体内倍他米松对妊娠期胎盘肾上腺髓质素的影响。

Emanuela Marinoni, Chrysoula Zacharopoulou, Alessia Di Rocco, Claudio Letizia, Massimo Moscarini, Romolo Di Iorio
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引用次数: 6

摘要

目的:本研究的目的是确定在有早产风险的患者体内给予倍他米松对母体和胎儿血浆中肾上腺髓质素(AM)浓度以及AM在胎盘和胎膜定位的影响。方法:对62例妊娠25 ~ 35周的孕妇进行研究。47名孕妇接受倍他米松(2 x 12mg肌注,间隔24小时)刺激胎儿肺成熟。在倍他米松给药前和第一次给药后不同时间点采集血样。在分娩时和未分娩的妇女在给予倍他米松1周和30天后进一步收集样本。分娩时采集胎盘和胎膜。15名未接受倍他米松治疗的相同胎龄分娩的患者为对照组。放射免疫法测定AM浓度。应用免疫组织化学方法检测AM在胎盘组织中的定位。结果:倍他米松使母体血浆AM在给药后1周增加约50%,而胎儿血浆AM在给药后48小时增加约90%。倍他米松给药后收集的胎胎盘组织中AM免疫组化染色增加。结论:这些结果为糖皮质激素在人类妊娠晚期对AM(可能是胎盘起源)的体内刺激提供了第一个证据。
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Effect of betamethasone in vivo on placental adrenomedullin in human pregnancy.

Objective: The aim of the current study was to determine the effects of in vivo administration of prenatal betamethasone in patients at risk for preterm delivery on adrenomedullin (AM) concentrations in maternal and fetal plasma and on AM localization in placenta and fetal membranes.

Methods: A total of 62 pregnant women between 25 and 35 weeks' gestation were studied. Forty-seven pregnant women received betamethasone (2 x 12 mg intramuscularly given 24 hours apart) for stimulation of fetal lung maturity. Blood samples were collected before betamethasone administration and at different time points after the first and the second dose. Further samples were collected at delivery and, in women who did not deliver, after 1 week and 30 days from betamethasone administration. At delivery, placenta and membranes were collected. Fifteen patients who delivered at the same gestational age not receiving betamethasone represented the control group. AM concentration was determined by radioimmunoassay. Localization of AM in placental tissues was assessed by immunohistochemistry.

Results: Betamethasone caused approximately 50% increase in maternal plasma AM at 1 week after administration, whereas in fetal plasma AM levels increased by about 90% at 48 hours after betamethasone administration. There was increased immunohistochemical staining for AM in fetoplacental tissues collected after betamethasone administration.

Conclusion: These results provide the first evidence for in vivo stimulation of AM, likely of placental origin, by glucocorticoids in the third trimester human pregnancy.

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