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
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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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