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http://purl.uniprot.org/citations/19029431http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/19029431http://www.w3.org/2000/01/rdf-schema#comment"

Background

beta(2)-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 beta(2)-AR gene, particularly at amino acid positions 16 and 27, have been shown to affect the response to beta(2)-AR agonist therapy. Our hypothesis is that genotypic differences contribute to patient response to beta(2)-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 beta(2)-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 beta(2)-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 beta(2)-AR therapy than those with Arg/Arg or Arg/Gly genotypes. No association existed among polymorphisms at amino acid position 27 and response to beta(2)-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 beta(2)-AR gene had a more rapid response to beta(2)-AR agonist treatment. The beta(2)-AR genotype appears to influence the response to therapy in this population."xsd:string
http://purl.uniprot.org/citations/19029431http://purl.org/dc/terms/identifier"doi:10.1378/chest.08-2041"xsd:string
http://purl.uniprot.org/citations/19029431http://purl.uniprot.org/core/author"Carroll C.L."xsd:string
http://purl.uniprot.org/citations/19029431http://purl.uniprot.org/core/author"Schramm C.M."xsd:string
http://purl.uniprot.org/citations/19029431http://purl.uniprot.org/core/author"Stoltz P."xsd:string
http://purl.uniprot.org/citations/19029431http://purl.uniprot.org/core/author"Zucker A.R."xsd:string
http://purl.uniprot.org/citations/19029431http://purl.uniprot.org/core/date"2009"xsd:gYear
http://purl.uniprot.org/citations/19029431http://purl.uniprot.org/core/name"Chest"xsd:string
http://purl.uniprot.org/citations/19029431http://purl.uniprot.org/core/pages"1186-1192"xsd:string
http://purl.uniprot.org/citations/19029431http://purl.uniprot.org/core/title"Beta2-adrenergic receptor polymorphisms affect response to treatment in children with severe asthma exacerbations."xsd:string
http://purl.uniprot.org/citations/19029431http://purl.uniprot.org/core/volume"135"xsd:string
http://purl.uniprot.org/citations/19029431http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/19029431
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