ABSTRACT
Despite advances in our understanding of the pathophysiology and immunobiology of asthma, death rate from this illness appears to be increasing. There is also increased incidence of patients with severe intractable disease with considerable impairment of lung function and a requirement for oral corticosteroids. Airway obstruction in asthma is not a completely reversible disorder and is presumed to be the result of inflammation-induced structural changesÐor remodelingÐ of the airways (1). These structural changes include epithelial detachment and regeneration, goblet cell hyperplasia, submucosal glands hypertrophy, subepithelial fibrosis (thickening of the basement membrane), inflammatory cell infiltration, hyperplasia and hypertrophy of the bronchial smooth muscle, and vascular changes. Increase in subepithelial and submucosal collagen depositions was found in asthmatic airway (2,3). Asthmatics are classified as severe if they are steroid-dependent, need frequent hospital administrations, have a long history of persistent asthma, and require time away
from work (4,5). In contrast, mild asthmatics occasionally use bronchodilators and/or inhaled steroids. Structural changes in mild asthma are less prominent than those observed in airways of severe or fatal asthma. This suggests that there is a progression in the degree of inflammation from mild to severe asthma with alterations in epithelial cell integ-rity and basement membrane, bronchial smooth muscle, and mucous gland. Patients with long-standing disease and altered airway structure are more likely to die from asthma.
