title: Myopathological features in skeletal muscle of patients with chronic obstructive pulmonary disease.
abstract: Despite the fact that muscle weakness is a major problem in chronic obstructive pulmonary disease (COPD), detailed information on myopathological changes at the microscopic level in these patients is scarce, if indeed available at all. Vastus lateralis biopsies of 15 COPD weight-stable patients (body mass index (BMI) 23.9+/-1.0 kg x m(-2); fat-free mass index (FFMI) 17.2+/-1.7 kg x m(-2)) and 16 healthy age-matched controls (BMI 26.3+/-0.8 kg x m(-2); FFMI 19.6+/-2.2 kg x m(-2)) were evaluated. Histochemistry was used to evaluate myopathological features. Immunohistochemistry was used for the detection of macrophages and leukocytes, and active caspase 3 and terminal deoxynucleotidyl transferase deoxyuridine triphosphate (dUTP) nick-end labelling (TUNEL) as markers of apoptosis. Fatty cell replacement and fibrosis were observed in both groups, the latter being slightly, but significantly, more pronounced in COPD. No differences between COPD and controls were found with respect to central nuclei, necrosis, regeneration, or fibre splitting. Signs of mitochondrial abnormalities were absent and normal numbers of inflammatory cells were found. Active caspase 3 positive myocytes were not observed and no difference was found in the number of TUNEL-positive myonuclei between controls and COPD patients (1.1% versus 1.0%, respectively). The cross-sectional area of type-IIX muscle fibres was smaller in COPD than in controls (2,566 versus 4,248 microm2). Except for the I to IIX shift in fibre types, the selective type-IIX atrophy and a slight accompanying increase in fibrosis and fat cell replacement in chronic obstructive pulmonary disease relative to age-matched controls, no other morphological abnormalities were observed in the muscle biopsies of chronic obstructive pulmonary disease patients. Also, in this group of clinically and weight stable chronic obstructive pulmonary disease patients, apoptosis appeared not to be involved in muscle pathology.
authors.affiliation: Dept of Pulmonology, Nutrition Toxicology and Environment Research Institute Maastricht, Maastricht, The Netherlands. H.Gosker@pul.unimaas.nl
authors.forename: H R
authors.initials: HR
authors.lastname: Gosker
authors.forename: B
authors.initials: B
authors.lastname: Kubat
authors.forename: G
authors.initials: G
authors.lastname: Schaart
authors.forename: G J
authors.initials: GJ
authors.lastname: van der Vusse
authors.forename: E F M
authors.initials: EF
authors.lastname: Wouters
authors.forename: A M W J
authors.initials: AM
authors.lastname: Schols
mesh_terms: D000328:Adult; D000368:Aged; D017209:Apoptosis; D016022:Case-Control Studies; D005260:Female; D005355:Fibrosis / Q000209:etiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D032342:Muscle Cells / Q000378:metabolism / Q000473:pathology; D018908:Muscle Weakness / Q000209:etiology / Q000473:pathology; D018482:Muscle, Skeletal / Q000378:metabolism / Q000473:pathology*; D009133:Muscular Atrophy / Q000209:etiology / Q000473:pathology; D029424:Pulmonary Disease, Chronic Obstructive / Q000150:complications / Q000378:metabolism / Q000473:pathology*