ADRB2 GENE POLYMORPHISMS AND SALBUTAMOL RESPONSIVENESS IN SERBIAN CHILDREN WITH ASTHMA
Jovicic N, Babic T, Dragicevic S, Nestorovic B, Nikolic A
*Corresponding Author: Dr. Nevena Jovicic, Department of Pulmonology and Allergology, University Children’s Hospital, Tirsova 10, 11000 Belgrade, Serbia. Tel: +38-164-115-6721. Fax: +38-111-268-5378. E-mail: jovicic.nevena@gmail.com
page: 33

RESULTS

The study included a group of 54 asthmatic children (6-18 years old, 22 girls and 32 boys), whose demographic and clinical characteristics are presented in Table 1. All asthmatic children were of a Serbian ethnic group. The patients were divided in accordance with GINA 2016 guidelines into three groups according to their asthmatic severity: mild, moderate and severe. There was no association of age or gender with asthma severity in this group of patients. All patients were genotyped for the ADRB2 gene polymorphisms +46A>G and +79C>G by direct DNA sequencing. Allele +46A was detected with a frequency of 41.7%, while allele +79G was detected with a frequency of 23.1% (Table 1). Response to salbutamol (measured by recording the change in the percentage of FEV1 before and after salbutamol administration and expressed as a percentage difference in FEV1 (dFEV1) after and before salbutamol administration) and severity of the disease were compared between carriers of different ADRB2 genotypes (Table 2). There was no significant difference in response to salbutamol between boys and girls. The presence of the +46G allele in the ADRB2 gene correlates with better bronchodilator response to salbutamol (p = 0.044). This allele was also associated with a mild form of the disease (p = 0.010). No significant association was found between the +79C>G polymorphism and asthma severity (p = 0.955) or better bronchodilator response to salbutamol (p = 0.316). In the analysis of the ADRB2 gene polymorphism distribution in respect to the clinical characteristics of asthmatic children, no significant association was found between carriers of the different genotypes (Table 2). The distribution of observed genotypes for +46A>G and +79C>G polymoprhisms were consistent with the Hardy-Weinberg equilibrium (p = 0.050 and p = 0.359, respectively). The three allele combinations were identified in our group of patients: +46A/+79C (41.7%), +46G/+79C (35.2%) and +46G/+79G (23.1%). The response to salbutamol and asthma severity were compared between carriers of these allele combinations. We found no statistically significant difference in severity of asthma. In the group of children with the +46A>G polymorphism and severe asthma, 41.2% of cases were carriers of the +46GG genotype that is associated with the best bronchodilator response. In patients with the +46A/+79C combination, the response to salbutamol was significantly worse than in patients with the other two allele combinations (dFEV1 9.4 ± 6.2 vs. 14.4 ± 6.1%, p = 0.026). There was no significant difference in response of the homozygous and heterozygous carriers of the +46A allele.



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