ABSTRACT
It is interesting to note, however, that as early as 1769 John Miller described a child who had died of asthma ‘with an abundance of gelatinous secretions obstructing the bronchi’.2
The first information on the pathology of asthma was gained from post-mortem examina-
widespread mucosal plugging of airways resulting in air trapping and hyperinflated lungs. Subsequent studies confirmed that the plugs contain not only plasma protein and sloughed epithelial cells but also inflammatory cells.4 It was also appreciated that the airway wall was affected with thickening of the smooth muscle and sub-basement membrane fibrosis as well as accumulation of inflammatory cells.5-8
These changes were subsequently also identified in the airways of even mild asthmatics with particular accumulation of eosinophils and mast cells in the lamina propria.1,9 However, this had already been highlighted from postmortem studies in which death had not been caused by asthma.10 The very first suggestion that airway inflammation even underlay mild asthma came from paediatricians. In 1978, Cutz and colleagues published information on ultrastructural examination of the airways of two asthmatic children undergoing open lung biopsies who by chance had asthma that was in remission and compared them with the lung tissue from two children who had died of status asthmaticus. All four had submucosal cellular
explain the inflammatory response and the implications of this for management of the disease.
