title: Early inflammation in the absence of overt infection in preterm neonates exposed to intensive care.
abstract: BACKGROUND
  Systemic inflammation, typically attributed to sepsis, has been repeatedly linked to adverse long-term outcomes in infants born prematurely. However, it is unclear whether other factors can contribute to potentially harmful systemic inflammatory responses.
  
  
  OBJECTIVE
  To determine the timing and extent of systemic inflammation occurring in absence of infection in preterm infants exposed to intensive care.
  
  
  METHODS
  First, we screened for inflammation biomarkers most strongly linked to infection in a large prospective cohort of 425 newborns (gestational age 24-42 weeks). Second, we longitudinally measured levels of infection-related inflammation biomarkers up to 42 days of post-natal life in a series of 58 infants born ≤30 weeks of gestation exposed to intensive care. Ante- or post-natal infections were excluded using stringent definitions including rigorous histological placental examination. Spearman correlations were used to identify putative clinical factors potentially linked to inflammation.
  
  
  RESULTS
  Three biomarkers were most strongly associated with neonatal sepsis (IL-6, IL-8 and G-CSF) in the first cohort. Using these markers, we found a predominant early high intensity systemic inflammation period within the first 72 h of preterm infants' extra-uterine life. Remarkably, this systemic inflammatory response was of magnitude comparable to that observed during sepsis in absence of ante- or post-natal signs of infection, and correlated with the amount of supplemental oxygen exposure (r=0.51-0.60).
  
  
  CONCLUSIONS
  Non-infectious sources of systemic inflammation are significant in preterm infants exposed to intensive care and may contribute to intensive care-related organ injury.
authors.affiliation: Child & Family Research Institute, Department of Pediatrics, University of British Columbia, Vancouver, BC, Canada.
authors.forename: Brent A
authors.initials: BA
authors.lastname: Chang
authors.forename: Qing
authors.initials: Q
authors.lastname: Huang
authors.forename: Joanne
authors.initials: J
authors.lastname: Quan
authors.forename: Vann
authors.initials: V
authors.lastname: Chau
authors.forename: Mihoko
authors.initials: M
authors.lastname: Ladd
authors.forename: Eddie
authors.initials: E
authors.lastname: Kwan
authors.forename: Deborah E
authors.initials: DE
authors.lastname: McFadden
authors.forename: Thierry
authors.initials: T
authors.lastname: Lacaze-Masmonteil
authors.forename: Steven P
authors.initials: SP
authors.lastname: Miller
authors.forename: Pascal M
authors.initials: PM
authors.lastname: Lavoie
mesh_terms: D015415:Biomarkers / Q000378:metabolism; D003141:Communicable Diseases / Q000150:complications* / Q000473:pathology*; D003422:Critical Care; D005260:Female; D006801:Humans; D007231:Infant, Newborn; D007234:Infant, Premature / Q000276:immunology*; D007249:Inflammation / Q000150:complications* / Q000473:pathology*; D008137:Longitudinal Studies; D008297:Male; D018805:Sepsis / Q000150:complications / Q000473:pathology; D013997:Time Factors
chemical_list: D015415:Biomarkers