweight or chorioamnionitis 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 infants; 1980s RR 0.71, 95% CI 0.58 to 0.87, six studies, 1127 infants; 1990s RR 0.69, 95% CI 0.59 to 0.81, ninestudies, 1064 infants) 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 reduced 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 studies, 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 corticosteroid-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 significantly 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