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Peripheral lung function in patients with stable and unstable asthma - 29/04/13

Doi : 10.1016/j.jaci.2013.01.054 
Bruce R. Thompson, PhD a, b, , Jo A. Douglass, MD c, Matthew J. Ellis, BSc a, b, Vanessa J. Kelly, PhD d, Robyn E. O’Hehir, MD a, b, Gregory G. King, MD b, e, Sylvia Verbanck, PhD f
a Department of Allergy, Immunology and Respiratory Medicine, The Alfred Hospital and Monash University, Melbourne, Australia 
b Cooperative Research Centre for Asthma and Airways, Camperdown, Sydney, Australia 
c Department of Clinical Immunology and Allergy, Royal Melbourne Hospital and University of Melbourne, Parkville, Australia 
d Department of Medicine, Pulmonary and Critical Care Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Mass 
e Woolcock Institute of Medical Research, Camperdown, Sydney, Australia 
f Respiratory Division, Academic Hospital, Vrije Universiteit Brussels, Brussels, Belgium 

Corresponding author: Bruce R. Thompson, PhD, Lung Function Laboratory, Department of Allergy, Immunology and Respiratory Medicine, The Alfred Hospital, Commercial Rd, Melbourne 3004, Victoria, Australia.

Abstract

Background

Exacerbations of asthma are thought to be caused by airflow obstruction resulting from airway inflammation, bronchospasm, and mucus plugging. Histologic evidence suggests the small airways, including acinar air spaces, are involved; however, this has not been corroborated in vivo by measurements of peripheral small-airway function.

Objective

We sought to determine whether asthma severity is linked to small-airway function, particularly in patients with acute severe asthma.

Methods

Eighteen subjects admitted for an asthma exacerbation underwent lung function testing, including measures of acinar ventilation heterogeneity (Sacin) and conductive ventilation heterogeneity (Scond) using the multiple-breath nitrogen washout. Treatment requirement was defined according to Global Initiative for Asthma scores. Data were compared with those obtained in 19 patients with stable asthma.

Results

For the asthma exacerbation group, the median FEV1 was 59% of predicted value (95% CI, 45% to 75% of predicted value), the median Scond value was 185% of predicted value (95% CI, 119% to 245% of predicted value), and the median Sacin value was 225% of predicted value (95% CI, 143% to 392% of predicted value). FEV1 (percent predicted) was correlated with Sacin (percent predicted) values (Spearman rho = −0.67, P = .006) but not with Scond (percent predicted) values (P > .1). The Global Initiative for Asthma score was significantly related to Sacin (percent predicted) (Spearman rho = 0.59, P = .016) but not to Scond (percent predicted) values (P > .1). The unstable group was characterized by considerably lower forced vital capacity (P < .001) and higher Scond (P = .001) values than the unstable group. In a subgroup of 11 unstable patients who could be reviewed after 4 weeks, FEV1, forced vital capacity, Sacin, and Scond values showed marked improvements.

Conclusion

Our findings suggest that unstable asthma is characterized by a combined abnormality in the acinar and conductive lung zones, both of which are partly reversible. Functional abnormality in the acinar lung zone in particular showed a direct correlation with airflow obstruction and treatment requirement in patients with acute severe asthma.

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Key words : Severe asthma, acinar airways, peripheral gas mixing

Abbreviations used : ACQ, FRC, FVC, GINA, MBW, Sacin, Scond, Sn


Plan


 Support for this study was provided by the Cooperative Research Centre for Asthma and Airways and the National Health and Medical Research Council, Australia.
 Disclosure of potential conflict of interest: B. R. Thompson, M. J. Ellis, V. J. Kelly, R. E. O’Hehir, and S. Verbanck have received grants from the National Health and Medical Research Council and the Cooperative Research Centre for Asthma and Airways. J. A. Douglass has received grants from the National Health and Medical Research Council and the Cooperative Research Centre for Asthma and Airways; is on an advisory board for Novartis; has received payment for lectures from AstraZeneca, GlaxoSmithKline, and Novartis; and has received royalties from Health Press Limited. G. G. King has received grants from the National Health and Medical Research Council, GlaxoSmithKline, Boehringer Ingelheim, Pharmaxis, and the Asthma Foundation; has received travel support from GlaxoSmithKline, Novartis, AstraZeneca, Boehringer Ingelheim, and Pfizer; has received subject payments for clinical trials from Pharmaxis; and is part of a consultancy agreement between GlaxoSmithKline, Novartis, AstraZeneca, Boehringer Ingelheim, Pfizer, and the Woolcock Institute of Medical Research, and his research group receives an unrestricted allocation as part of the monies received from the consultancy agreements.


© 2013  American Academy of Allergy, Asthma & Immunology. Publié par Elsevier Masson SAS. Tous droits réservés.
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Vol 131 - N° 5

P. 1322-1328 - mai 2013 Retour au numéro
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