The
Arg/Arg homozygosity at
codon 16 of the beta-2-adrenoreceptor (ADRB2) gene has been thought to predispose
asthma patients to a poorer therapeutic response to beta-2-mimetics, or to worse control of the disease. In contrast, the results of the studies analysing the effect of ADRB2 polymorphisms on the response to beta-2-adrenoreceptor agonists in
chronic obstructive pulmonary disease (
COPD) patients are sparse and inconclusive. The aim of this research was to verify if p.Arg16Gly (c.46A > G) and p.Gly27Glu (c.79G > C) single nucleotide polymorphisms (SNPs) exert a negative effect on the selected clinical indicators of
COPD. The SNPs of the ADRB2 were identified by multiplex allele-specific PCR on
DNA isolated from the venous blood leukocytes of 92 patients with stable grade
COPD. In addition, all of the patients were asked about the course of
COPD during the 12 months preceding the study, including the frequency of exacerbations requiring hospitalisation, the number of
antibiotic therapy courses given due to the lower
respiratory tract infection, and the number of courses of systemic
corticosteroid therapy administered due to the exacerbation of
COPD.
Arg/Arg homozygotes at
codon 16 required at least two courses of
antibiotic therapy administered as a result of a lower
respiratory tract infection significantly more frequently than carriers of other polymorphic variants of the ADRB2. Moreover, they were the only ones who required three or more courses of
corticosteroid therapy due to
COPD exacerbation. No significant relationships were observed between the polymorphism at
codon 27 and the analysed clinical indicators of
COPD severity. These data suggested that
Arg/Arg homozygosity at
codon 16 of the ADRB2 gene predisposes patients to a clinically more severe course of
COPD.