title: Insulin decreases hepatic acute phase protein levels in severely burned children.
abstract: BACKGROUND
  Severe burn induces the hepatic acute phase response. In this study, we wondered whether continuous insulin treatment decreases acute phase protein levels in the severely burned.
  
  
  METHODS
  Eighteen children aged 2 to 17 years with burns >40% of total body surface area were randomized to receive either insulin (n=9) or no treatment (n=9) within 72 hours after injury until the wounds were 95% healed. Insulin was given at a continuous rate of > or =1.5 microU/kg/min to maintain euglycemia (serum glucose 100-140 microg/dL). Plasma was examined at days 7, 14, 21, and 28 for acute phase protein levels including C-reactive protein, C3 complement, alpha1-acid glycoprotein, haptoglobin, alpha2-macroglobulin, prealbumin, transferrin, and retinol-binding protein. Statistical analysis was by ANOVA and t test.
  
  
  RESULTS
  With insulin treatment, alpha1-acid glycoprotein, C3 complement, alpha2-macroglobulin, and haptoglobin levels decreased (P<.05) after a severe burn compared with control, especially at days 21 and 28. Additionally, the hepatic constitutive proteins (prealbumin, transferrin, and retinol-binding protein) were lower in the insulin-treatment group than those of the control group at day 21 (P<.05).
  
  
  CONCLUSIONS
  Continuous insulin treatment decreases acute phase protein levels after a severe burn. The results suggest insulin downregulation of the hepatic acute phase response to injury.
authors.affiliation: Shriners Hospitals for Children and Department of Surgery, the University of Texas Medical Branch, Galveston, Tex 77550, USA.
authors.forename: Xiaowu
authors.initials: X
authors.lastname: Wu
authors.forename: Steven J
authors.initials: SJ
authors.lastname: Thomas
authors.forename: David N
authors.initials: DN
authors.lastname: Herndon
authors.forename: Arthur P
authors.initials: AP
authors.lastname: Sanford
authors.forename: Steven E
authors.initials: SE
authors.lastname: Wolf
mesh_terms: D000209:Acute-Phase Proteins / Q000378:metabolism*; D000328:Adult; D001786:Blood Glucose / Q000187:drug effects; D002056:Burns / Q000188:drug therapy* / Q000378:metabolism*; D002097:C-Reactive Protein / Q000378:metabolism; D002648:Child; D002675:Child, Preschool; D003176:Complement C3 / Q000378:metabolism; D005260:Female; D006801:Humans; D007004:Hypoglycemic Agents / Q000008:administration & dosage*; D007328:Insulin / Q000008:administration & dosage*; D008099:Liver / Q000378:metabolism; D008297:Male; D009961:Orosomucoid / Q000378:metabolism; D011228:Prealbumin / Q000378:metabolism; D012177:Retinol-Binding Proteins / Q000378:metabolism; D054839:Retinol-Binding Proteins, Plasma; D012720:Severity of Illness Index; D014168:Transferrin / Q000378:metabolism; D016896:Treatment Outcome; D000511:alpha-Macroglobulins / Q000378:metabolism
chemical_list: D000209:Acute-Phase Proteins; D001786:Blood Glucose; D003176:Complement C3; D007004:Hypoglycemic Agents; D007328:Insulin; D009961:Orosomucoid; D011228:Prealbumin; D012177:Retinol-Binding Proteins; D054839:Retinol-Binding Proteins, Plasma; D014168:Transferrin; D000511:alpha-Macroglobulins; D002097:C-Reactive Protein