title: Increased resting energy expenditure and weight loss are related to a systemic inflammatory response in lung cancer patients.
abstract: OBJECTIVE
  To determine whether an increased resting energy expenditure (REE) and weight loss in lung cancer patients are related to a systemic inflammatory response.
  
  
  METHODS
  REE was measured by indirect calorimetry using a ventilated hood system. Soluble tumor necrosis factor receptor 55 (sTNF-R55) and sTNF-R75, soluble intercellular adhesion molecule (sICAM)-1, soluble E (sE)-selectin, lipopolysaccharide (LPS)-binding protein (LBP), interleukin (IL)-6, and TNF-alpha were measured using sandwich enzyme-linked immunosorbent assay (ELISA), and C-reactive protein (CRP) was measured by turbidimetry. A cross-sectional study was performed to compare inflammatory mediators between hypermetabolic (REE/Harris Benedict [HB] equation > or = 110%) versus normometabolic (REE/HB < 110%) patients and between patients who lost weight (more than 10% loss of preillness weight) versus those whose weight remained stable.
  
  
  RESULTS
  Eighty-seven patients with primary non-small-cell lung cancer were consecutively entered onto the study. Mean REE expressed as a percentage of the HB reference values was 118% +/- 12%; 67 patients were considered hypermetabolic. Twenty-six patients had a substantial loss of more than 10% of their preillness weight. Hypermetabolic patients were found to have significantly increased levels of sTNF-R55, sE-selectin, LBP, and CRP compared with normometabolic patients. Weight loss was related with increased levels of the sTNF-Rs, sICAM-1, IL-6, LBP, and CRP.
  
  
  CONCLUSIONS
  Hypermetabolism and weight loss are related to the presence of a systemic inflammatory response as reflected by enhanced levels of inflammatory mediators and acute phase proteins in patients with primary non-small-cell lung cancer.
authors.affiliation: Department of Pulmonology, University Hospital, Maastricht, The Netherlands.
authors.forename: A J
authors.initials: AJ
authors.lastname: Staal-van den Brekel
authors.forename: M A
authors.initials: MA
authors.lastname: Dentener
authors.forename: A M
authors.initials: AM
authors.lastname: Schols
authors.forename: W A
authors.initials: WA
authors.lastname: Buurman
authors.forename: E F
authors.initials: EF
authors.lastname: Wouters
mesh_terms: D000209:Acute-Phase Proteins / Q000032:analysis; D000368:Aged; D000704:Analysis of Variance; D015703:Antigens, CD / Q000097:blood; D001685:Biological Factors / Q000097:blood*; D002289:Carcinoma, Non-Small-Cell Lung / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D016022:Case-Control Studies; D015815:Cell Adhesion Molecules / Q000097:blood; D003404:Creatinine / Q000097:blood; D004734:Energy Metabolism / Q000502:physiology*; D005260:Female; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D015850:Interleukin-6 / Q000097:blood; D008175:Lung Neoplasms / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D015431:Weight Loss / Q000502:physiology*
chemical_list: D000209:Acute-Phase Proteins; D015703:Antigens, CD; D001685:Biological Factors; D015815:Cell Adhesion Molecules; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D003404:Creatinine