Extended hypermetabolic response of the liver in severely burned pediatric patients

Marc G. Jeschke, Robert E. Barrow, David Herndon

Research output: Contribution to journalArticle

60 Citations (Scopus)

Abstract

Hypothesis: The acute phase response is a cascade of events contributing to hypermetabolism and substrate catabolism. It was believed to persist for only a short time after injury. There is now evidence that systemic catabolism and hypermetabolism associated with thermal injury persevere for a long time. We hypothesize that the proinflammatory hepatic acute phase response perseveres for an extended time and enhances hypermetabolism longer than previously believed. Design: Prospective study. Setting: Intensive Care Burn Unit, Shriners Hospital for Children. Patients: Twenty-three children (aged 1-16 years) sustaining a severe thermal injury (≥40% total-body surface area) who remained in the intensive care unit longer than 30 days. Main Outcome Measures: Patient demographics, nutritional support, incidence of sepsis, inhalation injury, mortality, and levels of serum constitutive proteins, type I and type II acute phase proteins, free fatty acids, proinflammatory cytokines, insulin-like growth factor (IGF) I, IGF binding protein-1, IGF binding protein-3, and hepatocyte growth factor. Results: After thermal injury, constitutive hepatic protein levels decreased 2- to 3-fold 80 days after burn, whereas acute phase protein levels increased. Free fatty acid levels were increased 5 days after burn. Proinflammatory cytokine levels (interleukin [IL] 1, IL-6, IL-8, IL-10, and tumor necrosis factor) and IGF binding protein-1 levels were elevated for 40 days after burn, whereas serum IGF-I and IGF binding protein-3 levels were decreased. Hepatocyte growth factor levels were increased immediately after burn but rapidly returned to the normal range. Conclusions: Despite adequate nutritional support, a severe thermal injury induces the proinflammatory acute phase response for a prolonged period. Thus, the liver with the hepatic acute phase response plays a more important role during catabolism after burn than previously believed. Pharmacologic agents that improve hepatic function may be an effective approach to attenuate hypermetabolism after trauma.

Original languageEnglish (US)
Pages (from-to)641-647
Number of pages7
JournalArchives of Surgery
Volume139
Issue number6
DOIs
StatePublished - Jun 2004

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Acute-Phase Reaction
Pediatrics
Liver
Wounds and Injuries
Hot Temperature
Insulin-Like Growth Factor Binding Protein 1
Insulin-Like Growth Factor Binding Protein 3
Hepatocyte Growth Factor
Nutritional Support
Acute-Phase Proteins
Insulin-Like Growth Factor I
Nonesterified Fatty Acids
Intensive Care Units
Cytokines
Burn Units
Body Surface Area
Interleukin-8
Interleukin-1
Interleukin-10
Inhalation

ASJC Scopus subject areas

  • Surgery

Cite this

Extended hypermetabolic response of the liver in severely burned pediatric patients. / Jeschke, Marc G.; Barrow, Robert E.; Herndon, David.

In: Archives of Surgery, Vol. 139, No. 6, 06.2004, p. 641-647.

Research output: Contribution to journalArticle

Jeschke, Marc G. ; Barrow, Robert E. ; Herndon, David. / Extended hypermetabolic response of the liver in severely burned pediatric patients. In: Archives of Surgery. 2004 ; Vol. 139, No. 6. pp. 641-647.
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abstract = "Hypothesis: The acute phase response is a cascade of events contributing to hypermetabolism and substrate catabolism. It was believed to persist for only a short time after injury. There is now evidence that systemic catabolism and hypermetabolism associated with thermal injury persevere for a long time. We hypothesize that the proinflammatory hepatic acute phase response perseveres for an extended time and enhances hypermetabolism longer than previously believed. Design: Prospective study. Setting: Intensive Care Burn Unit, Shriners Hospital for Children. Patients: Twenty-three children (aged 1-16 years) sustaining a severe thermal injury (≥40{\%} total-body surface area) who remained in the intensive care unit longer than 30 days. Main Outcome Measures: Patient demographics, nutritional support, incidence of sepsis, inhalation injury, mortality, and levels of serum constitutive proteins, type I and type II acute phase proteins, free fatty acids, proinflammatory cytokines, insulin-like growth factor (IGF) I, IGF binding protein-1, IGF binding protein-3, and hepatocyte growth factor. Results: After thermal injury, constitutive hepatic protein levels decreased 2- to 3-fold 80 days after burn, whereas acute phase protein levels increased. Free fatty acid levels were increased 5 days after burn. Proinflammatory cytokine levels (interleukin [IL] 1, IL-6, IL-8, IL-10, and tumor necrosis factor) and IGF binding protein-1 levels were elevated for 40 days after burn, whereas serum IGF-I and IGF binding protein-3 levels were decreased. Hepatocyte growth factor levels were increased immediately after burn but rapidly returned to the normal range. Conclusions: Despite adequate nutritional support, a severe thermal injury induces the proinflammatory acute phase response for a prolonged period. Thus, the liver with the hepatic acute phase response plays a more important role during catabolism after burn than previously believed. Pharmacologic agents that improve hepatic function may be an effective approach to attenuate hypermetabolism after trauma.",
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