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Published Online First: 2 May 2006. doi:10.1136/thx.2005.052241
Thorax 2006;61:671-677
Copyright © 2006 BMJ Publishing Group Ltd & British Thoracic Society.

EPIDEMIOLOGY

Bronchial hyperresponsiveness and the development of asthma and COPD in asymptomatic individuals: SAPALDIA Cohort Study

M H Brutsche1, S H Downs2, C Schindler2, M W Gerbase3, J Schwartz4, M Frey5, E W Russi6, U Ackermann-Liebrich3, P Leuenberger7 for the SAPALDIA Team

1 Pneumology, University Hospital Basel, Basel, Switzerland
2 Institute for Social and Preventive Medicine, University of Basel, Switzerland
3 Pneumology, Hôpital Cantonal Universitaire, Geneva, Switzerland
4 Harvard School of Public Health, Boston, USA
5 Klinik Barmelweid, Barmelweid, Switzerland
6 Pneumology, University Hospital Zurich, Zurich, Switzerland
7 Pneumology, Centre Hôpitalier Universitaire Vaudois, Lausanne, Switzerland

Correspondence to:
Dr M H Brutsche
Pneumologie, University Hospital Basel, Petersgraben 4, CH-4031 Basel, Switzerland; mbrutsche{at}uhbs.ch

Background: Bronchial hyperresponsiveness (BHR) is a common feature of asthma. However, BHR is also present in asymptomatic individuals and its clinical and prognostic significance is unclear. We hypothesised that BHR might play a role in the development of chronic obstructive pulmonary disease (COPD) as well as asthma.

Methods: In 1991 respiratory symptoms and BHR to methacholine were evaluated in 7126 of the 9651 participants in the SAPALDIA cohort study. Eleven years later 5825 of these participants were re-evaluated, of whom 4852 performed spirometric tests. COPD was defined as an FEV1/FVC ratio of <0.70.

Results: In 1991 17% of participants had BHR, of whom 51% were asymptomatic. Eleven years later the prevalence of asthma, wheeze, and shortness of breath in formerly asymptomatic subjects with or without BHR was, respectively, 5.7% v 2.0%, 8.3% v 3.4%, and 19.1% v 11.9% (all p<0.001). Similar differences were observed for chronic cough (5.9% v 2.3%; p = 0.002) and COPD (37.9% v 14.3%; p<0.001). BHR conferred an adjusted odds ratio (OR) of 2.9 (95% CI 1.8 to 4.5) for wheezing at follow up among asymptomatic participants. The adjusted OR for COPD was 4.5 (95% CI 3.3 to 6.0). Silent BHR was associated with a significantly accelerated decline in FEV1 by 12 (5–18), 11 (5–16), and 4 (2–8) ml/year in current smokers, former smokers and never smokers, respectively, at SAPALDIA 2.

Conclusions: BHR is a risk factor for an accelerated decline in FEV1 and the development of asthma and COPD, irrespective of atopic status. Current smokers with BHR have a particularly high loss of FEV1.

Abbreviations: BHR, bronchial hyperresponsiveness; COPD, chronic obstructive pulmonary disease; FEV1, forced expiratory volume in 1 second; FVC, forced vital capacity

Keywords: bronchial hyperresponsiveness; asthma; chronic obstructive pulmonary disease; smoking; epidemiological study


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