title: The effects of treatment with chemotherapy on energy metabolism and inflammatory mediators in small-cell lung carcinoma.
abstract: A disturbed energy balance has been demonstrated in lung cancer patients. Both an enhanced resting energy expenditure (REE) and a decreased energy intake contribute to weight loss. Enhanced systemic levels of inflammatory mediators were found to be related to the enhanced REE in lung cancer. The aim of the present study was to investigate energy metabolism and systemic levels of inflammatory mediators in small-cell lung carcinoma (SCLC) patients before and after treatment with chemotherapy. Hypermetabolism and an enhanced inflammatory response have already been demonstrated in SCLC by our group before. Twelve newly diagnosed SCLC patients were consecutively included in the study. REE was measured by indirect calorimetry and body composition was determined by bioelectrical impedance (BIA) before and 1 month after treatment. To assess the inflammatory state the acute-phase proteins, C-reactive protein (CRP) and lipopolysaccharide-binding protein (LBP), both soluble tumour necrosis factor (TNF) receptors, (sTNF-R)-55 and sTNF-R75, and soluble intercellular adhesion molecule (sICAM)-1 were measured in plasma before and 1 month after treatment. CRP was assessed by turbidemetry, whereas the other inflammatory parameters were measured by enzyme-linked immunosorbent assay (ELISA). A significant reduction in REE was found irrespective of therapeutic outcome, whereas body weight and body composition remained stable. The acute-phase proteins CRP and LBP were reduced significantly after treatment with chemotherapy, whereas both sTNF receptors and sICAM-1 remained enhanced. No correlation, however, existed between the decrease in REE and the decrease in the acute-phase proteins. In conclusion, chemotherapeutic treatment attenuates the tumour-related metabolic derangements and acute-phase response.
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: A M
authors.initials: AM
authors.lastname: Schols
authors.forename: M A
authors.initials: MA
authors.lastname: Dentener
authors.forename: G P
authors.initials: GP
authors.lastname: ten Velde
authors.forename: W A
authors.initials: WA
authors.lastname: Buurman
authors.forename: E F
authors.initials: EF
authors.lastname: Wouters
mesh_terms: D000328:Adult; D000368:Aged; D018288:Carcinoma, Small Cell / Q000188:drug therapy* / Q000378:metabolism; D004734:Energy Metabolism / Q000187:drug effects*; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000032:analysis*; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis; D008175:Lung Neoplasms / Q000188:drug therapy* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D018124:Receptors, Tumor Necrosis Factor / Q000032:analysis
chemical_list: D018836:Inflammation Mediators; D018124:Receptors, Tumor Necrosis Factor; D018799:Intercellular Adhesion Molecule-1