Marc G Jeschke1, Robert E Barrow, David N Herndon. 1. Department of Plastic and Hand Surgery, Friedrich-Alexander University of Erlangen, Erlangen, Germany. mcjeschke@hotmail.com
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.
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.
Authors: Eva C Diaz; David Newcomb Herndon; Mario Alberto Cleves; Ronald P Mlcak; Asle Aarsland; Elisabet Børsheim Journal: J Trauma Acute Care Surg Date: 2019-05 Impact factor: 3.313
Authors: Marc G Jeschke; Gerd G Gauglitz; Juquan Song; Gabriela A Kulp; Celeste C Finnerty; Robert A Cox; José M Barral; David N Herndon; Darren Boehning Journal: J Cell Mol Med Date: 2009-08 Impact factor: 5.310
Authors: Junru Wu; Anthony Cyr; Danielle Gruen; Tyler Lovelace; Panayiotis Benos; Tianmeng Chen; Francis Guyette; Mark Yazer; Brian Daley; Richard Miller; Brian Harbrecht; Jeffrey Claridge; Herb Phelan; Brian Zuckerbraun; Matthew Neal; Pär Johansson; Jakob Stensballe; Rami Namas; Yoram Vodovotz; Jason Sperry; Timothy Billiar; PAMPer Study Group Journal: Res Sq Date: 2021-01-08
Authors: Marc G Jeschke; Robert Kraft; Juquan Song; Gerd G Gauglitz; Robert A Cox; Natasha C Brooks; Celeste C Finnerty; Gabriela A Kulp; David N Herndon; Darren Boehning Journal: Mol Med Date: 2011-01-19 Impact factor: 6.354
Authors: Mile Stanojcic; Peter Chen; Rachael A Harrison; Vivian Wang; Jeremy Antonyshyn; Juan Carlos Zúñiga-Pflücker; Marc G Jeschke Journal: Crit Care Med Date: 2014-06 Impact factor: 7.598
Authors: Yaeko Hiyama; Alexandra H Marshall; Robert Kraft; Nour Qa'aty; Anna Arno; David N Herndon; Marc G Jeschke Journal: Mol Med Date: 2013-03-05 Impact factor: 6.354
Authors: Marc G Jeschke; David L Chinkes; Celeste C Finnerty; Gabriela Kulp; Oscar E Suman; William B Norbury; Ludwik K Branski; Gerd G Gauglitz; Ronald P Mlcak; David N Herndon Journal: Ann Surg Date: 2008-09 Impact factor: 12.969