Effects Of Short-term Treatment With Inhaled Corticosteroid on Airway Wall Thickening in Asthma
Niimi A, Matsumoto H, Amitami R, et al. Am J Med. 2004;116:725–731
Purpose of the Study.
To examine the effect of inhaled corticosteroids (ICSs) on thickening of the asthmatic airway wall as measured by computed tomography (CT), pulmonary function, and serum levels of eosinophilic cationic protein (ECP).
Fifty-one patients (mean age: 54.4 ± 13.8 years) with persistent asthma and 28 healthy controls (mean age: 48.1 ± 15.9 years).
Patients fulfilled American Thoracic Society criteria for asthma, and none had ever received systemic or inhaled steroids, cromomes, or antileukotriene agents. Exclusion criteria included asthma exacerbations or respiratory tract infections within 8 weeks before enrollment or a history of smoking. Cross-sectional, thin-section CT images of the right upper lobe apical bronchus were obtained before and after treatment. Using an enlarged image on a workstation, luminal and total airway areas (in millimeters squared) were calculated after manually tracing the internal and external perimeters of the airway. The airway wall area and airway wall area as a percentage of total wall area were used as indices of airway wall thickness. In asthmatic patients, CT, blood sampling for ECP, and pulmonary function tests were performed before and after treatment with beclomethasone dipropionate (400 μg) administered twice daily for 12 weeks.
Before treatment, airway wall thickness was greater in asthma patients than controls (P < .0001). After treatment, airway wall thickness decreased by 11% (P < .001) but remained high (P < .0001 vs control). Serum ECP levels decreased significantly after treatment (P < .001). Forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), and FEV1/FVC improved significantly after treatment, but the values remained lower than in controls. The decrease in wall thickness was associated with a decrease in the level of ECP (r = 0.39; P = .009) and an increase in the FEV1 (r = 0.45; P = .003) and was inversely related to disease duration at entry (r = −0.38; P = .009). Posttreatment wall thickness was related to disease duration (r = 0.45; P = .003) and remaining airflow obstruction.
In patients with persistent asthma, treatment with inhaled beclomethasone for 12 weeks significantly reduced airway wall thickness as assessed by CT. Airway wall thickness remained significantly greater than in controls. ICSs had less of an effect on airway wall thickening in patients with long-standing asthma.
This study raises questions. Is the reduction in airway wall thickness indicative of reductions in airway inflammation? Additional studies (eg, with airway biopsy specimens) are needed to confirm this. Would earlier intervention with ICSs result in normalization of airway wall thickness? This is a particularly important question for those who treat children with asthma.