title: Systemic and pulmonary inflammation is independent of skeletal muscle changes in patients with chronic obstructive pulmonary disease.
abstract: BACKGROUND
  Nutritional depletion is an important manifestation of chronic obstructive pulmonary disease (COPD), which has been related to systemic inflammation. It remains unclear to what degree airway inflammation contributes to the presence or progression of nutritional depletion.
  
  
  OBJECTIVE
  To determine whether airway inflammation and lung bacterial colonization are related to nutritional status or predict progressive weight loss and muscle atrophy in patients with COPD.
  
  
  METHODS
  Body composition using dual energy X-ray absorptiometry, indices of airway inflammation, and bacterial colonization were measured in 234 COPD patients. Systemic inflammation was assessed from serum C reactive protein (CRP) and circulating total and differential leukocyte counts. Nutritional depletion was defined as a body mass index (BMI) less than 21 kg/m(2) and/or fat-free mass index (FFMI) less than 15 or 17 kg/m(2) in women and men, respectively. FFMI was calculated as the fat-free mass (FFM) corrected for body surface area. Measurements were repeated in 94 patients after a median 16-month follow-up. Regression analysis was used to assess the relationships of weight change and FFM change with indices of bacterial colonization and airway and systemic inflammation.
  
  
  RESULTS
  Nutritional depletion occurred in 37% of patients. Lung function was worsened in patients with nutritional depletion compared to those without (forced expiratory volume in 1 second 1.17 L versus 1.41 L, mean difference 0.24, 95% confidence interval 0.10 to 0.38, P<0.01). There were no differences in airway inflammation and bacterial colonization in patients with and without nutritional depletion. At baseline, BMI correlated positively with serum CRP (rs=0.14, P=0.04). Change in weight and change in FFM over time could not be predicted from baseline patient characteristics.
  
  
  CONCLUSIONS
  Nutritional depletion and progressive muscle atrophy are not related to airway inflammation or bacterial colonization. Overspill of pulmonary inflammation is not a key driver of muscle atrophy in COPD.
authors.affiliation: Institute for Lung Health, NIHR Respiratory Biomedical Research Unit, Department of Infection, Immunity and Inflammation, University of Leicester, Leicester, United Kingdom.
authors.forename: Bethan L
authors.initials: BL
authors.lastname: Barker
authors.affiliation: Institute for Lung Health, NIHR Respiratory Biomedical Research Unit, Department of Infection, Immunity and Inflammation, University of Leicester, Leicester, United Kingdom.
authors.forename: Susan
authors.initials: S
authors.lastname: McKenna
authors.affiliation: Institute for Lung Health, NIHR Respiratory Biomedical Research Unit, Department of Infection, Immunity and Inflammation, University of Leicester, Leicester, United Kingdom.
authors.forename: Vijay
authors.initials: V
authors.lastname: Mistry
authors.affiliation: Institute for Lung Health, NIHR Respiratory Biomedical Research Unit, Department of Infection, Immunity and Inflammation, University of Leicester, Leicester, United Kingdom.
authors.forename: Mitesh
authors.initials: M
authors.lastname: Pancholi
authors.affiliation: Department of Clinical Microbiology, University Hospitals of Leicester NHS Trust, Leicester, United Kingdom.
authors.forename: Hemu
authors.initials: H
authors.lastname: Patel
authors.affiliation: Department of Infection, Immunity, and Inflammation, University of Leicester, Leicester, United Kingdom.
authors.forename: Koirobi
authors.initials: K
authors.lastname: Haldar
authors.affiliation: Department of Infection, Immunity, and Inflammation, University of Leicester, Leicester, United Kingdom.
authors.forename: Michael R
authors.initials: MR
authors.lastname: Barer
authors.affiliation: Respiratory Medicine Unit, Nuffield Department of Clinical Medicine, University of Oxford, Old Road Campus, Oxford, United Kingdom.
authors.forename: Ian D
authors.initials: ID
authors.lastname: Pavord
authors.affiliation: Institute for Lung Health, NIHR Respiratory Biomedical Research Unit, Department of Infection, Immunity and Inflammation, University of Leicester, Leicester, United Kingdom.
authors.forename: Michael C
authors.initials: MC
authors.lastname: Steiner
authors.affiliation: Institute for Lung Health, NIHR Respiratory Biomedical Research Unit, Department of Infection, Immunity and Inflammation, University of Leicester, Leicester, United Kingdom.
authors.forename: Christopher E
authors.initials: CE
authors.lastname: Brightling
authors.affiliation: Respiratory Medicine Unit, Nuffield Department of Clinical Medicine, University of Oxford, Old Road Campus, Oxford, United Kingdom.
authors.forename: Mona
authors.initials: M
authors.lastname: Bafadhel
mesh_terms: D015502:Absorptiometry, Photon; D050154:Adiposity; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000097:blood; D015992:Body Mass Index; D002097:C-Reactive Protein / Q000032:analysis; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood; D008137:Longitudinal Studies; D008168:Lung / Q000382:microbiology / Q000503:physiopathology*; D008297:Male; D044342:Malnutrition / Q000175:diagnosis / Q000209:etiology* / Q000503:physiopathology; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000473:pathology / Q000503:physiopathology*; D009133:Muscular Atrophy / Q000175:diagnosis / Q000209:etiology* / Q000503:physiopathology; D009752:Nutritional Status; D011014:Pneumonia / Q000097:blood / Q000175:diagnosis / Q000209:etiology* / Q000382:microbiology / Q000503:physiopathology; D011446:Prospective Studies; D029424:Pulmonary Disease, Chronic Obstructive / Q000150:complications* / Q000175:diagnosis / Q000503:physiopathology; D012307:Risk Factors; D013997:Time Factors; D015431:Weight Loss
chemical_list: D015415:Biomarkers; D018836:Inflammation Mediators; D002097:C-Reactive Protein
keywords: airway inflammation; bacteria; dual-energy X-ray absorptiometry (DEXA); fat-free mass; muscle atrophy