AIRWAY AND LUNG ELASTIC FIBER IS NOT REDUCED IN ASTHMA NOR IN ASTHMATICS FOLLOWING CORTICOSTEROID TREATMENT

By morphometric investigation of the relative content of elastic and c ollagen fibres, we have tested the hypothesis that loss of elastic fib res in the conducting airways and lung parenchyma may reduce tissue el astic recoil, resulting in increased airway maximal closure and appare nt increased responsiveness. The study groups comprised: Group A (n-11 ) with relatively mild atopic asthma using inhaled bronchodilators pm (i.e. short-term corticosteroids users); Group B (n=9) with more sever e asthma requiring inhaled bronchodilators regularly, and daily inhale d 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 bef ore and after a 4 wk treatment period with inhaled corticosteroids (20 0 mu g b.i.d.) and the relative elastic and collagen fibre content of a subepithelial zone was determined from electron micrographs, In a pa rallel 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 br onchi) from subjects suffering a fatal asthma attack (n-11), and non-a sthmatic suffering sudden death (n=9), were determined using Miller's elastic and eosin counterstain for light microscopy. In bronchial biop sies of normal subjects, 4.6 (SEM 1.1)% of subepithelial connective ti ssue was elastic fibre, similar to mild asthmatic subjects, 1.9 (SEM 0 .48)%. Neither short-term (4 weeks) inhaled corticosteroid (200 mu g b .i.d.) nor long-term (<6 months) treatment with variable doses of inha led steroids (100-1000 mu g b.i.d.) significantly altered the elastic or collagen content of the tissue. In fatal asthma, the relative propo rtions of elastic fibre (SEM) were 17.0 (6), 10.4 (1.1), and 13.4 (1.8 )% for bronchial wall, lung parenchyma and alveolar/bronchial attachme nt zones respectively compared with 22.3 (3.9), 9.0 (1.1) and 13.0 (2. 1)% in nine cases of non-asthmatic sudden death controls. The results indicate that reduction of elastic fibre content is not a feature of m ild or fatal asthma, and is unlikely to be a contributory factor to th e reported reduction of elastic recoil and the development of airway h yperresponsiveness.