title: Propranolol does not increase inflammation, sepsis, or infectious episodes in severely burned children.
abstract: BACKGROUND
  Propranolol, a nonselective beta1-2 antagonist, attenuates hypermetabolism and catabolism in severely burned patients. However, recent data suggest that propranolol impairs immune function and enhances inflammation. The purpose of the present study was to determine the effect of propranolol administration on infection, sepsis, and inflammation in severely burned pediatric patients.
  
  
  METHODS
  A prospective, intent-to-treat study was performed; patient demographics (age, gender, burn size, and mortality); infectious episodes (colony count greater then 10); and sepsis (guidelines by the society of critical care medicine) were determined. Hypermetabolic response was determined by resting energy expenditure (REE), and the inflammatory response was determined by measuring serum cytokine expression.
  
  
  RESULTS
  Two hundred forty-five patients (143 controls, 102 propranolol) were included into the study. There were no differences between the control and propranolol groups for age, gender distribution, burn size, third degree burn, and length of stay. Mortality was 6% in the control group and 5% in the propranolol group. Propranolol significantly decreased REE and predicted REE during acute hospital stay. Forty-three patients developed infections in the control group (30%), whereas 21 developed infections in the propranolol group (21%). The incidence of sepsis was 10% for controls and 7% for propranolol. Analysis of the cytokine expression profile in 20 patients in each group revealed that propranolol significantly decreased serum tumor necrosis factor and interleukin-1beta compared with controls (p < 0.05).
  
  
  CONCLUSIONS
  Propranolol treatment attenuates hypermetabolism and does not cause increased incidence of infection and sepsis.
authors.affiliation: Department of Surgery, Shriners Hospitals for Children, University of Texas Medical Branch, TX 77550, USA. majeschk@utmb.edu
authors.forename: Marc G
authors.initials: MG
authors.lastname: Jeschke
authors.forename: William B
authors.initials: WB
authors.lastname: Norbury
authors.forename: Celeste C
authors.initials: CC
authors.lastname: Finnerty
authors.forename: Ludwik K
authors.initials: LK
authors.lastname: Branski
authors.forename: David N
authors.initials: DN
authors.lastname: Herndon
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000009:adverse effects / Q000627:therapeutic use*; D045930:Anabolic Agents / Q000009:adverse effects / Q000627:therapeutic use*; D002056:Burns / Q000188:drug therapy* / Q000276:immunology / Q000378:metabolism; D002648:Child; D004734:Energy Metabolism; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood; D008297:Male; D011433:Propranolol / Q000009:adverse effects / Q000627:therapeutic use*; D018805:Sepsis / Q000276:immunology*; D018746:Systemic Inflammatory Response Syndrome / Q000209:etiology / Q000276:immunology*
chemical_list: D000319:Adrenergic beta-Antagonists; D045930:Anabolic Agents; D018836:Inflammation Mediators; D011433:Propranolol