Background: The beta2-adrenergic receptors are cell surface receptors playing a central role in the pharmacological targeting asthma and chronic obstructive pulmonary disease [COPD]. Recent studies suggest that patients who are homozygous for one of the two important polymorphisms of the beta2-adrenergic receptor [ADRB2] gene at codon 16 (arginine to glycine) and 27 (glutamine to glutamate) may have a reduced response to ss2-agonists. Since smoking patients who are Gly16 homozygotes have an increased risk of airway obstruction we hypothesized that beta2-adrenoreceptor gene polymorphisms may be also a cofounder for COPD development and disease severity.
Methods: We investigated 190 COPD patients and 172 healthy volunteers in a case-control study. DNA was isolated from whole blood and beta2-AR gene polymorphisms Arg/Gly16 and Gln/Glu27 were determined using allele-specific polymerase chain reaction [PCR].
Results: In COPD patients with Gly/Gly16 was found more frequently than in healthy smokers [29.47% COPD versus 18.18% controls, p = 0.026]. All other gene polymorphisms of the ADRB2 gene at codon 16 were equally distributed between groups. ss2-adrenoreceptor gene polymorphisms were neither a cofounder for COPD exacerbations [>or= 3 hospitalizations within the last 3 years] nor for disease severity [FEV1 <or= 30% predicted].
Conclusion: Our study suggests that the Gly16 allele of the beta2-AR gene predisposes to COPD development but not for exacerbation rates and disease severity. In contrast, Gln/Glu27 polymorphism was irrelevant in our COPD cohort.