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Published online before print July 24, 2008
Eur Respir J 2008, doi:10.1183/09031936.00114007
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ORIGINAL ARTICLE

INCREASED AIRWAY CLOSURE IS A DETERMINANT OF AIRWAY HYPERRESPONSIVENESS

D.G. Chapman 1*, N. Berend 1, G.G. King 2, C.M. Salome 1

1 Woolcock Institute of Medical Research, Camperdown, NSW, Australia; Cooperative Research Centre for Asthma, Camperdown, NSW, Australia; and University of Sydney, Sydney, Australia
2 Woolcock Institute of Medical Research, Camperdown, NSW, Australia; Cooperative Research Centre for Asthma, Camperdown, NSW, Australia; University of Sydney, Sydney, Australia; and Dept Respiratory Medicine, Royal North Shore Hospital, St Leonards, NSW, Australia

* To whom correspondence should be addressed. E-mail: dcha7069{at}woolcock.org.au.


   Abstract

To investigate whether increased airway closure is a component of airway hyperresponsiveness (AHR), airway closure was compared during induced bronchoconstriction in 62 asthmatic, 41 non-asthmatic non-obese (control) and 20 non-asthmatic obese (obese) subjects.

Airway closure and airway narrowing were measured by spirometry as the %{Delta}FVC and {Delta}(FEV1/FVC), or forced expiratory ratio ({Delta}FER). Multiple regression analyses were used to assess the determinants of AHR, assessed by the dose response slope (DRS).

DRS was increased in asthmatics compared to controls (P<0.001), but did not differ between obese and controls. The spirometric predictors of logDRS were baseline FER, {Delta}FER, BMI and %{Delta}FVC (R2adj=0.36, p<0.0001). There was a negative relationship between BMI and logDRS in the regression, suggesting a protective effect.

These findings suggest that the extent of airway closure during induced bronchoconstriction is a determinant of AHR, independent of the level of airway narrowing. However, after adjusting for airway closure, obesity appears to protect against AHR.

Keywords:  Airway hyperresponsiveness, asthma – small airways




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