Asthma is a common lung disease defined by reversible airway obstruction, airway inflammation, and increased airway responsiveness to a wide variety of stimuli. It is characterized by paroxysmal bronchospasm, hypersecretion of mucus, airway wall edema, and bronchial hyperreactivity. There is substantial evidence for the role of inflammation in asthma and bronchial hyperreactivity. Early autopsy studies of patients who had died in status asthmaticus showed epithelial denudation, mucosal edema, glandular hypertrophy, and dense eosinophilic infiltration. More recently, bronchoalveolar lavage (BAL) studies in patients challenged with aeroallergens consistently reveal increased numbers of BAL fluid eosinophils, mast cell mediators, and products of other inflammatory cells (1,2). Furthermore, transbronchial biopsies, even of patients with mild, well-controlled disease, have shown significant inflammatory changes. Biopsies have not only shown inflammation, but also an association between the degree of inflammatory changes and measurements of nonspecific bronchial hyperresponsiveness (3,4). Finally, therapy directed toward airway inflammation has been most effective in the treatment of chronic asthma and in attenuating bronchial hyperreactivity.
KeywordsCorticosteroid Ozone Heparin Enzymatic Degradation Prostaglandin
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