PT  - JOURNAL ARTICLE
AU  - C. Rebordosa
AU  - M. Kogevinas
AU  - S. Guerra
AU  - F. Castro-Giner
AU  - D. Jarvis
AU  - L. Cazzoletti
AU  - I. Pin
AU  - V. Siroux
AU  - M. Wjst
AU  - J.M. Antò
AU  - R. de Marco
AU  - X. Estivill
AU  - A.G. Corsico
AU  - R. Nielsen
AU  - C. Janson
TI  - <em>ADRB2</em> Gly16Arg polymorphism, asthma control and lung function decline
AID  - 10.1183/09031936.00146310
DP  - 2011 Nov 01
TA  - European Respiratory Journal
PG  - 1029--1035
VI  - 38
IP  - 5
4099  - http://erj.ersjournals.com/content/38/5/1029.short
4100  - http://erj.ersjournals.com/content/38/5/1029.full
SO  - Eur Respir J2011 Nov 01; 38
AB  - Arg/Arg homozygotes for the Gly16Arg polymorphism in the β2-adrenoreceptor gene (ADRB2) have a reduced response to short-acting β2-agonists but no effect has been associated with long-acting β2-agonists (LABAs). We selected 604 subjects with current asthma from the European Community Respiratory Health Study to evaluate whether asthma control and lung function decline were associated with Gly16Arg polymorphism, and to test whether LABA or inhaled corticosteroid (ICS) use modified these effects. There was an increased risk of noncontrolled asthma (OR 1.33, 95% CI 1.01–1.75; p=0.046) for each Arg allele. Among nonusers of ICS, the odds ratio of noncontrolled asthma among Arg/Arg versus Gly/Gly subjects was 2.73 (95% CI 1.28–5.82; p=0.009). No increased risk of noncontrolled asthma associated with the Arg allele was observed among ICS and/or LABA users. For each Arg allele, a mean±se decrease in decline in forced expiratory volume in 1 s of 7.7±2.5 mL·yr−1 was found (p-value for trend 0.003), irrespective of ICS or LABA use. Arg/Arg subjects had an increased risk of bronchial hyperresponsiveness (BHR) versus Gly/Gly subjects, with an odds ratio of 2.51 (95% CI 1.12–5.63; p=0.025) if they did not use ICS. The Arg allele was associated with poorer asthma control, a steeper lung function decline and BHR. Absence of genotypic effects on asthma control among ICS users may be due to reversed β2-adrenoreceptor desensitisation.