Schwenzel W, Jung H, Lahmann H, Etzrodt A, Sticherling C, Korz K, Liedtke B, Chantraine H
Z Geburtshilfe Perinatol. 1975 Feb;179(1):45-52.
Because of premature labour, probability of fetal retardation, discrepance at term of delivery, Rh-incompatibility or EPH-gestosis 185 patients were hospitalized. 76 pregnant women received twice 1.5 ml Celestan Depot i.m. (4.5 betamethasone acetate and 6mg betamethasome dinatrium phosphate per injection) within an interval of 24 hours. It was necessary to maintain a tocolysis for at least 48 hours as a minimum after the first injection of Celestan Depot. The other 109 patients without treatment of glucocorticoids were considered as a controlgroup. We could show that antepartum application of betamethasone before the 38. week of gestation was associated with a reduction of RDS in our premature infants. Only one baby of the betamethasone-treated infants died of hyaline membrane disease during the first 7 days of life compared with 11 of the control group. In 11 patients patients amniocentesis was performed before the first injection of glucocorticoids and was repeated 2 to 7 days later. The amniotid fluid lecithin phosphorus concentration was determined. In the same period of pregnancy and the same iterval the lecithin phosphours level of amniotic fluid was analysed in 11 other patients who were not rreated with glucocorticoids. The difference between amniotic fluid lecithin phosphorus concentration in the first and second anslysis was found significant by a level of significance of alpha = 5%. There was no evidence of an influence of the therapy with Celestan Depot on this increase. The excretion of oestorgens in the urine of 24 hours was analysed in 22 gradidae before and 7 days after the treatment with betamethasone. The oestogen values of the day before application of betamethasone served as baseline figures. All patients showed a market fall in urinary oestrogens excretion, especially after the second day of therapy. After day 2 the values returned rapidly to baseline values. There were no differences between treated and control groups in Apgar scores at birth or in the incidence of icterus neonatroum (bilirubine level is greater that 10 mg% in the serum). The results of our study support the hypothesis that in humans glucocorticoid administration to the fetus accelerates lung maturation. Relatively brief intrauterine exposure of human infants to pharmacological doses of betamethasone was associated with a substantial reduction in the incidense of RDS.
由于早产、胎儿发育迟缓的可能性、分娩时的差异、Rh血型不合或妊娠高血压综合征,185名患者住院治疗。76名孕妇在24小时内分两次肌肉注射1.5毫升长效倍他米松(每次注射含4.5毫克醋酸倍他米松和6毫克倍他米松二钠)。在首次注射长效倍他米松后,至少需要维持48小时的保胎治疗。另外109名未接受糖皮质激素治疗的患者被视为对照组。我们可以证明,在妊娠38周前产前应用倍他米松与降低早产儿呼吸窘迫综合征的发生率有关。在接受倍他米松治疗的婴儿中,只有1名婴儿在出生后7天内死于透明膜病,而对照组有11名。11名患者在首次注射糖皮质激素前进行了羊膜穿刺术,并在2至7天后重复进行。测定了羊水卵磷脂磷浓度。在相同的孕期和相同的时间间隔内,对另外11名未接受糖皮质激素治疗的患者的羊水卵磷脂磷水平进行了分析。首次和第二次分析的羊水卵磷脂磷浓度差异在α=5%的显著性水平上被发现具有显著性。没有证据表明长效倍他米松治疗对这种增加有影响。在22名孕妇接受倍他米松治疗前和治疗后7天分析了她们24小时尿液中的雌激素排泄情况。应用倍他米松前一天的雌激素值作为基线数据。所有患者的尿雌激素排泄量均显著下降,尤其是在治疗第二天后。第二天后,这些值迅速恢复到基线值。治疗组和对照组在出生时的阿氏评分或新生儿黄疸发生率(血清胆红素水平大于10mg%)方面没有差异。我们的研究结果支持这样的假设,即对胎儿给予糖皮质激素可加速肺成熟。人类婴儿在子宫内相对短暂地接触药理剂量的倍他米松与呼吸窘迫综合征发生率的大幅降低有关。