Contribution of preterm delivery to perinatal mortality.

Rush, R. W.; Keirse, Marc J. N. C.; Howat, P; Baum, J D; Anderson, Anne B. M.; Turnbull, A. C.

doi:10.1136/bmj.2.6042.965

Cited by 305 publications

(72 citation statements)

References 7 publications

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“…36,37 Therefore, the significant increased risk for preterm births found after in utero exposure to SGAs (OR, 1.85; 95% CI, 1.20-2.86) may pose a significant health care issue. Furthermore, a study by Russell et al 38 (2007) reported that preterm births use significant amounts of health care resources, causing longer hospital stays, and almost 50% of the costs of infant hospitalizations.…”

Section: Discussionmentioning

confidence: 98%

Pregnancy Outcomes Following In Utero Exposure to Second-Generation Antipsychotics

Terrana

Koren

Pivovarov³

et al. 2015

Journal of Clinical Psychopharmacology

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Second-generation antipsychotics (SGAs) are increasingly used for a variety of mental illnesses; however, the data regarding the safety of these medications during pregnancy are inconclusive and contradictory. We examined the risk of adverse pregnancy outcomes associated with in utero exposure to SGAs by conducting a systematic review and meta-analysis. We searched the databases EMBASE and MEDLINE from January 1990 to December 2014. Eligible studies had to report pregnant women who took SGAs during pregnancy (first trimester exposure if analyzing congenital malformations), follow a healthy comparison group in a similar manner, and report data on pregnancy outcomes. There was no restriction on language, sample size, or publication date. The primary outcome analyzed was major congenital malformations, and secondary outcomes included miscarriages, stillbirths, preterm births, small or large for gestational age neonates, and differences in gestational ages and birth weights. A total of 12 studies met our inclusion criteria, totalling 1782 cases and 1,322,749 controls. The use of SGA during the first trimester of pregnancy was associated with a significant increased risk for major congenital malformations (odds ratio, 2.03; 95% confidence interval, 1.41-2.93); however, no specific pattern of malformations was found. An increased risk was also found for preterm births (odds ratio, 1.85; 95% CI, 1.20-2.86). The use of SGA during pregnancy was not found to be associated with an increased risk for secondary outcomes analyzed. The absence of a specific pattern of malformations makes it difficult to identify an explicit risk posed by SGAs, and therefore, further studies sufficiently controlling for confounding factors are needed to validate these findings.

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Section: Discussionmentioning

confidence: 98%

Pregnancy Outcomes Following In Utero Exposure to Second-Generation Antipsychotics

Terrana

Koren

Pivovarov³

et al. 2015

Journal of Clinical Psychopharmacology

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“…Preterm labor occurs in 5%-10% of all pregnancies and accounts for 70% of neonatal morbidities and mortality not attributable to congenital anomalies [1]. Long-term morbidities, including neurological handicap and learning difficulties, impose a substantial cost on the health care and education systems as well as placing emotional hardship and stress on families [2].…”

Section: Introductionmentioning

confidence: 99%

Altered Fetal Pituitary-Adrenal Function in the Ovine Fetus Treated with RU486 and Meloxicam, an Inhibitor of Prostaglandin Synthase-II1

McKeown

Challis

Small

et al. 2000

Biology of Reproduction

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Term and preterm labor are associated with increased fetal hypothalamic-pituitary-adrenal (HPA) activation and synthesis of prostaglandins (PGs) generated through the increased expression of prostaglandin H synthase-II (PGHS-II) in the placenta. Inhibition of PGHS-II has been advocated as a means of producing uterine tocolysis, but the effects of such treatment on fetal endocrine functions have not been thoroughly examined. Because PGE(2) is known to activate the fetal HPA axis, we hypothesized that administration of meloxicam, a PGHS-II inhibitor, to sheep in induced labor would suppress fetal HPA function. Chronically catheterized pregnant ewes were treated with RU486, a progesterone receptor antagonist, to produce active labor, and then treated with either high-maintenance-dose meloxicam, graded-maintenance-dose meloxicam, or a saline infusion. Maternal uterine contraction frequency increased 24 h after the RU486 injection and the animals were in active labor by 48 +/- 4 h. RU486 injection led to increased concentrations of PGE(2), ACTH, and cortisol in the fetal circulation, and increased concentrations of 13,14 dihydro 15-ketoprostaglandin F(2 alpha) (PGFM) in the maternal circulation. Uterine activity was inhibited within 12 h of beginning meloxicam infusion at both infusion regimes. During meloxicam infusion there were significant decreases in fetal plasma PGE(2), ACTH, and cortisol concentrations, and PGFM concentrations in maternal plasma. In control animals, frequency of uterine contractions, maternal plasma PGFM, fetal plasma PGE(2), ACTH, and cortisol concentrations increased after RU486 administration, and continued to rise during saline infusion until delivery occurred. We conclude that RU486-provoked labor in sheep is associated with activation of fetal HPA function, and that this is attenuated during meloxicam treatment to a level considered compatible with pregnancy maintenance.

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“…Complications resulting from idiopathic preterm birth, defined as delivery before 37 weeks of gestation, account for the majority of perinatal deaths of infants without anomalies in developed nations (1,2). Preterm premature rupture of the membranes (PPROM) 1 occurs in ϳ1% of all pregnancies and is associated with 30 -40% of preterm deliveries (3).…”

mentioning

confidence: 99%

A Single Nucleotide Polymorphism in the Matrix Metalloproteinase-1 (MMP-1) Promoter Influences Amnion Cell MMP-1 Expression and Risk for Preterm Premature Rupture of the Fetal Membranes

Fujimoto¹,

Parry²,

Urbanek³

et al. 2002

Journal of Biological Chemistry

160

108

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Interstitial collagen gives fetal membranes tensile strength, and membrane rupture has been attributed to collagen degradation. A polymorphism at ؊1607 in the matrix metalloproteinase-1 (MMP-1) promoter (an insertion of a guanine (G)) creates a core Ets binding site and increases promoter activity. We investigated whether this polymorphism is functionally significant for MMP-1 expression in amnion cells and whether it is associated with preterm premature rupture of the membranes (PPROM). The 2G promoter had >2-fold greater activity than the 1G allele in amnion mesenchymal cells and WISH amnion cells. Phorbol 12-myristate 13-acetate (PMA) increased mesenchymal cell nuclear protein binding with greater affinity to the 2G allele. Induction of MMP-1 mRNA by PMA was significantly greater in cells with a 1G/2G or 2G/2G genotype compared with cells homozygous for the 1G allele. When treated with PMA, the 1G/2G and 2G/2G cells produced greater amounts of MMP-1 protein than 1G/1G cells. A significant association was found between fetal carriage of a 2G allele and PPROM. We conclude that the 2G allele has stronger promoter activity in amnion cells, that it confers increased responsiveness of amnion cells to stimuli that induce MMP-1, and that this polymorphism contributes to the risk of PPROM.Complications resulting from idiopathic preterm birth, defined as delivery before 37 weeks of gestation, account for the majority of perinatal deaths of infants without anomalies in developed nations (1, 2). Preterm premature rupture of the membranes (PPROM) 1 occurs in ϳ1% of all pregnancies and is associated with 30 -40% of preterm deliveries (3). PPROM is thus the leading identifiable cause of preterm birth and its complications, including respiratory distress syndrome, neonatal infection, and intraventricular hemorrhage (3, 4). Consequently, identification of markers that identify patients at risk for PPROM is a subject of considerable interest.Interstitial collagens (type I and type III collagen) of the amnion confer upon the fetal membranes tensile strength (5). Rupture of fetal membranes at term as well as preterm has been attributed, in part, to degradation of the collagens in the extracellular matrix. The breakdown of the interstitial collagens is mediated by matrix metalloproteinases (MMPs). The first step in interstitial collagen catabolism is catalyzed by collagenases including matrix metalloproteinase 1 (MMP-1), the primary collagenase elaborated by fibroblasts (6). It is also produced by monocytic cells (7). MMP-1 is produced as a proenzyme; after proteolytic activation, it cleaves through the fibrillar triple helix at a specific site, producing fragments that can be further degraded by other MMPs, including the gelatinases MMP-2 and MMP-9 (8 -12). Evidence that MMP activity is important for fetal membrane rupture includes the observation that fetal membrane MMP expression increases at the time of parturition (13, 14). Moreover, MMP levels are elevated in human amniotic fluid in association with PPROM (15-18).A single n...

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Contribution of preterm delivery to perinatal mortality.

Cited by 305 publications

References 7 publications

Pregnancy Outcomes Following In Utero Exposure to Second-Generation Antipsychotics

Pregnancy Outcomes Following In Utero Exposure to Second-Generation Antipsychotics

Altered Fetal Pituitary-Adrenal Function in the Ovine Fetus Treated with RU486 and Meloxicam, an Inhibitor of Prostaglandin Synthase-II1

A Single Nucleotide Polymorphism in the Matrix Metalloproteinase-1 (MMP-1) Promoter Influences Amnion Cell MMP-1 Expression and Risk for Preterm Premature Rupture of the Fetal Membranes

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