Background: Variable airflow obstruction and airway hyperresponsiveness (AHR) are features of asthma, which are absent in nonasthmatic eosinophilic bronchitis (EB). Airway remodelling is characteristic of both conditions suggesting that remodelling and airway dysfunction are disassociated, but whether the airway geometry differs between asthma and nonasthmatic EB is uncertain.
Methods: We assessed airway geometry by computed tomography (CT) imaging in asthma vs EB. A total of 12 subjects with mild-moderate asthma, 14 subjects with refractory asthma, 10 subjects with EB and 11 healthy volunteers were recruited. Subjects had a narrow collimation (0.75 mm) CT scan from the aortic arch to the carina to capture the right upper lobe apical segmental bronchus (RB1). In subjects with asthma and EB, CT scans were performed before and after a 2-week course of oral prednisolone (0.5 mg/kg).
Results: Mild-moderate and refractory asthma were associated with RB1 wall thickening in contrast to subjects with nonasthmatic EB who had maintained RB1 patency without wall thickening [mean (SD) % wall area and luminal area mild-t0-moderate asthma 67.7 (7.3)% and 6.6 (2.8) mm(2)/m(2), refractory asthma 67.3 (5.6)% and 6.7 (3.4) mm(2)/m(2), healthy control group 59.7 (6.3)% and 8.7 (3.8) mm(2)/m(2), EB 61.4 (7.8)% and 11.1 (4.6) mm(2)/m(2) respectively; P < 0.05]. Airway wall thickening of non-RB1 airways generation three to six was a feature of asthma only. There was no change in airway geometry of RB1 after prednisolone. Proximal airway wall thickening was associated with AHR in asthma (r = -0.56; P = 0.02).
Conclusions: Maintained airway patency in EB may protect against the development of AHR, whereas airway wall thickening may promote AHR in asthma.