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Original Research: ASTHMA |

β2-Adrenergic Receptor Polymorphisms Affect Response to Treatment in Children With Severe Asthma Exacerbations

Christopher L. Carroll, MD, FCCP; Petronella Stoltz, APRN; Craig M. Schramm, MD; Aaron R. Zucker, MD
Author and Funding Information

*From the Department of Pediatrics, Connecticut Children's Medical Center, Hartford, CT.

Correspondence to: Christopher L. Carroll, MD, FCCP, Division of Pediatric Critical Care, Connecticut Children's Medical Center, 282 Washington St, Hartford, CT 06106; e-mail: ccarrol@ccmckids.org


This research was supported by the University of Connecticut Health Center General Clinical Research Center (grant M01 RR006192).

The authors have reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/site/misc/reprints.xhtml).


© 2009 American College of Chest Physicians


Chest. 2009;135(5):1186-1192. doi:10.1378/chest.08-2041
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Background:  β2-adrenergic receptor (AR) agonists are the mainstay of treatment for severe asthma exacerbations, one of the most common causes of critical illness in children. Genotypic differences in the β2-AR gene, particularly at amino acid positions 16 and 27, have been shown to affect the response to β2-AR agonist therapy. Our hypothesis is that genotypic differences contribute to patient response to β2-AR agonist treatment during severe asthma exacerbations in children.

Methods:  Children admitted to the hospital ICU for a severe asthma exacerbation between 2002 and 2005 were located, and genetic samples were obtained from saliva. Children hospitalized during this period were treated with a protocol that titrated β2-AR therapy (first nebulized, then IV) according to a validated clinical asthma score.

Results:  Thirty-seven children hospitalized during the study period were enrolled into the study. At amino acid position 16 in the β2-AR gene, 13 children were homozygous for the glycine (Gly) allele (Gly/Gly), 8 were homozygous for the arginine (Arg) allele (Arg/Arg), and 16 were heterozygous (Arg/Gly). Despite similar clinical asthma scores on hospital admission, the children with the Gly/Gly genotype had significantly shorter hospital ICU length of stay and duration of continuously nebulized albuterol therapy and were significantly less likely to require IV β2-AR therapy than those with Arg/Arg or Arg/Gly genotypes. No association existed among polymorphisms at amino acid position 27 and response to β2-AR therapy.

Conclusions:  In this cohort of children with severe asthma exacerbations, children whose genotypes were homozygous for Gly at amino acid position 16 of the β2-AR gene had a more rapid response to β2-AR agonist treatment. The β2-AR genotype appears to influence the response to therapy in this population.

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