Nifedipine versus atosiban for threatened preterm birth (APOSTEL III): a multicentre, randomised controlled trial

Vliet, Elvira O.G. van; Nijman, Tobias A.J.; Schuit, Ewoud; Heida, Karst Y.; Opmeer, Brent C.; Kok, Marjolein; Gyselaers, Wilfried; Porath, Martina; Woiski, Mallory; Bax, Caroline J.; Bloemenkamp, Kitty W. M.; Scheepers, Hubertina C.J.; Jacquemyn, Yves; Beek, Erik van; Duvekot, Johannes J.; Franssen, Maureen; Papatsonis, Dimitri; Kok, Joke H.; Post, Joris A. M. van der; Franx, Arie; Mol, Ben Willem; Oudijk, Martijn A.

doi:10.1016/s0140-6736(16)00548-1

Cited by 76 publications

(50 citation statements)

References 36 publications

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“…Van Vliet et al recently published, that in women with threatened preterm birth, 48 h of tocolysis with nifedipine or atosiban resulted in similar perinatal outcomes [125]. However, more cases of intrauterine fetal demise (IUFD) were registered in the nifidipine group (5% vs. 2% in the atosiban group; RR 2.20, 95% CI 0.91-5.33, n.s.…”

Section: Tocolysismentioning

confidence: 97%

Mid-trimester preterm premature rupture of membranes (PPROM): etiology, diagnosis, classification, international recommendations of treatment options and outcome

Tchirikov

Schlabritz‐Loutsevitch

Mäher

et al. 2017

Journal of Perinatal Medicine

188

153

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Mid-trimester preterm premature rupture of membranes (PPROM), defined as rupture of fetal membranes prior to 28 weeks of gestation, complicates approximately 0.4%-0.7% of all pregnancies. This condition is associated with a very high neonatal mortality rate as well as an increased risk of long-and short-term severe neonatal morbidity. The causes of the mid-trimester PPROM are multifactorial. Altered membrane morphology including marked swelling and disruption of the collagen network which is seen with PPROM can be triggered by bacterial products or/and pro-inflammatory cytokines. Activation of matrix metalloproteinases (MMP) have been implicated in the mechanism of PPROM. The propagation of bacteria is an important contributing factor not only in PPROM, but also in adverse neonatal and maternal outcomes after PPROM. Inflammatory mediators likely play a causative role in both disruption of fetal membrane integrity and activation of uterine contraction. The "classic PPROM" with oligo/anhydramnion is associated with a short latency period and worse neonatal outcome compared to similar gestational aged neonates delivered without antecedent PPROM. The "high PPROM" syndrome is defined as a defect of the chorio-amniotic membranes, which is not located over the internal cervical os. It may be associated with either a normal or reduced amount of amniotic fluid. It may explain why sensitive biochemical tests such as the Amniosure (PAMG-1) or IGFBP-1/alpha fetoprotein test can have a positive result without other signs of overt ROM such as fluid leakage with Valsalva. The membrane defect following fetoscopy also fulfils the criteria for "high PPROM" syndrome. In some cases, the rupture of only one membrane -either the chorionic or amniotic membrane, resulting in "pre-PPROM" could precede "classic PPROM" or "high PPROM". The diagnosis of PPROM is classically established by identification of nitrazine positive, fern positive watery leakage from the cervical canal observed during in specula investigation. Other more recent diagnostic tests include the vaginal swab assay for placental alpha macroglobulin-1 test or AFP and IGFBP1. In some rare cases amniocentesis and infusion of indigo carmine has been used to confirm the diagnosis of PPROM. The management of the PPROM requires balancing the potential neonatal benefits from prolongation of the pregnancy with the risk of intraamniotic infection and its consequences for the mother and infant. Close monitoring for signs of chorioamnionitis (e.g. body temperature, CTG, CRP, leucocytes, IL-6, procalcitonine, amniotic fluid examinations) is necessary to minimize the risk of neonatal and maternal complications. In addition to delayed delivery, broad spectrum antibiotics of penicillin or cephalosporin group and/or macrolide and corticosteroids have been show to improve neonatal outcome [reducing risk of chorioamnionitis (average risk ratio (RR) = 0.66), neonatal infections (RR = 0.67) and abnormal ultrasound scan of neonatal brain (RR = 0.67)]. The positive effect of continuo...

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Section: Tocolysismentioning

confidence: 97%

Mid-trimester preterm premature rupture of membranes (PPROM): etiology, diagnosis, classification, international recommendations of treatment options and outcome

Tchirikov

Schlabritz‐Loutsevitch

Mäher

et al. 2017

Journal of Perinatal Medicine

188

153

View full text Add to dashboard Cite

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“…Of patients with suspected preterm labor, approximately one-half deliver at term (3). This information is derived from both observational studies (6–9), randomized clinical trials (10–20), and meta-analysis of such trials (16, 20–26) to which patients were allocated as placebo or acute intravenous tocolysis. The management of women with suspected preterm labor and the decision about the need for hospitalization affect the women and their families as well as the health care system.…”

mentioning

confidence: 99%

Is an episode of suspected preterm labor that subsequently leads to a term delivery benign?

Romero

Erez

Maymon

et al. 2017

American Journal of Obstetrics and Gynecology

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“…More specifically, Oxtr has been reported to be increased in the human uterus following the onset of labour, both at term and preterm (23). Furthermore, an Oxtr antagonist, atosiban, elicited similar outcomes to nifedipine during tocolysis (24). Increased Cox2 expression has also been detected in the human myometrium during preterm labour (25).…”

Section: Discussionmentioning

confidence: 97%

Effect of molecular hydrogen on uterine inflammation during preterm labour

et al. 2018

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Abstract. Intrauterine inflammation causes preterm birth and is associated with complications in preterm neonates. Thus, strategies aimed at suppressing inflammation are expected to be effective for reducing the risk of preterm birth and associated complications. Our previous studies demonstrated that molecular hydrogen (H 2 ), an anti-inflammatory agent, prevented inflammation-induced impairment in foetal brain and lung tissues in lipopolysaccharide (LPS)-induced rodent models. However, it remains unclear whether H 2 is capable of inhibiting preterm labour. The aim of the current study was therefore to investigate the effect of H 2 on inflammation-induced preterm labour. Pregnant ICR (CD-1) mice were divided into three groups: Control, LPS and H 2 water (HW) + LPS. In the control and LPS groups, vehicle and LPS, respectively, were intraperitoneally injected on embryonic day 15.5. In the HW + LPS group, HW was administered 24 h prior to LPS injection. The time from LPS administration to parturition was compared between the LPS and HW + LPS groups. Maternal uterus was collected 6 h after LPS injection and the transcript levels of pro-inflammatory cytokines, contractile-associated proteins (CAPs), matrix metalloproteinase-3 (Mmp3) and endothelin-1 (Et1)were assessed by reverse transcription-quantitative polymerase chain reaction. The protein levels of cyclooxygenase-2 (Cox2) were also evaluated by immunohistochemistry. The time from LPS administration to parturition in the HW + LPS group was significantly increased compared with that in the LPS group (33.5±3.4 vs. 18.3±8.8 h, respectively, P=0.020). H 2 administration also resulted in significantly higher progesterone levels compared with LPS treatment alone (P=0.002). The transcript levels of pro-inflammatory cytokines, CAPs, Mmp3 and Et1 in the uteri of the LPS group were significantly higher than those in the control group (all P<0.05). In turn, all these levels with the exception of interleukin-8 and Mmp3 were significantly lower in the HW + LPS group compared with those in the LPS group (all P<0.05). The protein levels of Cox2 in the LPS group were also significantly increased compared with those in the control (P<0.001) and HW + LPS (P= 0.003) groups. These results suggest that inflammation-induced changes in the uterus may be ameliorated through maternal H 2 administration. Preventive H 2 administration may therefore represent an effective strategy for the suppression of inflammation during preterm labour.

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Nifedipine versus atosiban for threatened preterm birth (APOSTEL III): a multicentre, randomised controlled trial

Cited by 76 publications

References 36 publications

Mid-trimester preterm premature rupture of membranes (PPROM): etiology, diagnosis, classification, international recommendations of treatment options and outcome

Mid-trimester preterm premature rupture of membranes (PPROM): etiology, diagnosis, classification, international recommendations of treatment options and outcome

Is an episode of suspected preterm labor that subsequently leads to a term delivery benign?

Effect of molecular hydrogen on uterine inflammation during preterm labour

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