For decades, COPD management has largely focused on bronchodilation, with long-acting beta-agonists (LABAs) and long-acting muscarinic antagonists (LAMAs) serving as primary treatment options.1 However, growing evidence supports the role of airway inflammation in COPD pathophysiology, particularly in patients with eosinophilic inflammation. This has led to the exploration of biologic therapies that selectively target inflammatory pathways.2
Monoclonal antibodies directed at IL-4 and IL-13 have emerged as a promising therapeutic approach for COPD patients with elevated eosinophils.2 These biologics, already utilized in asthma and eosinophilic esophagitis, modulate type 2 inflammation, reducing exacerbation rates and improving lung function. Unlike traditional COPD treatments, which primarily address airflow limitation, these agents directly modulate the inflammatory response, potentially altering disease progression in select patients.2
The differentiation of biologics from inhaled corticosteroids is particularly relevant, as ICS therapy has been widely used in eosinophilic COPD but has limitations secondary to elevated pneumonia risk in some populations. Precisely targeting IL-4 and IL-13 signaling offers a selective approach to inflammation management, potentially reducing systemic side effects associated with broad immunosuppression.2
As pulmonologists integrate these novel therapies into practice, patient selection will be critical. Blood eosinophil counts and biomarker-driven strategies will help identify individuals most likely to benefit.3The future of COPD treatment is shifting toward a more personalized model, allowing for tailored interventions that extend beyond symptomatic relief to address underlying disease mechanisms.
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