ANALYSIS OF THE RELATIONSHIP OF POLYMORPHISM OF THE β2-ADRENORECEPTOR GENE TO BRONCHIAL ASTHMA FORMS AS WELL AS INDICATORS OF EXTERNAL RESPIRATORY ACTIVITY
Keywords:
bronchial asthma, Gln27Glu polymorphism of β2-adrenoreceptor gene, external respiratory function, salbutamolAbstract
Although significant progress has been made in the diagnosis and treatment of bronchial asthma (BA), the variety of forms of the disease, severe withdrawal options and responses to individual treatment leave it as one of the pressing problems in the health system.
Research objective. To assess how the ADRB2 gene is distributed in the different phenotypes of the Gln27Glu Polymorph locus BA, and to determine to what extent the most basic parameters of external respiratory function are associated with this polymorphism.
Research material and methods: 120 people of Uzbek nationality were examined in order to learn that the Gln27Glu polymorphism of the ADRB2 gene is associated with various pathogenetic variants of Ba, the main indicators of their external respiratory activity, 80 of them patients with BA.
Results of the study: the results of the study of the genotype ADRB2 Gene Gln27Gln in allergic BA (ABA) patients found that the frequency of the homozygous variant of the gene being examined in this group of patients was reliably higher than in the control group (73% as well as 44.6%, respectively, χ2=4.7; p<0.05; OR=2.67). Variants of the homozygous genotype Glu27Glu were not observed among ABA patients. Patients with BA with the genotype Gln27Gln were found to respond to salbutamol-induced bronchodilation with a significant increase in FEV1 compared to those with the genotype Gln27Glu and Glu27Glu.
Conclusion: in Aba, the ADRB2 gene confirms that the gln27gln genotype, the Gln27 allele, may be an important factor in the development of BA. The greatest increase in FEV₁ in bronchodilating Synapse (salbutamol) was recorded in the genotype Gln27Gln, and the potential for maximum benefit from β₂-agonists was found to be higher in this genotype.
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