Single Versus Weekly Courses of Antenatal Corticosteroids in Preterm Premature Rupture of Membranes

Lee, Men Jean; Davies, Jill; Guinn, Debra A.; Sullivan, Lisa M.; Atkinson, M.; McGregor, Scott; Parilla, Barbara V.; Hanlon‐Lundberg, Kathleen M.; Simpson, Lynn; Stone, Joanne; Wing, Deborah A.; Ogasawara, Keith K.; Muraskas, Jonathon

doi:10.1097/01.aog.0000110249.84858.90

Cited by 58 publications

(53 citation statements)

References 11 publications

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“…A 48-hour antenatal corticosteroid therapy is recommended before 34 weeks of gestation in order to reduce the risk of neonatal complications [11]. It is not recommended to repeat corticosteroid therapy if delivery does not occur within seven days, during the period of their optimum action [12]. The results of randomized trials suggest that the use of prophylactic antibiotics in PPROM before the onset of contractions before 37 weeks of gestation can reduce the risk of intrauterine infection and lengthen the pregnancy.…”

Section: Recommendationmentioning

confidence: 99%

Polish Gynecological Society Recommendations for Labor Induction

Bomba‐Opoń¹,

Drews²,

Huras³

et al. 2017

Ginekol Pol

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Section: Recommendationmentioning

confidence: 99%

Polish Gynecological Society Recommendations for Labor Induction

Bomba‐Opoń¹,

Drews²,

Huras³

et al. 2017

Ginekol Pol

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“…However, because of lingering concern about the preterm delivery in the setting of chorioamnionitis largely stemming from a trial of weekly antenatal corticosteroids, ACOG still does not fully endorse corticosteroid administration after 32 weeks gestation. 47,48 …”

Section: Safety Of Antenatal Corticosteroid Treatmentmentioning

confidence: 99%

Antenatal Corticosteroids in the Management of Preterm Birth: Are We Back Where We Started?

Bonanno

Wapner

2012

Obstetrics and Gynecology Clinics of North America

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“…Later obstetricians all over the world started using multiple courses of steroids when delivery did not occur after the first course of steroids [6][7][8]. Multiple courses of corticosteroids did not improve outcome but have been associated with higher incidence of chorioamnionitis, severe IVH, intra-uterine growth restriction and impaired postnatal stress regulation [9,10]. Based on epidemiologic data, prenatal corticosteroid use has been implicated in long-term programming of the foetus leading to increased risk of cardiovascular, metabolic and neuroendocrine disorders in adult life [11,12].…”

Section: Introductionmentioning

confidence: 99%

Antenatal Dexamethasone Treatment Leads to Changes in Gene Expression in a Murine Late Placenta

Baisden

Sonne

Joshi³

et al. 2007

Placenta

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Antenatal steroids like dexamethasone (DEX) are used to augment foetal lung maturity and there is a major concern that they impair foetal growth. If delivery is delayed after using antenatal DEX, placental function and hence foetal growth may be compromised even further. To investigate the effects of DEX on placental function, we treated 9 pregnant C57/BL6 mice with DEX and 9 pregnant mice were injected with saline to serve as controls. Placental gene expression was studied using microarrays in 3 pairs and other 6 pairs were used to confirm microarray results by semi-quantitative RT-PCR, real-time PCR, in situ hybridization, western blot analysis and Oligo ApopTaq assay. DEXtreated placentas were hydropic, friable, pale, and weighed less (80.0±15.1 mg compared to 85.6.8 ±7.6 mg, p=0.05) (n=62 placentas). Foetal weight was significantly reduced after DEX use (940±32 mg compared to 1162±79 mg, p=0.001) (n=62 foetuses). There was > 99% similarity within and between the three gene chip data sets. DEX led to down-regulation of 1212 genes and up-regulation of 1382 genes. RT-PCR studies showed that DEX caused a decrease in expression of genes involved in cell division such as cyclins A2, B1, D2, cdk 2, cdk 4 and M-phase protein kinase along with growth-promoting genes such as EGF-R, BMP4 and IGFBP3. Oligo ApopTaq assay and western blot studies showed that DEX-treatment increased apoptosis of trophoblast cells. DEX-treatment led to up-regulation of aquaporin 5 and tryptophan hydroxylase genes as confirmed by real-time PCR, and in situ hybridization studies. Thus antenatal DEX treatment led to a reduction in placental and foetal weight, and this effect was associated with a decreased expression of several growth-promoting genes and increased apoptosis of trophoblast cells.

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Single Versus Weekly Courses of Antenatal Corticosteroids in Preterm Premature Rupture of Membranes

Abstract: I

Cited by 58 publications

References 11 publications

Polish Gynecological Society Recommendations for Labor Induction

Polish Gynecological Society Recommendations for Labor Induction

Antenatal Corticosteroids in the Management of Preterm Birth: Are We Back Where We Started?

Antenatal Dexamethasone Treatment Leads to Changes in Gene Expression in a Murine Late Placenta

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