Airway wall thickening has been observed in postmortem studies of patients with status asthmaticus. The wall thickening is accompanied by airway structural changes, such as subbasement membrane thickening, mucous gland and goblet-cell hyperplasia, increased vascularity, and smooth-muscle hypertrophy and hyperplasia, as well as with chronic inflammation such as mucosal edema and inflammatory cell infiltration. These changes have been further confirmed by studies using bronchial biopsy in living patients. With the advent of high-resolution CT, noninvasive assessment of airway dimensions in asthma has become available. We and others have quantitatively assessed airway wall thickening and its clinical implication in asthma.
Chronic cough is a common problem for which patients seek medical attention from primary care physicians and pulmonologists. Although chronic cough itself is not fatal, it severely impairs quality of life. One of the most common causes of chronic cough is cough variant asthma (CVA), which lacks the typical manifestation of asthma such as wheezing or dyspnea but presents airway hyperresponsiveness and bronchodilator responsive coughing. CVA is clinically considered as a variant type of asthma as well as a precursor of classic asthma with wheezing. Pathologically, CVA shares common features such as eosinophilic inflammation and remodeling changes, including subbasement membrane thickening and goblet-cell hyperplasia with classic asthma.
Chronic cough due to other causes, such as gastroesophageal reflux disease (GERD) and postnasal drip syndrome, which is currently referred to as upper airway cough syndrome,16 is often grouped as nonasthmatic chronic cough (NAC). Patients with NAC also have features of airway inflammation and remodeling. In a study examining BAL fluid of patients with NAC, mast cells, eosinophils, and histamine levels were increased; while in another study, sputum neutrophilia and increased levels of interleukin-8 and tumor necrosis factors were observed. Increase of bronchoalveolar lymphocytes in idiopathic chronic cough is also reported. In terms of remodeling, the presence of submucosal fibrosis in the airways of patients with NAC was first described by Boulet and colleagues. A biopsy study of NAC has further demonstrated an increase of submucosal mast cells, subbasement membrane thickness, goblet-cell area, vascularity, and smooth-muscle area. Nonasthmatic eosinophilic bronchitis, another cause of chronic cough characterized by airway eosinophilia and absence of airway hyperresponsiveness, also involves subbasement membrane thickening. Regardless of the accumulating evidence of airway remodeling based on bronchial biopsies in patients with chronic cough, only one study of nonasthmatic eosinophilic bronchitis has examined whole airway wall thickness using CT scans, and has shown that in contrast with the biopsy study, wall area of large airways in patients with nonasthmatic eosinophilic bronchitis is not different from that of healthy control subjects and is less than that of intermittent or mild persistent asthmatics with sputum eosinophilia, suggesting the importance of assessment by CT that may extend and compensate the information of endobronchial biopsy studies in chronic cough.
In this study, we examined airway dimensions by CT in patients with CVA and those with NAC. Correlations between the CT parameters and clinical indexes, such as age, disease duration, pulmonary function, cough sensitivity, and sputum cell differentials, were also studied.