The variability of the pharmacological response to beta 2 (β2)-agonists may be due to the polymorphism of the gene of β2 adrenergic receptor (ADRβ2). The objective of our research was to evaluate the significance of ADRβ2 gene polymorphism in the 16th amino acid position in the efficiency of broncholytic therapy by β2-agonists among children with bronchial asthma.Materials and methods
We defined the type of ADRβ2 gene among 208 children with bronchial asthma of various severity by means of polymerase chain reaction. The distribution of the patients into two groups was carried out subject to the efficiency of the β2-agonists based short-term therapy during the exacerbation of bronchial asthma. 171 children received the inhaled glucocorticoids.Results
Singled out statistically significant differences of the genotype distribution. The Gly/Gly16 homozygous allele was discovered twice as often in the group with an insufficient response to β2-agonists than in the group with a good response (66 vs 38%, P<0.001), while the distribution of heterozygous allele was detected the opposite pattern (55 vs 28%, P<0.001). In the Arg/Arg16 genotype distribution, there were no considerable differences in both groups (6% in each group). In the subgroups of children, receiving the high doses of the inhaled glucocorticoids, there was a trend for the prevalence of Gly/Gly16 homozygous allele prevalence.Conclusion
We have discovered the association of the Gly/Gly16 genotype of the ADRβ2 gene with an insufficient effect of broncholytic therapy by means of short-term β2-agonists; we also revealed the participation of the Gly16 allele in the phenotype formation with the severe run of bronchial asthma and tolerance towards the therapy both by β2-agonists and inhaled glucocorticoids.