Objective: The purpose of this study was to determine whether prenatal inflammation (as assessed by clinical chorioamnionitis, maternal temperature >38°C, or histologic chorioamnionitis) is associated with a composite adverse neonatal outcome.
Study Design: We performed a prospective cohort study of women at 22 weeks to 33 weeks 6 days' gestation with symptoms of labor (April 2009 to March 2012). Relevant maternal and neonatal exposures and outcomes were recorded. Multivariable logistic regression was performed to determine the association between prenatal inflammation and neonatal outcomes that were controlled for potential confounders.
Results: We analyzed 871 mother-infant pairs. The preterm birth rate was 42.0%. When we controlled for infant sex and modified the data by gestational age at delivery, prenatal inflammation remains a significant risk factor for adverse neonatal outcomes, despite advancing gestational age: clinical chorioamnionitis at 32 weeks' gestation (odds ratio [OR], 3.12; 95% confidence interval [CI], 1.02-9.52], at 36 weeks' gestation (OR, 8.88; 95% CI, 4.32-18.25), and at 40 weeks' gestation (OR, 25.30; 95% CI, 9.25-69.19); maternal temperature >38°C at 32 weeks' gestation (OR, 3.18; 95% CI, 0.66-15.42), at 36 weeks gestation (OR, 8.40; 95% CI, 3.60-19.61), and at 40 weeks gestation (OR, 22.19; 95% CI, 8.15-60.44); histologic chorioamnionitis at 32 weeks gestation (OR, 1.25; 95% CI, 0.64-2.46), at 36 weeks gestation (OR, 2.56; 95% CI, 1.54-4.23), and at 40 weeks gestation (OR, 5.23; 95% CI, 1.95-13.99).
Conclusion: The protective association with advancing gestational age is diminished when prenatal inflammation is present.
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http://dx.doi.org/10.1016/j.ajog.2013.12.024 | DOI Listing |
Nutrients
December 2024
Department of Nutrition, Texas A&M University, College Station, TX 77843, USA.
Background/objectives: This study builds on previous findings from mouse models, which showed that maternal overnutrition induced by a high-fat diet (HFD) promotes metabolic-associated fatty liver disease (MAFLD) in offspring, linked to global DNA hypermethylation. We explored whether epigenetic modulation with 5-Aza-CdR, a DNA methylation inhibitor, could prevent MAFLD in offspring exposed to maternal overnutrition.
Methods: The offspring mice from dams of maternal overnutrition were fed either a chow diet or a high-fat diet (HFD) for 10 weeks.
J Proteomics
January 2025
Necker Proteomics, Université Paris Cité - Structure Fédérative de Recherche Necker, INSERM US24/CNRS UAR3633, Paris, France.
Despite numerous studies on fetal therapy for myelomeningoceles (MMC), the pathophysiology of this malformation remains poorly understood. This study aimed to analyze the biochemical profile and proteome of amniotic fluid (AF) supernatants from MMC fetuses to explore the prenatal pathophysiology. Biochemical analysis of 61 AF samples from MMC fetuses was compared with 45 healthy fetuses' samples.
View Article and Find Full Text PDFPlacenta
December 2024
Johns Hopkins University Bloomberg School of Public Health, USA. Electronic address:
Chronic arsenic exposure affects over 140 million people globally. While arsenic easily crosses the placenta, the specific mechanisms impacting placental immune cell populations and fetal health are unclear. Maternal arsenic exposure is epidemiologically linked to increased infection risk, mortality, and cancer susceptibility in offspring, emphasizing the importance of understanding placentally-mediated immune effects.
View Article and Find Full Text PDFCurr Obes Rep
January 2025
Department of Medicine, University of Washington, Seattle, WA, USA.
Purpose Of Review: To evaluate the role of hypothalamic inflammation and gliosis in human obesity pathogenesis and other disease processes influenced by obesity.
Recent Findings: Recent studies using established and novel magnetic resonance imaging (MRI) techniques to assess alterations in hypothalamic microarchitecture in humans support the presence of hypothalamic inflammation and gliosis in adults and children with obesity. Studies also identify prenatal exposure to maternal obesity or diabetes as a risk factor for hypothalamic inflammation and gliosis and increased obesity risk in offspring.
Int J Mol Sci
December 2024
Laboratory of Comparative Developmental Physiology, Koltzov Institute of Developmental Biology of the Russian Academy of Sciences, 119334 Moscow, Russia.
Available evidence from animal studies suggests that placental serotonin plays an important role in proper fetal development and programming by altering brain circuit formation, which later translates into altered abnormal adult behaviors. Several environmental stimuli, including stress and maternal inflammation, affect placental and, hence, fetal serotonin levels and thus may disturb fetal brain development. We investigated the effect of prenatal stress of varying intensities on the formation of adaptive behaviors in mouse offspring and the role of placental serotonin in these processes.
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