Lung function of adult patients with bronchial asthma or chronic obstructive lung disease prior to and following a 3-month-stay in the Dutch Asthma Center in Davos]

The effect of a multidisciplinary treatment for obstructive airway disease at high altitude has not been well established for adult patients. One hundred and fifty patients with obstructive airway disease were examined at admission and at discharge after a 3-month hospitalization period in an Alpine clinic. Body plethysmographic data were collected at admission and at discharge as was medication use. Patients were subdivided into three groups, one group (n = 34) with bronchial asthma, one group (n = 97) with moderately severe chronic obstructive pulmonary disease (COPD) and one group (n = 19) with severe COPD. The greatest improvement in lung function data occurred in the moderately severe COPD group (at discharge before salbutamol administration there was an increase in FEV1 of 6%, after salbutamol administration there was an increase in FEV1 of 7%). When we divided the patient groups into atopic and non-atopic, it appeared that the non-atopic moderately severe COPD group showed the greatest improvement in lung function variables. The histamine threshold (expressed in 10logPC20) improved only in the moderately severe COPD group. There was a reduction from mean 7.5 mg per day in oral corticosteroids use to mean 5.0 mg per day in the moderately severe COPD group. We conclude that after 3 months' multidisciplinary treatment in the Alpine climate there is an improvement in lung function and a reduction in medication use in patients with airflow limitation.     

Chronic obstructive pulmonary disease is associated with enhanced bronchial expression of FGF-1, FGF-2, and FGFR-1

An important feature of chronic obstructive pulmonary disease (COPD) is airway remodelling, the molecular mechanisms of which are poorly understood. In this study, the role of fibroblast growth factors (FGF-1 and FGF-2) and their receptor, FGFR-1, was assessed in bronchial airway wall remodelling in patients with COPD (FEV1 < 75%; n = 15) and without COPD (FEV1 > 85%; n = 16). FGF-1 and FGFR-1 were immunolocalized in bronchial epithelium, airway smooth muscle (ASM), submucosal glandular epithelium, and vascular smooth muscle. Quantitative digital image analysis revealed increased cytoplasmic expression of FGF-2 in bronchial epithelium (0.35 +/- 0.03 vs 0.20 +/- 0.04, p < 0.008) and nuclear localization in ASM (p < 0.0001) in COPD patients compared with controls. Elevated levels of FGFR-1 in ASM (p < 0.005) and of FGF-1 (p < 0.04) and FGFR-1 (p < 0.001) in bronchial epithelium were observed. In cultured human ASM cells, FGF-1 and/or FGF-2 (10 ng/ml) induced cellular proliferation, as shown by [3H]thymidine incorporation and by cell number counts. Steady-state mRNA levels of FGFR-1 were elevated in human ASM cells treated with either FGF-1 or FGF-2. The increased bronchial expression of fibroblast growth factors and their receptor in patients with COPD, and the mitogenic response of human ASM cells to FGFs in vitro suggest a potential role for the FGF/FGFR-1 system in the remodelling of bronchial airways in COPD.     

Sputum microbiome profiles identify severe asthma phenotypes of relative stability at 12 to 18 months

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