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Fetal inflammation associated with minimal acute morbidity in moderate/late preterm infants
  1. Tate Gisslen1,2,
  2. Manuel Alvarez1,
  3. Casey Wells3,
  4. Man-Ting Soo1,4,
  5. Donna S Lambers5,
  6. Christine L Knox6,
  7. Jareen K Meinzen-Derr7,
  8. Claire A Chougnet3,
  9. Alan H Jobe1,
  10. Suhas G Kallapur1
  1. 1Divisions of Neonatology and Pulmonary Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA
  2. 2Division of Neonatology, University of Minnesota, Minneapolis, Minnesota, USA
  3. 3Department of Immunobiology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA
  4. 4Department of Pediatrics, Kwong Wah Hospital, Hong Kong, Hong Kong
  5. 5Department of Obstetrics and Gynecology, Good Samaritan Hospital, Cincinnati, Ohio, USA
  6. 6Institute of Health and Biomedical Innovation, Faculty of Health, Queensland University of Technology, Brisbane, Australia
  7. 7Biostatistics and Epidemiology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA
  1. Correspondence to Dr Suhas G Kallapur, Division of Neonatology and Pulmonary Biology, Cincinnati Children's Hospital/University of Cincinnati 3333 Burnet Avenue, ML#7029, Cincinnati, OH 45229-3039, USA; suhas.kallapur{at}cchmc.org

Abstract

Objective To determine whether exposure to acute chorioamnionitis and fetal inflammation caused short-term adverse outcomes.

Design This is a prospective observational study: subjects were mothers delivering at 32–36 weeks gestation and their preterm infants at a large urban tertiary level III perinatal unit (N=477 infants). Placentae and fetal membranes were scored for acute histological chorioamnionitis based on the Redline criteria. Fetal inflammation was characterised by histological diagnosis of funisitis (umbilical cord inflammation), increased cord blood cytokines measured by ELISA, and activation of the inflammatory cells infiltrating the placenta and fetal membranes measured by immunohistology. Maternal and infant data were collected.

Results Twenty-four per cent of 32–36-week infants were exposed to histological chorioamnionitis and 6.9% had funisitis. Immunostaining for leucocyte subsets showed selective infiltration of the placenta and fetal membranes with activated neutrophils and macrophages with chorioamnionitis. Interleukin (IL) 6, IL-8 and granulocyte colony-stimulating factor were selectively increased in the cord blood of preterm infants with funisitis. Compared with infants without chorioamnionitis, funisitis was associated with increased ventilation support during resuscitation (43.8% vs 15.4%) and more respiratory distress syndrome postnatally (27.3% vs 10.2%) in univariate analysis. However, these associations disappeared after adjusting for prematurity.

Conclusions Despite fetal exposure to funisitis, increased cord blood cytokines and activated placental inflammatory cells, we could not demonstrate neonatal morbidity specifically attributable to fetal inflammation after adjusting for gestational age in moderate and late preterm infants.

  • Neonatology
  • Fetal Medicine
  • Resuscitation
  • Immunology

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Footnotes

  • Contributors All authors have fulfilled requirements based on ICMJE guidelines.

  • Funding This research was funded in part by National Institute of Health and Human Development grants HL 97064 and HD 57869 (SGK and AHJ). REDCap technology was provided through Center for Clinical and Translational Science and Training support (UL1-RR026314-01 NCRR/NIH).

  • Competing interests None declared.

  • Ethics approval Institutional review boards of Good Samaritan Hospital, Cincinnati, OH and Cincinnati Children's Hospital Medical Center.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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