title: Therapeutic hypothermia delays the C-reactive protein response and suppresses white blood cell and platelet count in infants with neonatal encephalopathy.
abstract: BACKGROUND
  Therapeutic hypothermia (HT) delays the cytokine response in infants with neonatal encephalopathy (NE).
  
  
  OBJECTIVE
  To determine if HT delayed the C-reactive protein (CRP) response and altered white blood cell (WBC), neutrophil and platelet count course during the first week of life in infants with NE.
  
  
  METHODS
  Retrospective cohort study.
  
  
  METHODS
  Regional neonatal intensive care unit, UK.
  
  
  METHODS
  104 term infants with NE (38 normothermia (NT) and 66 HT) born between 1998 and 2010. Infants not exposed to prenatal sepsis risk factors were classified as group 'A' and exposed infants to group 'B'. CRP >10 mg/L was defined as significant response.
  
  
  METHODS
  Time to CRP >10 mg/L, peak CRP, WBC, neutrophil and platelet count.
  
  
  RESULTS
  Blood cultures were negative in all the infants. In babies who had CRP response, HT delayed time to CRP >10 mg/L (median (95% CI): group A, HT: 36 h (28.3 to 48.0); NT: 24 h (0.0 to 24.0); p=0.001; group B, HT: 30 h (15.2 to 56.8); NT: 12 h (0.0 to 24.0); p=0.009) and time to peak CRP (median (95% CI): group A, HT: 60 h (60.0 to 72.0); NT: 36 h (0.0 to 48.0); p=0.001; group B, HT: 84 h (62.1 to 120.0); NT: 24 h (0.0 to 36.0); p=0.001). Compared with NT, HT was associated with reduction in slope of CRP elevation by 0.5 (95% CI 0.04 to 0.97), WBC by 2.18×10(9)/L (95% CI 0.002 to 4.35) and platelet count by 32.3×10(9)/L (95% CI 2.75 to 61.8) independent of exposure to sepsis risk, meconium aspiration and severity of asphyxia.
  
  
  CONCLUSIONS
  Therapeutic hypothermia delayed the initiation of CRP and its peak response, and depressed the WBC and platelet count compared with NT.
authors: Neonatal Neuroscience, School of Clinical Medicine, St Michael's Hospital, University of Bristol, Bristol, UK.
authors: Elavazhagan
authors: E
authors: Chakkarapani
authors: Neonatal Neuroscience, School of Clinical Medicine, St Michael's Hospital, University of Bristol, Bristol, UK.
authors: Jonathan
authors: J
authors: Davis
authors: Neonatal Neuroscience, School of Clinical Medicine, St Michael's Hospital, University of Bristol, Bristol, UK Department of Physiology, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
authors: Marianne
authors: M
authors: Thoresen
mesh_terms: D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism*; D005260:Female; D005865:Gestational Age; D006801:Humans; D007036:Hypothermia, Induced; D020925:Hypoxia-Ischemia, Brain / Q000097:blood / Q000628:therapy*; D007231:Infant, Newborn; D018836:Inflammation Mediators / Q000097:blood*; D053208:Kaplan-Meier Estimate; D007958:Leukocyte Count; D008297:Male; D009504:Neutrophils / Q000473:pathology; D010976:Platelet Count; D012189:Retrospective Studies; D018805:Sepsis / Q000175:diagnosis / Q000209:etiology
chemical_list: D015415:Biomarkers; D018836:Inflammation Mediators; D002097:C-Reactive Protein