Alterations in Airway Inflammation and Lung Function During Corticosteroid Therapy for Atopic Asthma
Corticosteroids are the most effective therapy for asthma, and current guidelines emphasize their use in all but mild asthma. Corticosteroid therapy down-regulates airway inflammation and improves lung function. Some studies suggest that steroid-induced changes in bronchial inflammation and lung function are closely associated. Other data suggest that changes in these two processes occur independently. Heterogeneity of asthma within subject groups and variations in dose and duration of therapy could explain this paradox. We hypothesized that repeat measures of airway inflammation (by endobronchial biopsy) and lung function during corticosteroid therapy might provide insights into their kinetics of change. A complete understanding of the relation between changes in airway physiology and lung function during corticosteroid therapy for asthma might allow accurate titration of anti-inflammatory therapy.
Airway inflammation in asthma is characterized by infiltrates of several cell types, including T lymphocytes, macrophages, and eosinophils. Although many cell types have been shown to play an important role in disease activity, asthma may occur in the absence of one or more of these “effector” cells. Moreover, lung function in patients with asthma is also characterized by several distinct features, including air trapping, airflow limitation, and airway hyperreactivity. To date, no single inflammatory or lung function parameter is entirely reliable at predicting disease severity, or response to antiasthma therapy. There is a need for more data on the relation between airway inflammation and lung function in asthma.
Flexible fiberoptic bronchoscopy with endobronchial biopsy allows precise quantification of airway inflammation in asthma.