Source: Annual Congress 2002 - Regulation of responsiveness and inflammation in airway disease
Disease area: Airway diseases, Paediatric lung diseases

Abstract

Objective: Increased airway responsiveness is not unique to asthma and can be demonstrated in a number of inflammatory airway diseases. It is related to inflammation, but indirect mechanisms remain unknown. Different mechanisms may underlie bronchial hyperresponsiveness (BHR) in different diseases. Cystic fibrosis (CF) is an autosomal recessive disease, caused by mutations of CFTR gene, characterised by progressive pulmonary tissue injury due to chronic bacterial infection and excessive immune- mediated inflammatory process. The importance of BHR and treatment with bronchodilators and corticosteroids in management of patients with CF is poorly understood. The aim of this study was to investigate bronchial reactivity using bronchial challenge test with carbachol in CF patients and to establish influencing factors (atopy, prechallenge pulmonary function tests). Methods: 33 CF patients (14 boys, 19 girls) aged 12,7 ±] 3,6 (mean ±] SD) with mild course of the disease (Shwachman- Kulczycki score>70) were studied. Bronchial challenge test with carbachol was performed according to standard guidelines (tidal breathing method) in all individuals. Patients having PC₂₀<4,8mg/ml were defined as having BHR. Results: BHR was found in 27 patients (81%), PC₂₀ was 1,46 ±] 1,21mg/ml (mean ±] SD). There was correlation between PC₂₀ and baseline pulmonary function tests (standardised values): SDSFVC-p=0,001, r=0,53 SDSFEV₁- p=0,003, r=0,50 and SDSMEF₅₀- p=0,007, r=0,46, SDSMEF₂₅- p=0,002, r=0,51. There was no correlation between PC₂₀ and athopy (positive prick skin tests and total serum IgE). Conclusion: There was a high incidence of BHR in studied CF patients. BHR was related to baseline pulmonary function tests, but was not related to atopy.

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Citations should be made in the following way:
M. Bielecka-Zylbersztejn, A. Milanowski, D. Sands (Warsaw, Poland). Bronchial hyperreactivity in cystic fibrosis. Eur Respir J 2002; 20: Suppl. 38, 3144

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