title: Insulin treatment improves the systemic inflammatory reaction to severe trauma.
abstract: OBJECTIVE
  Determine the effect of insulin on the systemic inflammatory response, pro- and anti-inflammatory cytokines and hepatic acute-phase-response in severely burned pediatric patients.
  
  
  BACKGROUND
  The systemic inflammatory and hepatic acute-phase-response contribute to hypermetabolism, multi-organ failure, and mortality. Insulin has been recently shown to decrease mortality and to prevent the incidence of multi-organ failure in critically ill patients; however, the underlying mechanisms have not been defined.
  
  
  METHODS
  Thirteen thermally injured children received insulin to maintain blood glucose at a range from 120 to 180 mg/dl, 15 children received no insulin with blood glucose levels also at range from 120 to 180 mg/dl and served as controls. Our outcome measures encompassed the effect of insulin on pro-inflammatory mediators, the hepatic acute-phase-response, fat, and the IGF-I system.
  
  
  RESULTS
  Insulin administration decreased pro-inflammatory cytokines and proteins, while increasing constitutive-hepatic proteins (P < 0.05). Burned children receiving insulin required significantly less albumin substitution to maintain normal levels compared with control (P < 0.05). Insulin decreased free fatty acids and serum triglycerides when compared with controls (P < 0.05). Serum IGF-I and IGFBP-3 significantly increased with insulin administration (P < 0.05).
  
  
  CONCLUSIONS
  Insulin attenuates the inflammatory response by decreasing the pro-inflammatory and increasing the anti-inflammatory cascade, thus restoring systemic homeostasis, which has been shown critical for organ function and survival in critically ill patients.
authors.affiliation: Klinik und Poliklinik für Chirurgie, Klinikum der Universität Regensburg, Germany. Mcjeschke@hotmail.com
authors.forename: Marc G
authors.initials: MG
authors.lastname: Jeschke
authors.forename: Dagmar
authors.initials: D
authors.lastname: Klein
authors.forename: David N
authors.initials: DN
authors.lastname: Herndon
mesh_terms: D000210:Acute-Phase Reaction / Q000276:immunology; D002056:Burns / Q000150:complications / Q000188:drug therapy* / Q000276:immunology*; D002648:Child; D002675:Child, Preschool; D016638:Critical Illness; D016207:Cytokines / Q000097:blood / Q000276:immunology; D005260:Female; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D007328:Insulin / Q000627:therapeutic use*; D008297:Male; D009752:Nutritional Status / Q000502:physiology; D012189:Retrospective Studies; D018746:Systemic Inflammatory Response Syndrome / Q000188:drug therapy* / Q000209:etiology / Q000276:immunology*
chemical_list: D016207:Cytokines; D007004:Hypoglycemic Agents; D007328:Insulin