Silver R K, Vyskocil C, Solomon S L, Ragin A, Neerhof M G, Farrell E E
Division of Maternal-Fetal Medicine, Evanston Hospital, Northwestern University Medical School, Chicago, Illinois, USA.
Obstet Gynecol. 1996 May;87(5 Pt 1):683-91. doi: 10.1016/0029-7844(96)00033-6.
To determine if an additive effect exists between antenatal corticosteroid administration and postnatal surfactant therapy in the prevention of respiratory distress syndrome (RDS) in preterm infants.
A randomized, double-blind trial was conducted from April 1990 to June 1994, in which dexamethasone (5 mg every 12 hours for a total of four doses) or saline was given to women at risk for delivery at 24-29 weeks' gestation. At birth, prophylactic surfactant was administered to all study infants. Main outcome measures were RDS occurrence and severity. Secondary clinical end points included bronchopulmonary dysplasia, pneumothorax, patent ductus arteriosus, necrotizing enterocolitis, retinopathy, intraventricular hemorrhage, and death.
Seventy-five of the 124 randomized subjects delivered 96 infants within the studied gestational age range (dexamethasone, n = 54; placebo, n = 42). Similar maternal demographics and obstetric complications were noted between study groups. A greater population of infants were delivered from multi-fetal gestations in the dexamethasone cohort (26 of 54 versus 12 of 42 newborns; P = .05). There were no significant differences in the occurrence or severity of RDS between the dexamethasone and placebo infants (none or mild, 67 versus 67%; moderate, 24 versus 26%; severe, 9 versus 7%, respectively), or differences in any of the secondary clinical outcomes. The study size was sufficient to exclude a 50% reduction in RDS incidence as a consequence of dexamethasone exposure. An analysis restricted to singletons (dexamethasone, n = 28; placebo, n = 30) revealed similar overall occurrence of intraventricular hemorrhage (12 of 28 versus ten of 30; P = .63), but significantly fewer grade 3 and 4 intraventricular hemorrhages in dexamethasone-exposed neonates (two of 12 versus six of ten; P = .048).
Antenatal dexamethasone does not appear to decrease the incidence or severity of RDS in surfactant-treated infants delivered at 24-29 weeks' gestation, but may be associated with reduced severity of intraventricular hemorrhages in surfactant-treated singletons in this gestational age range.
确定产前使用糖皮质激素与产后使用表面活性剂疗法在预防早产儿呼吸窘迫综合征（RDS）方面是否存在相加效应。
1990年4月至1994年6月进行了一项随机双盲试验，对妊娠24 - 29周有分娩风险的妇女给予地塞米松（每12小时5毫克，共4剂）或生理盐水。出生时，对所有研究婴儿给予预防性表面活性剂。主要观察指标为RDS的发生情况和严重程度。次要临床终点包括支气管肺发育不良、气胸、动脉导管未闭、坏死性小肠结肠炎、视网膜病变、脑室内出血和死亡。
124名随机分组的受试者中有75名在研究的孕周范围内分娩了96名婴儿（地塞米松组，n = 54；安慰剂组，n = 42）。研究组之间产妇人口统计学特征和产科并发症相似。地塞米松队列中多胎妊娠分娩的婴儿更多（54名新生儿中有26名，42名新生儿中有12名；P = 0.05）。地塞米松组和安慰剂组婴儿RDS的发生率或严重程度无显著差异（无或轻度，分别为67%对67%；中度，24%对26%；重度，9%对7%），任何次要临床结局也无差异。该研究规模足以排除因暴露于地塞米松而使RDS发生率降低50%的情况。对单胎婴儿的分析（地塞米松组，n = 28；安慰剂组，n = 30）显示脑室内出血的总体发生率相似（28名中有12名，30名中有10名；P = 0.63），但暴露于地塞米松的新生儿中3级和4级脑室内出血明显较少（12名中有2名，10名中有6名；P = 0.048）。
产前使用地塞米松似乎不会降低妊娠24 - 29周接受表面活性剂治疗的婴儿RDS的发生率或严重程度，但可能与该孕周范围内接受表面活性剂治疗的单胎婴儿脑室内出血严重程度降低有关。
