Asthma is a chronic disease that may cause remodeling of the airways. We aimed to observe the effects of the combined use of inhaled budesonide and formoterol on both the reversibility of remodeling and structural changes in the airways. Thirty-six male patients (age range, 20-31) with mild-to-moderate persistent asthma were given inhaled formoterol and budesonide treatment for three months. Bronchial diameter (BD) and bronchial wall thickness (BWT), as measured by high-resolution computerized tomography, and reticular basement membrane thickness (RBMT), assessed in bronchoscopic biopsy specimens, were compared with pretreatment findings. Twenty-two age-matched male controls were also enrolled. BDs of the patients were significantly smaller than in the controls, whereas BWT and RBMT were greater. After three months BWT and RBMT of the subsegmental airways significantly decreased and BD increased. There was a prominent eosinophilic and lymphocytic infiltration in the bronchial mucosa of the asthmatics, and the eosinophilic infiltration significantly improved with treatment. Both serum total IgE and eosinophil counts were related to eosinophilic infiltration in the biopsy samples (r = 0.494 and r = 0.463, respectively). FEV(1) was positively correlated with the diameters of the segmental and subsegmental airways (r = 0.491 and r = 0.265, respectively) and negatively correlated with BWT of the subsegmental airways (r = -0.293) and with the RBMT of both the segmental and subsegmental airways (r = -0.597 and r = -0.590, respectively). We suggest that treatment with inhaled formoterol and budesonide may reverse increased RBMT and BWT as part of remodeling in patients with asthma.

Anti-Helicobacter pylori IgG serum levels were measured in 31 young male bronchiectasis patients without gastrointestinal symptoms, and 56 healthy males. The possible presence of H. pylori was also investigated by rapid urease tests, culture and histopathological examination of protected catheter brush and biopsy specimens from the bronchiectatic site. No serological, microbiological or histological evidence of H. pylori infection was found in the bronchiectasis patient group. H. pylori did not appear to be an agent of infection or chronic colonisation in bronchiectasis, and may not have a significant role in the progression of this disease.