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Published ahead of print on June 23, 2005, doi:10.1164/rccm.200501-092OC

Am. J. Respir. Crit. Care Med., Volume 172, Number 6, September 2005, 700-703

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Submitted on January 20, 2005
Accepted on May 9, 2005

Bronchodilator Response in Relation to Beta-adrenoceptor Haplotype in Patients with Asthma

D. Robin Taylor1*, Michael J Epton2, Martin A Kennedy3, Andrew D Smith1, Steven Iles2, Allison L Miller3, Matthew D Littlejohn3, Jan O Cowan1, Tracey Hewitt2, Maureen P Swanney2, Karen P Brassett1, and G. Peter Herbison4

1 Otago Respiratory Research Unit, University of Otago, Dunedin School of Medicine, Dunedin, Otago, New Zealand, 2 Canterbury Respiratory Research Unit, University of Otago, Christchurch School of Medicine, Christchurch, Canterbury, New Zealand, 3 Department of Pathology, Gene Structure and Function Laboratory, University of Otago, Christchurch School of Medicine, Christchurch, Canterbury, New Zealand, 4 Department of Preventive and Social Medicine, University of Otago, Dunedin School of Medicine, Dunedin, Otago, New Zealand

* To whom correspondence should be addressed. E-mail: robin.taylor{at}stonebow.otago.ac.nz.

Rationale Genetic variation of the {beta}2-adrenoceptor influences receptor function in vitro. There are reports that, in vivo, bronchodilator response is related to {beta}2-adrenoceptor genotype, and that clinical outcomes during chronic therapy with {beta}2-agonist drugs are also influenced by genotype. Whether these features are related to single nucleotide polymorphisms or to combinations (haplotypes) is unclear. Objectives Our aim was to measure bronchodilator response in patients with asthma stratified by {beta}2- adrenoceptor haplotype. This was done after eliminating the confounding effect of prior drug treatment with inhaled {beta}2-agonists and corticosteroids. Methods and measurements {beta}2-adrenoceptor haplotype was determined in 176 patients with asthma of whom 161 harbored the six most common combinations. Treatment with inhaled {beta}2-agonists and inhaled corticosteroids were withheld for appropriate intervals. Spirometric changes 20 minutes following a single dose of albuterol (2.5mg by nebuliser) were then recorded. Main results There were no significant differences in bronchodilator response (% improvement in forced expiratory volume in one second) with respect to any of the major {beta}2- adrenoceptor haplotypes or genotypes. Conclusions Genetic variation of the {beta}2-adrenoceptor does not influence the immediate response to inhaled {beta}2-agonist. The confounding effect of tolerance resulting from regular {beta}2-agonist use requires to be controlled in assessing the pharmacogenetics influences on clinical outcomes with {beta}2-agonists.
Key words: beta2-adrenoceptor, haplotype, beta2-agonist, asthma therapy




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