title: Endotoxin immunity and the development of the systemic inflammatory response syndrome in critically ill children.
abstract: BACKGROUND
  The systemic inflammatory response syndrome (SIRS) may be triggered by endotoxin. Humans have antibodies directed against the core of endotoxin (endotoxin core antibodies, EndoCAb) that appear to be protective following surgery and in sepsis. We hypothesised that children with elevated antibodies to endotoxin core would be less likely to develop SIRS in their initial period on intensive care. Because of the existing literature we defined two sub-groups according to the primary reason for ICU admission: infection and non-infection.
  
  
  METHODS
  We recruited 139 consecutive patients admitted to a paediatric intensive care unit (PICU) with more than one organ failure for longer than 12 h as part of another study. Patients were classified on admission to PICU as having an infectious or a non-infections diagnosis. The occurrence of SIRS within 48 h of admission was recorded along with detailed clinical and demographic data, EndoCAb concentration and the potential confounding variables C-reactive protein and mannose-binding lectin.
  
  
  RESULTS
  In the 71 patients admitted without infection (primarily post-operative and head injured) IgG EndoCAb was significantly lower in patients who developed SIRS than those who did not (72 vs. 131 MU/ml), independent of potential confounding variables. In patients with infection there was no significant difference in IgG EndoCAb between children developing SIRS and those who did not (111 vs. 80 MU/ml).
  
  
  CONCLUSIONS
  Head injured and post-operative patients admitted to PICU who develop early SIRS have significantly lower serum IgG EndoCAb levels than those who do not.
authors.affiliation: Critical Care Group, Portex Unit, Institute of Child Health, 30 Guilford Street, WC1N 1EH, London, UK. r.stephens@ich.ucl.ac.uk.
authors.forename: R C M
authors.initials: RCM
authors.lastname: Stephens
authors.affiliation: Infectious Diseases & Microbiology Unit, Institute of Child Health, 30 Guilford Street, WC1N 1EH, London, UK.
authors.forename: K
authors.initials: K
authors.lastname: Fidler
authors.affiliation: Paediatric Intensive Care Unit, Great Ormond Street Hospital for Children NHS Trust, Great Ormond Street, WC1N 3JH, London, UK.
authors.forename: P
authors.initials: P
authors.lastname: Wilson
authors.affiliation: John Hughes Bennett Laboratory, Scottish National Blood Transfusion Service, Western General Hospital, Edinburgh, UK.
authors.forename: G R
authors.initials: GR
authors.lastname: Barclay
authors.affiliation: Critical Care Group, Portex Unit, Institute of Child Health, 30 Guilford Street, WC1N 1EH, London, UK.
authors.forename: M G
authors.initials: MG
authors.lastname: Mythen
authors.affiliation: Infectious Diseases & Microbiology Unit, Institute of Child Health, 30 Guilford Street, WC1N 1EH, London, UK.
authors.forename: G L J
authors.initials: GLJ
authors.lastname: Dixon
authors.affiliation: Immunobiology Unit, Institute of Child Health, 30 Guilford Street, WC1N 1EH, London, UK.
authors.forename: M W
authors.initials: MW
authors.lastname: Turner
authors.affiliation: Infectious Diseases & Microbiology Unit, Institute of Child Health, 30 Guilford Street, WC1N 1EH, London, UK.
authors.forename: N J
authors.initials: NJ
authors.lastname: Klein
authors.affiliation: Paediatric Intensive Care Unit, Great Ormond Street Hospital for Children NHS Trust, Great Ormond Street, WC1N 3JH, London, UK.
authors.forename: M J
authors.initials: MJ
authors.lastname: Peters
mesh_terms: D000293:Adolescent; D002648:Child; D002675:Child, Preschool; D016638:Critical Illness; D019446:Endotoxemia / Q000150:complications* / Q000276:immunology*; D005260:Female; D006801:Humans; D007223:Infant; D008297:Male; D012307:Risk Factors; D018709:Statistics, Nonparametric; D018746:Systemic Inflammatory Response Syndrome / Q000097:blood / Q000209:etiology* / Q000276:immunology*