Beta2-adrenergic receptor polymorphisms in African American children with status asthmaticus.
BACKGROUND
The beta2-adrenergic receptor plays a central role in the bronchodilator response to beta2-agonists in patients with asthma. Genetic polymorphisms within the gene coding for this receptor influence responsiveness of the receptor. A number of these polymorphisms differ in frequency in the African American and white populations.


OBJECTIVE
To determine the frequency of specific beta2-adrenergic receptor polymorphisms in African American children with status asthmaticus and to examine whether a specific genotype is associated with the clinical response to therapy.


METHODS
Cohort of African American children diagnosed with status asthmaticus.


METHODS
Tertiary care children's hospital.


METHODS
A total of 31 African American children with status asthmaticus.


METHODS
Blood samples were obtained from children at admission. Genotypes were determined by polymerase chain reaction amplification and restriction enzyme digestion.


METHODS
The requirement for admission to the pediatric intensive care unit, need for mechanical ventilation, institution of various therapies, and length of stay.


RESULTS
The genotypes of the polymorphic sites at amino acid positions 16 and 27 in the beta2-adrenergic receptor were determined. There were no significant differences between the various genotypes in the percentage of children requiring pediatric intensive care unit admission, mechanical ventilation, terbutaline treatment, or length of stay. However, in children heterozygous for Glu at position 27 of the beta2-adrenergic receptor, the percentage of patients requiring aminophylline treatment, in addition to beta2-agonist therapy, was significantly higher than that seen in patients homozygous for Gln at that position (5/10 [50%] vs. 1/21 [5%], respectively; p = .002).


CONCLUSIONS
African American children with status asthmaticus who have the Gln/Glu genotype at amino acid position 27 of the beta2-adrenergic receptor may benefit from aminophylline treatment in addition to beta2-agonist therapy.
Elbahlawan
Lama
L
St. Jude Children's Research Hospital, University of Tennessee Health Science Center, Memphis, TN, USA
Binaei
Saeed
S
Christensen
Michael L
ML
Zhang
Qing
Q
Quasney
Michael W
MW
Dahmer
Mary K
MK
D000293:Adolescent; D058666:Adrenergic beta-2 Receptor Agonists; D000318:Adrenergic beta-Agonists / Q000008:administration & dosage / Q000494:pharmacology*; D001741:Black or African American / Q000235:genetics*; D000628:Aminophylline / Q000008:administration & dosage / Q000494:pharmacology; D002648:Child; D002675:Child, Preschool; D004359:Drug Therapy, Combination; D005260:Female; D005787:Gene Frequency; D006239:Haplotypes; D006801:Humans; D008297:Male; D010641:Phenotype; D010726:Phosphodiesterase Inhibitors / Q000008:administration & dosage / Q000494:pharmacology; D020641:Polymorphism, Single Nucleotide; D018343:Receptors, Adrenergic, beta-2 / Q000235:genetics*; D013224:Status Asthmaticus / Q000188:drug therapy* / Q000208:ethnology / Q000235:genetics*; D013714:Tennessee / Q000453:epidemiology
D058666:Adrenergic beta-2 Receptor Agonists; D000318:Adrenergic beta-Agonists; D010726:Phosphodiesterase Inhibitors; D018343:Receptors, Adrenergic, beta-2; D000628:Aminophylline