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复旦大学：《循证医学》课程教学资源（预习资料）系统综述与meta分析预习

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Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth( Review) Roberts d, dalziel s Status: New This record should be cited as: Roberts D, Dalziel S Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth. Cochrane Database of Systematic Reviews 2006, Issue 3. Art. No CD004454. DO: 10.1002/14651858 CD004454 Pub2 This version first published online: 19 July 2006 in Issue 3, 2006. Date of most recent substantive amendment: 15 May 2006 ABSTRACT Respiratory distress syndrome(RDS) is a serious complication of preterm birth and the primary cause of early neonatal mortality and assess of administering corticosteroids to the mother before anticipated preterm birth We searched the Cochrane Pregnancy and Childbirth Group Trials Register(30 October 2005) Randomised controlled comparisons of antenatal corticosteroid administration( betamethasone, dexamethasone, or hydrocortisone) with placebo or with no treatment given to women with a singleton or multiple pregnancy, expected to deliver preterm as a result of either spontaneous preterm labour, preterm prelabour rupture of the membranes or elective preterm delivery Data collection and analysis Two review authors assessed trial quality and extracted data independently. Main results Twenty-one studies(3885 women and 4269 infants)are included. Treatment with antenatal corticosteroids does not increase risk to the mother of death, chorioamnionitis or puerperal sepsis. Treatment with antenatal corticosteroids is associated with an overall reduction in neonatal death(relative risk(rr)0.69, 95% confidence interval( CD)0.58 to 0.81, 18 studies, 3956 infants), RDS(RR 0.66, 95% CI0.59 to 0.73, 21 studies, 4038 infants), cerebroventricular haemorrhage(RR 0.54, 95%CI 0 43 to 0.69, 13 studies, 2872 infants), necrotising enterocolitis(RR 0.46, 95%CI 0. 29 to 0.74, eight studies, 1675 infants), respirator rt,intensive care admissions (RR 0.80, 95%CI 0.65 to 0.99, two studies, 277 infants)and systemic infections in the first 48 hours of life(RR 0.56, 95%CI 0.38 to 0.85, five studies, 1319 infants). Antenatal corticosteroid use is effective in women with premature rupture of membranes and pregnancy related hypertension syndromes Authors conclusions maturation in women at risk of preterm birth. A single course of antenatal corticosteroids should be considered routine for pre uing The evidence from this new review supports the continued use of a single course of antenatal corticosteroids to accelerate fetal delivery with few exceptions. Further information is required concerning optimal dose to delivery interval, optimal corticosteroid to use, effects in multiple pregnancies, and to confirm the long-term effects into adulthood. 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

Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth (Review) Roberts D, Dalziel S Status: New This record should be cited as: Roberts D, Dalziel S. Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth. Cochrane Database of Systematic Reviews 2006, Issue 3. Art. No.: CD004454. DOI: 10.1002/14651858.CD004454.pub2. This version first published online: 19 July 2006 in Issue 3, 2006. Date of most recent substantive amendment: 15 May 2006 A B S T R A C T Background Respiratory distress syndrome (RDS) is a serious complication of preterm birth and the primary cause of early neonatal mortality and disability. Objectives To assess the effects on fetal and neonatal morbidity and mortality, on maternal mortality and morbidity, and on the child in later life of administering corticosteroids to the mother before anticipated preterm birth. Search strategy We searched the Cochrane Pregnancy and Childbirth Group Trials Register (30 October 2005). Selection criteria Randomised controlled comparisons of antenatal corticosteroid administration (betamethasone, dexamethasone, or hydrocortisone) with placebo or with no treatment given to women with a singleton or multiple pregnancy, expected to deliver preterm as a result of either spontaneous preterm labour, preterm prelabour rupture of the membranes or elective preterm delivery. Data collection and analysis Two review authors assessed trial quality and extracted data independently. Main results Twenty-one studies (3885 women and 4269 infants) areincluded. Treatment with antenatal corticosteroids does not increase risk to the mother of death, chorioamnionitis or puerperal sepsis. Treatment with antenatal corticosteroids is associated with an overall reduction in neonatal death (relative risk (RR) 0.69, 95% confidence interval (CI) 0.58 to 0.81, 18 studies, 3956 infants), RDS (RR 0.66, 95% CI 0.59 to 0.73, 21 studies, 4038 infants), cerebroventricular haemorrhage (RR 0.54, 95% CI 0.43 to 0.69, 13 studies, 2872 infants), necrotising enterocolitis (RR 0.46, 95% CI 0.29 to 0.74, eight studies, 1675 infants), respiratory support, intensive care admissions (RR 0.80, 95% CI 0.65 to 0.99, two studies, 277 infants) and systemic infections in the first 48 hours of life (RR 0.56, 95% CI 0.38 to 0.85, five studies, 1319 infants). Antenatal corticosteroid use is effective in women with premature rupture of membranes and pregnancy related hypertension syndromes. Authors’ conclusions The evidence from this new review supports the continued use of a single course of antenatal corticosteroids to accelerate fetal lung maturation in women at risk of preterm birth. A single course of antenatal corticosteroids should be considered routine for preterm delivery with few exceptions. Further information is required concerning optimal dose to delivery interval, optimal corticosteroid to use, effects in multiple pregnancies, and to confirm the long-term effects into adulthood. Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth (Review) 1 Copyright © 2006 The Cochrane Collaboration. Published by John Wiley & Sons, Ltd 第 95 页

PLAIN LANGUAGE SUMMARY Corticosteroids given to women in early labour help the babies' lungs to mature and so reduce the number of babies who die or suffer Babies born very early are at risk of breathing difficulties(respiratory distress syndrome)and other complications at birth. Some babies have developmental delay and some do not survive the initial complications. In animal studies, corticosteroids are shown to help the lungs to mature and so it was suggested these drugs may help babies in preterm labour too. This review of 21 trials shows that a singl course of corticosteroid, given to the mother in preterm labour and before the baby is born, helps to develop the baby's lungs and reduces complications like respiratory distress syndrome. Furthermore, this treatment results in fewer babies dying and fewer commo serious neurological and abdominal problems, e.g. cerebroventricular haemorrhage and necrotising enterocolitis, that affect babies born very early. There does not to be any negative effects of the corticosteroid on the mother. Long-term outcomes on both baby and BACKGR。UND Mature lungs contain more than 40 different cell types derived from this early tissue. From 8 to 16 weeks' gestation, the major Respiratory distress syndrome(RDS) is a serious complication of bronchial airways and associated respiratory units of the lung are preterm birth and the primary cause of early neonatal death and progressively formed. At this time the lung blood vessels also be- disability. It affects up to one fifth of low birthweight babies(less gin to grow in parallel. From 17 to 25 weeks gestation, the air- than 2500 g) and two thirds of extremely low birthweight babies ways grow, widen and lengthen( canalisation). Terminal bronchi- oles with enlargements that subsequently give rise to terminal sacs (the primitive alveoli)are formed. These are the functional Respiratory failure in these infants occurs as a result of surfactant of the lung (respiratory lobules). It is at this stage that the increas- deficiency, poor lung ar other organs. Neonatal survival after preterm birth improves with ing proximity of blood capillaries begins the air-blood interface gestation(Doyle 2001a), reflecting improved maturity of organ required for effective air exchange. This can only take place at the terminal bronchioles. At the end of the canalicular stage, type systems. However, those who survive early neonatal care are at and Il pneumocytes can be seen in the alveoli. From 28 to 35 ncreased risk of long-term neurological disability(Doyle 2001b). weeks'gestation, the alveoli can be counted and with increasing age they become more mature. Lung volume increases four-fold While researching the effects of the steroid dexamethasone on pre- between 29 weeks and term Alveolar number shows a curvilinear mature parturition in fetal sheep in 1969, Liggins found that there increase with age but a linear relationship with bodyweight. At as some inflation of the lungs oflambs born at gestations at which birth there are an average of 150 million alveoli(half the expected the lungs would be expected to be airless(Liggins 1969). He the- adult number). The alveoli produce surfactant. The alveolar stage orised, from these observations, that dexamethasone might have continues for one to two years after birth. In the preterm infant, accelerated the appearance of pulmonary surfactant. The hypoth- low alveolar numbers probably contribute to respiratory dysfunc esis is that corticosteroids act to trigger the synthesis of ribonucleic tion of phospholipids or in the breakdown of glycogen. Subsequent tation. Lamellar bodis, which store surfactant, appear at 22 to a number of organ systems(Padbury 1996; Vyas 1997). Liggins 24 weeks. Surfactant is a complex mixture of lipids and apopro. and Howie performed the first randomised controlled trial in hu. choline, phosphatidylglycerol and apoproteins A, B, C and D tion of RDS in 1972(Lig. Surfactant is needed to maintain stability when breathing prevent collapse of the alveoli. Premature infants have a qualita- Fetal lung development rIve ative deficiency of surfactant, which predisposes to Some understanding of fetal lung development may be useful in RDS. Ar the low lung volume associated with expiration, surface understanding why RDS occurs and why corticosteroids work. tension becomes very high, leading to atelectasis with subsequent Fetal lung development can be divided into five stages: embryonic, intrapulmonary shunting, ventilation perfusion inequalities and pseudoglandular, canalicular, terminal sac and alveolar. The lung ultimately respiratory failure. Capillary leakage allows inhibitors first appears as an outgrowth of the foregut at 22 to 26 from plasma to reach alveoli and inactivate any surfactant that may days after conception. By 34 days, the outgrowth has divided into be present. Hypoxia, acidosis and hypothermia(common prob- ft and right sides and further to form the major units of the lung. lems in the very preterm infant) can reduce surfactant synthesis 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

P L A I N L A N G U A G E S U M M A R Y Corticosteroids given to women in early labour help the babies’ lungs to mature and so reduce the number of babies who die or suffer breathing problems at birth Babies born very early are at risk of breathing difficulties (respiratory distress syndrome) and other complications at birth. Some babies have developmental delay and some do not survive the initial complications. In animal studies, corticosteroids are shown to help the lungs to mature and so it was suggested these drugs may help babies in preterm labour too. This review of 21 trials shows that a single course of corticosteroid, given to the mother in preterm labour and before the baby is born, helps to develop the baby’s lungs and reduces complications like respiratory distress syndrome. Furthermore, this treatment results in fewer babies dying and fewer common serious neurological and abdominal problems,e.g. cerebroventricular haemorrhageand necrotising enterocolitis, that affect babies born very early. There does not appear to be any negative effects of the corticosteroid on the mother. Long-term outcomes on both baby and mother are also good. B A C K G R O U N D Respiratory distress syndrome (RDS) is a serious complication of preterm birth and the primary cause of early neonatal death and disability. It affects up to one fifth of low birthweight babies (less than 2500 g) and two thirds of extremely low birthweight babies (less than 1500 g). Respiratory failure in these infants occurs as a result of surfactant deficiency, poor lung anatomical development and immaturity in other organs. Neonatal survival after preterm birth improves with gestation (Doyle 2001a), reflecting improved maturity of organ systems. However, those who survive early neonatal care are at increased risk of long-term neurological disability (Doyle 2001b). History Whileresearching theeffects of thesteroid dexamethasone on premature parturition in fetal sheep in 1969, Liggins found that there wassomeinflation of thelungs of lambs born at gestationsatwhich the lungs would be expected to be airless (Liggins 1969). He theorised, from these observations, that dexamethasone might have accelerated the appearance of pulmonary surfactant. The hypothesis is thatcorticosteroidsact to trigger thesynthesis of ribonucleic acid that codes for particular proteins involved in the biosynthesis of phospholipids or in the breakdown of glycogen. Subsequent work has suggested that, in animal models,corticosteroids mature a number of organ systems (Padbury 1996; Vyas 1997). Liggins and Howie performed the first randomised controlled trial in humans of betamethasone for the prevention of RDS in 1972 (Liggins 1972b). Fetal lung development Some understanding of fetal lung development may be useful in understanding why RDS occurs and why corticosteroids work. Fetal lung developmentcan be divided into fivestages:embryonic, pseudoglandular, canalicular, terminal sac and alveolar. The lung first appears as an outgrowth of the primitive foregut at 22 to 26 days after conception. By 34 days, the outgrowth has divided into leftand right sides and further to form the major units of thelung. Mature lungs contain more than 40 different cell types derived from this early tissue. From 8 to 16 weeks’ gestation, the major bronchial airways and associated respiratory units of the lung are progressively formed. At this time the lung blood vessels also begin to grow in parallel. From 17 to 25 weeks’ gestation, the airways grow, widen and lengthen (canalisation). Terminal bronchioles with enlargements that subsequently give rise to terminal sacs (the primitive alveoli) are formed. These are the functional units of the lung (respiratory lobules). It is at this stage that the increasing proximity of blood capillaries begins the air-blood interface, required for effective air exchange. This can only take place at the terminal bronchioles. At the end of the canalicular stage, type I and II pneumocytes can be seen in the alveoli. From 28 to 35 weeks’ gestation, the alveoli can be counted and with increasing age they become more mature. Lung volume increases four-fold between 29 weeks and term. Alveolar number shows a curvilinear increase with age but a linear relationship with bodyweight. At birth there are an average of 150 million alveoli (half the expected adult number). The alveoli produce surfactant. The alveolar stage continues for one to two years after birth. In the preterm infant, low alveolar numbers probably contribute to respiratory dysfunction. The fetal lung also matures biochemically with increasing gestation. Lamellar bodies, which store surfactant, appear at 22 to 24 weeks. Surfactant is a complex mixture of lipids and apoproteins, the main constituents of which are dipalmitoylphosphatidyl choline, phosphatidylglycerol and apoproteins A, B, C and D. Surfactant is needed to maintain stability when breathing out, to prevent collapse of the alveoli. Premature infants have a qualitativeand quantitative deficiency of surfactant, which predisposes to RDS. At the low lung volume associated with expiration, surface tension becomes very high, leading to atelectasis with subsequent intrapulmonary shunting, ventilation perfusion inequalities and ultimately respiratory failure. Capillary leakage allows inhibitors from plasmato reach alveoliand inactivateany surfactant that may be present. Hypoxia, acidosis and hypothermia (common problems in the very preterm infant) can reduce surfactant synthesis Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth (Review) 2 Copyright © 2006 The Cochrane Collaboration. Published by John Wiley & Sons, Ltd 第 96 页

om the system. The pul- antenatal exposure to corticosteroids( Clark 1998; Dodic 1999; monary antioxidant system develops in parallel to the surfactant Edwards 2001). Thus this review will consider blood pressure, stem and deficiency in this also puts the preterm infant at risk glucose intolerance, dyslipidaemia, and hypothalamo-pituitary adrenal axis function in childhood and adulthood Effects of antenatal corticosteroids for preterm birth Experimental animal studies have shown decreased brain growth Several clinical trials have been performed on the effects of cor- in preterm and term infants exposed to single courses of corticos- ticosteroids before preterm birth since the original Liggins study. teroid(Huang 1999: Jobe 1998).This review will therefore also The first structured review on corticosteroids in preterm birth was address long-term neurodevelopment and other childhood and published in 1990(Crowley 1990). This review showed that corti. adult outcomes after antenatal corticosteroid exposure. costeroids given prior to preterm birth(as a result of either preterm The reasons for an updated review labour or elective preterm delivery) are effective in preventing res- There is need for an updated systematic review of the effects of piratory distress syndrome and neonatal mortality. Corticosteroid treatment was also associated with a significant reduction in the prophylactic corticosteroids for preterm birth, as a result of current sk of intraventricular haemorrhage. Corticosteroids appear to ex- nterest and due to further published trials. We also have the ability to re-analyse the Auckland Steroid Study by intention to treat. ert major vasoconstrictive effects on fetal cerebral blood flow, pro- This study contributes a third of the participants to the review so tecting the fetus against intraventricular haemorrhage at rest and this is an important development for the review. Because of this, when challenged by conditions causing vasodilatation such as hy- the he since the last version of the review( Crowley 1996),new percapnia(Schwab 2000).Crowley found no effect on necrotising Cochrane guidelines for inclusion and exclusion of studies and enterocolitis or chronic lung disease from antenatal corticosteroid administration. The infuence of the results of the original trial the need for the review to be standardised with the repeat courses the subject of a Wellcome Witness Sem- Crowther 2000), it seemed preferable to start with a new ar( Wellcome 2005) held in 2004 protocol to set out the rationale and the proposed methods. This te has been developed following this new Corticosteroids have become the mainstay of prophylactic treat ment in preterm birth, as a result of these findings and subsequen work. However, there have remained a number of outstanding is- OBJECTIVES sues regarding the use of antenatal corticosteroids. The original ial by Liggins suggested an increased rate of stillbirth in women To assess the effects on fetal and neonatal morbidity and mortality, with hypertension syndromes(Liggins 1976). There is concern on maternal mortality and morbidity, and on the child in later life about using corticosteroids in women with premature rupture of of administering corticosteroids to the mother prior to anticipated branes due to the possible increased risk of neonatal and ma- preterm birth. The review addresses whether corticosteroids rnal infection( Imseis 1996: NIH 1994). The efficacy of this more effective than placebo or no corticosteroids in reducing the treatment in multiple births has only been addressed retrospec. risk of respiratory distress syndrome, neonatal death, intraventric- tively(Turrentine 1996). From the time of the original Liggins ular haemorrhage, necrotising enterocolitis, chronic lung disease paper, debate has continued around whether the treatment is ef- in survivors of neonatal intensive care, the use of surfactant in the fective at lower gestations and at differing treatment-to-delivery newborn, the cost of neonatal care, and the duration of neonatal intervals. These issues will be addressed in this review in subgroup hospital care. The review will also address the effect of corticos- nalyses. The effectiveness and safety of repeat doses of corticos- teroids on the risk of stillbirth, fetal or neonatal infection,ma- teroids for women who remain undelivered, but at increased risk ternal infection, and long-term abnormality in survivors during of preterm birth after an initial course of treatment, is addressed childhood and adulthood. a separate review( Crowther 2000) Recent epidemiological evidence and animal work strongly sug- CRITERIA FOR CONSIDERING gests that there may be adverse long-term consequences of ante- STUDIES FOR THIS REVIEW natal exposure to corticosteroids(Seckl 2000). Exposure to excess corticosteroids before birth is hypothesised to be a key mechanism underlying the fetal of adult disease hypothesis( Barker 1998: Benediktsson 1993). This hypothesis postulates a link be- All randomised controlled comparisons of antenatal corticosteroid tween impaired fetal growth and cardiovascular disease and type administration(betamethasone, dexamethasone, or hydrocorti 2 diabetes in later life and their risk factors of impaired glucose sone) with placebo, or with no treatment, given to women prior to tolerance, dyslipidaemia, and hypertension(Barker 1998). A large anticipated preterm delivery (elective, or following spontaneous body of animal experimental work has documented impaired glu- labour), regardless of other co-morbidity, were considered for in- cose tolerance and increased blood pressure in adult animals after clusion in this review. Quasi-randomised trials(e.g allocation by 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

required to replenish surfactant lost from the system. The pulmonary antioxidant system develops in parallel to the surfactant system and deficiency in this also puts the preterm infant at risk of chronic lung disease. Effects of antenatal corticosteroids for preterm birth Several clinical trials have been performed on the effects of corticosteroids before preterm birth since the original Liggins study. The first structured review on corticosteroids in preterm birth was published in 1990 (Crowley 1990). This review showed thatcorticosteroids given prior to preterm birth (asaresult ofeither preterm labour or elective preterm delivery) are effective in preventing respiratory distress syndrome and neonatal mortality. Corticosteroid treatment was also associated with a significant reduction in the risk of intraventricular haemorrhage.Corticosteroidsappear to exert major vasoconstrictive effects on fetalcerebral blood flow, protecting the fetus against intraventricular haemorrhage at rest and when challenged by conditions causing vasodilatation such as hypercapnia (Schwab 2000). Crowley found no effect on necrotising enterocolitis or chronic lung disease from antenatal corticosteroid administration. The influence of the results of the original trial and Crowley’s review was thesubject of a Wellcome Witness Seminar (Wellcome 2005) held in 2004. Corticosteroids have become the mainstay of prophylactic treatment in preterm birth, asa result of these findings and subsequent work. However, there have remained a number of outstanding issues regarding the use of antenatal corticosteroids. The original trial by Liggins suggested an increased rate of stillbirth in women with hypertension syndromes (Liggins 1976). There is concern about using corticosteroids in women with premature rupture of membranes due to the possible increased risk of neonatal and maternal infection ( Imseis 1996: NIH 1994). The efficacy of this treatment in multiple births has only been addressed retrospectively (Turrentine 1996). From the time of the original Liggins paper, debate has continued around whether the treatment is effective at lower gestations and at differing treatment-to-delivery intervals. Theseissues will be addressed in this review in subgroup analyses. The effectiveness and safety of repeat doses of corticosteroids for women who remain undelivered, but at increased risk of preterm birth after an initial course of treatment, is addressed in a separate review (Crowther 2000). Recent epidemiological evidence and animal work strongly suggests that there may be adverse long-term consequences of antenatal exposure to corticosteroids (Seckl 2000). Exposure to excess corticosteroids before birth is hypothesised to be a key mechanism underlying the fetal origins of adult disease hypothesis (Barker 1998; Benediktsson 1993). This hypothesis postulates a link between impaired fetal growth and cardiovascular disease and type 2 diabetes in later life and their risk factors of impaired glucose tolerance, dyslipidaemia,and hypertension (Barker 1998). A large body of animal experimental work has documented impaired glucose tolerance and increased blood pressure in adult animals after antenatal exposure to corticosteroids (Clark 1998; Dodic 1999; Edwards 2001). Thus this review will consider blood pressure, glucose intolerance, dyslipidaemia, and hypothalamo-pituitaryadrenal axis function in childhood and adulthood. Experimental animal studies have shown decreased brain growth in preterm and term infants exposed to single courses of corticosteroid (Huang 1999; Jobe 1998).This review will therefore also address long-term neurodevelopment and other childhood and adult outcomes after antenatal corticosteroid exposure. The reasons for an updated review There is need for an updated systematic review of the effects of prophylacticcorticosteroids for preterm birth,asaresult ofcurrent interestand dueto further published trials. Wealso havetheability to re-analyse the Auckland Steroid Study by intention to treat. This study contributes a third of the participants to the review so this is an important development for the review. Because of this, the time since the last version of the review (Crowley 1996), new Cochrane guidelines for inclusion and exclusion of studies and the need for the review to be standardised with the repeat courses review (Crowther 2000), it seemed preferable to start with a new protocol to set out the rationale and the proposed methods. This update has been developed following this new protocol. O B J E C T I V E S To assess theeffects on fetaland neonatal morbidity and mortality, on maternal mortality and morbidity, and on thechild in later life ofadministering corticosteroids to the mother prior to anticipated preterm birth. The review addresses whether corticosteroids are more effectivethan placebo or ’no corticosteroids’ in reducing the risk of respiratory distress syndrome, neonatal death, intraventricular haemorrhage, necrotising enterocolitis, chronic lung disease in survivors of neonatal intensive care, the use of surfactant in the newborn, the cost of neonatal care, and the duration of neonatal hospital care. The review will also address the effect of corticosteroids on the risk of stillbirth, fetal or neonatal infection, maternal infection, and long-term abnormality in survivors during childhood and adulthood. C R I T E R I A F O R C O N S I D E R I N G S T U D I E S F O R T H I S R E V I E W Types of studies Allrandomised controlled comparisons ofantenatalcorticosteroid administration (betamethasone, dexamethasone, or hydrocortisone) with placebo, or with no treatment, given to women prior to anticipated preterm delivery (elective, or following spontaneous labour), regardless of other co-morbidity, were considered for inclusion in this review. Quasi-randomised trials (e.g. allocation by Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth (Review) 3 Copyright © 2006 The Cochrane Collaboration. Published by John Wiley & Sons, Ltd 第 97 页

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