Send to

Choose Destination
Respir Med. 2009 Jan;103(1):98-103. doi: 10.1016/j.rmed.2008.07.025. Epub 2008 Sep 11.

CT scanning-based phenotypes vary with ADRB2 polymorphisms in chronic obstructive pulmonary disease.

Author information

Department of Internal Medicine, College of Medicine, Kangwon National University, Chuncheon, South Korea.



Chronic obstructive pulmonary disease (COPD) is a heterogeneous disease that is characterized by varying degrees of involvement of airway and lung parenchyma. Although cigarette smoke is the major risk factor for COPD, the principal determining factors of involvement of the airway or lung parenchyma have not been clearly defined. Genetic variability in COPD patients might influence the varying degrees of involvement of airway and parenchyma. We therefore studied whether airway and parenchyma involvement might be associated with the ADRB2 genotype, which has been reported to be associated with COPD susceptibility and the bronchodilator response.


One hundred and eleven COPD subjects, whose post-bronchodilator FEV(1)/FVC values were less than 0.7, and who had histories of smoking exceeding 10 pack-years, were prospectively recruited from pulmonology clinics of 11 hospitals in Seoul, Korea. The degrees of involvement of airway and parenchyma were evaluated by volumetric computed tomography (CT) scans. In-house software automatically calculated luminal areas, airway wall areas, percentages of wall areas in segmental bronchi, emphysema indices, and mean lung densities in the whole lung parenchyma. The ADRB2 genotypes at codon 16 were determined for all patients.


Gly16 was associated with lumen diameter, luminal area, and percentage of wall area in patients with COPD (p=0.02), whereas neither wall area nor wall thickness differed with ADRB2 genotype. Neither emphysema index nor mean lung density was associated with ADRB2 genotype.


Gly16 variant in ADRB2 gene was associated with airway wall phenotypes measured using CT scanning in COPD patients.

[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center