| Summary: | <p>Abstract</p> <p>Background</p> <p>Chronic obstructive pulmonary disease (COPD) is characterized by irreversible airflow limitation and airway inflammation, accompanied by decreased health status. It is still unknown which factors are responsible for the impaired health status in COPD. We postulated that airway inflammation negatively contributes to health status in COPD.</p> <p>Methods</p> <p>In 114 COPD patients (99 male, age: 62 ± 8 yr, 41 [31–55] pack-years, no inhaled or oral corticosteroids, postbronchodilator FEV<sub>1</sub>: 63 ± 9% pred, FEV<sub>1</sub>/IVC: 48 ± 9%) we obtained induced sputum and measured health status (St. George's respiratory questionnaire (SGRQ)), postbronchodilator FEV<sub>1</sub>, hyperinflation (RV/TLC), and airway hyperresponsiveness to methacholine (PC<sub>20</sub>). Sputum was induced by hypertonic saline and differential cell counts were obtained in 102 patients.</p> <p>Results</p> <p>Univariate analysis showed that SGRQ total and symptom score were positively associated with % sputum macrophages (r = 0.20, p = 0.05; and r = 0.20, p = 0.04, respectively). Multiple regression analysis confirmed these relationships, providing significant contributions of % sputum macrophages (B = 0.25, p = 0.021) and RV/TLC (B = 0.60, p = 0.002) to SGRQ total score. Furthermore, SGRQ symptom score was associated with % sputum macrophages (B = 0.30, p = 0.03) and RV/TLC (B = 0.48, p = 0.044), whilst SGRQ activity score was associated with % sputum macrophages (B = 0.46, p = 0.002), RV/TLC (B = 0.61, p = 0.015), and PC<sub>20 </sub>(B = -9.3, p = 0.024). Current smoking and FEV<sub>1 </sub>were not significantly associated with health status in the multiple regression analysis.</p> <p>Conclusion</p> <p>We conclude that worse health status in COPD patients is associated with higher inflammatory cell counts in induced sputum. Our findings suggest that airway inflammation and hyperinflation independently contribute to impaired health status in COPD. This may provide a rationale for anti-inflammatory therapy in this disease.</p>
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