title: Airway and lung elastic fibre is not reduced in asthma nor in asthmatics following corticosteroid treatment.
abstract: By morphometric investigation of the relative content of elastic and collagen fibres, we have tested the hypothesis that loss of elastic fibres in the conducting airways and lung parenchyma may reduce tissue elastic recoil, resulting in increased airway maximal closure and apparent increased responsiveness. The study groups comprised: Group A (n = 11) with relatively mild atopic asthma using inhaled bronchodilators prn (i.e. short-term corticosteroids users); Group B (n = 9) with more severe asthma requiring inhaled bronchodilators regularly, and daily inhaled glucocorticosteroids (i.e. longterm corticosteroid users); Group C (n = 12) normal healthy workers. Bronchial biopsy samples were taken from three sites from the left lung. Group A biopsy samples were taken before and after a 4 wk treatment period with inhaled corticosteroids (200 micrograms b.i.d.) and the relative elastic and collagen fibre content of a subepithelial zone was determined from electron micrographs. In a parallel study, the relative proportion of elastic fibre in post mortem lung tissue samples (inner aspect of the bronchial wall, alveolar wall, and points of attachment of surrounding alveoli to intrapulmonary bronchi) from subjects suffering a fatal asthma attack (n = 11), and non-asthmatic suffering sudden death (n = 9), were determined using Miller's elastic and eosin counterstain for light microscopy. In bronchial biopsies of normal subjects, 4.6 (SEM 1.1)% of subepithelial connective tissue was elastic fibre, similar to mild asthmatic subjects, 1.9 (SEM 0.48)%. Neither short-term (4 weeks) inhaled corticosteroid (200 micrograms b.i.d.) nor long-term (< 6 months) treatment with variable doses of inhaled steroids (100-1000 micrograms b.i.d.) significantly altered the elastic or collagen content of the tissue.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Dept of Lung Pathology, Royal Brompton NHLI, London, UK.
authors.forename: R W
authors.initials: RW
authors.lastname: Godfrey
authors.forename: S
authors.initials: S
authors.lastname: Lorimer
authors.forename: S
authors.initials: S
authors.lastname: Majumdar
authors.forename: E
authors.initials: E
authors.lastname: Adelroth
authors.forename: P W
authors.initials: PW
authors.lastname: Johnston
authors.forename: A V
authors.initials: AV
authors.lastname: Rogers
authors.forename: S A
authors.initials: SA
authors.lastname: Johansson
authors.forename: P K
authors.initials: PK
authors.lastname: Jeffery
mesh_terms: D000293:Adolescent; D000328:Adult; D001249:Asthma / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D001980:Bronchi / Q000187:drug effects / Q000473:pathology; D001999:Bronchoscopy; D003238:Connective Tissue / Q000187:drug effects / Q000473:pathology; D004311:Double-Blind Method; D004547:Elastic Tissue / Q000187:drug effects* / Q000473:pathology; D005260:Female; D005938:Glucocorticoids / Q000494:pharmacology* / Q000627:therapeutic use; D006801:Humans; D008168:Lung / Q000187:drug effects / Q000473:pathology; D008297:Male; D008854:Microscopy, Electron; D008875:Middle Aged; D012137:Respiratory System / Q000187:drug effects / Q000473:pathology
chemical_list: D005938:Glucocorticoids