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Real-world effectiveness of dupilumab in COPD: a German multicenter analysis
Mustafa Abdo1, Dirk Skowasch2, Timm Greulich3,4
1Department of Internal Medicine I, University Medical Center Schleswig-Holstein Campus Kiel, Airway Research Center North (ARCN), German Center for Lung Research (DZL), Arnold-Heller-Str 3, 24105, Kiel, Germany. respabdo@gmail.com.
Background:
Dupilumab reduced exacerbations in patients with COPD and type 2 inflammation in clinical trials; however, multicenter real-world data remain limited.
Methods:
We performed a multicenter analysis of patients with COPD treated with dupilumab across centers in Germany. Patients with comorbid asthma were included to compare outcomes between COPD-only patients and those with comorbid asthma, as well as between patients with and without chronic bronchitis (CB). The primary endpoint was change in the annualized rate of moderate-to-severe exacerbations. Changes in lung function and CAT score were also assessed.
Results:
A total of 99 patients were included (60% male, mean age 66 years, FEV₁ 37% predicted, DLCO 41% predicted, 45% comorbid asthma, 58% CB, 7% current smokers). Over a median follow-up of 11 months [IQR 8-14], dupilumab reduced the annualized moderate-to-severe exacerbation rate from 3.52 (95% CI 2.94-4.09) at baseline to 1.04 (95% CI 0.71-1.37) during follow-up, corresponding to a 70% reduction. Reductions in exacerbation rates were consistent irrespective of exacerbation severity, comorbid asthma, CB, or emphysema severity. CAT improved by a mean of 4.5 points. FEV₁ improved by 50 mL (p = 0.077), while greater improvements were observed for residual volume (- 150 mL; p = 0.071) and total airway resistance (- 12.6%; p < 0.001). Eight patients were non-responders and had no reduction in exacerbation under treatment.
Conclusion:
In this real-world multicenter cohort, dupilumab effectively reduced exacerbation burden in patients with COPD and type 2 inflammation. Exploratory subgroup analyses suggested consistent treatment effects across different clinical phenotypes, although these findings require confirmation in larger studies. The high baseline exacerbation burden may partly explain the marked treatment response.
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