Comparison of pulmonary function in patients with COPD, asthma-COPD overlap syndrome, and asthma with airflow limitation.
BACKGROUND
This study was conducted in order to investigate the differences in the respiratory physiology of patients with chronic obstructive pulmonary disease (COPD), asthma-COPD overlap syndrome (ACOS), and asthma with airflow limitation (asthma FL(+)).


METHODS
The medical records for a series of all stable patients with persistent airflow limitation due to COPD, ACOS, or asthma were retrospectively reviewed and divided into the COPD group (n=118), the ACOS group (n=32), and the asthma FL(+) group (n=27). All the patients underwent chest high-resolution computed tomography (HRCT) and pulmonary function tests, including respiratory impedance.


RESULTS
The low attenuation area score on chest HRCT was significantly higher in the COPD group than in the ACOS group (9.52±0.76 vs 5.09±1.16, P<0.01). The prevalence of bronchial wall thickening on chest HRCT was significantly higher in the asthma FL(+) group than in the COPD group (55.6% vs 25.0%, P<0.01). In pulmonary function, forced expiratory volume in 1 second (FEV1) and peak expiratory flow rate were significantly higher in the asthma FL(+) group than in the ACOS group (76.28%±2.54% predicted vs 63.43%±3.22% predicted, P<0.05 and 74.40%±3.16% predicted vs 61.08%±3.54% predicted, P<0.05, respectively). Although residual volume was significantly lower in the asthma FL(+) group than in the COPD group (112.05%±4.34% predicted vs 137.38%±3.43% predicted, P<0.01) and the ACOS group (112.05%±4.34% predicted vs148.46%±6.25% predicted, P<0.01), there were no significant differences in functional residual capacity or total lung capacity. The increase in FEV1 in response to short-acting β2-agonists was significantly greater in the ACOS group than in the COPD group (229±29 mL vs 72±10 mL, P<0.01) and the asthma FL(+) group (229±29 mL vs 153±21 mL, P<0.05). Regarding respiratory impedance, resistance at 5 Hz and resistance at 20 Hz, which are oscillatory parameters of respiratory resistance, were significantly higher in the asthma FL(+) group than in the COPD group at the whole-breath (4.29±0.30 cmH2O/L/s vs 3.41±0.14 cmH2O/L/s, P<0.01 and 3.50±0.24 cmH2O/L/s vs 2.68±0.10 cmH2O/L/s, P<0.01, respectively), expiratory, and inspiratory phases.


CONCLUSIONS
Although persistent airflow limitation occurs in patients with COPD, ACOS, and asthma FL(+), they may have distinct characteristics of the respiratory physiology and different responsiveness to bronchodilators.
First Department of Internal Medicine, Shinshu University School of Medicine, Matsumoto, Japan.
Yoshiaki
Y
Kitaguchi
First Department of Internal Medicine, Shinshu University School of Medicine, Matsumoto, Japan.
Masanori
M
Yasuo
First Department of Internal Medicine, Shinshu University School of Medicine, Matsumoto, Japan.
Masayuki
M
Hanaoka
D000280:Administration, Inhalation; D058666:Adrenergic beta-2 Receptor Agonists / Q000008:administration & dosage; D000368:Aged; D000403:Airway Resistance; D001249:Asthma / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology*; D001993:Bronchodilator Agents / Q000008:administration & dosage; D005260:Female; D005541:Forced Expiratory Volume; D006801:Humans; D008168:Lung / Q000000981:diagnostic imaging / Q000187:drug effects / Q000503:physiopathology*; D008297:Male; D008499:Medical Records; D036501:Metered Dose Inhalers; D010366:Peak Expiratory Flow Rate; D010641:Phenotype; D017265:Procaterol / Q000008:administration & dosage; D029424:Pulmonary Disease, Chronic Obstructive / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology*; D011656:Pulmonary Emphysema / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology*; D012189:Retrospective Studies; D013147:Spirometry; D013577:Syndrome; D014057:Tomography, X-Ray Computed
D058666:Adrenergic beta-2 Receptor Agonists; D001993:Bronchodilator Agents; D017265:Procaterol
ACOS; FOT; MostGraph; respiratory impedance