Elevating COPD Management: Enhancing Treatment and Improving Patient Outcomes - Episode 8
Prevalence and Clinical Features of Type 2 Inflammation in COPD
Panelists discuss the prevalence and complexity of type 2 inflammation in chronic obstructive pulmonary disease (COPD), noting that blood eosinophil counts—using thresholds of 150 to 300 cells/µL—identify roughly 30% to 50% of patients with this phenotype, while emphasizing that not all elevated eosinophil cases reflect true type 2 inflammation; they highlight additional markers like allergen sensitization and immunoglobulin E (IgE), the association of type 2 inflammation with increased symptoms and exacerbations, and the ongoing need for refined phenotyping and targeted therapies to address the heterogeneity of COPD inflammation.
Type 2 inflammation in COPD is recognized in a substantial subset of patients, with blood eosinophil counts serving as the primary biomarker for identification. Estimates suggest that approximately 30% to 40% of patients with COPD exhibit features consistent with type 2 inflammation when a threshold of 300 cells/µL is applied. Lowering this cutoff to 150 cells/µL may increase the prevalence to around 40% to 50%, though precise figures remain uncertain and debated in the literature. It is also important to note that not all patients with elevated eosinophils fully display type 2 inflammatory characteristics, highlighting the complexity and heterogeneity of this phenotype. Moreover, a significant portion of patients with COPD do not have type 2 inflammation, representing an ongoing challenge in understanding and managing the broader COPD population.
Clinically, elevated eosinophil levels have been associated with increased symptoms and a higher frequency of exacerbations in COPD, though this relationship appears less consistent than in asthma. Beyond eosinophil counts, other clues to the presence of type 2 inflammation include allergen sensitization and elevated IgE levels, particularly in patients with upper airway symptoms. This allergic phenotype of COPD, while less studied, may represent an important subgroup with type 2 inflammation that does not always correlate directly with eosinophil counts. Phenotyping based on eosinophil counts and allergen sensitization can help guide therapeutic decisions, especially in patients with frequent exacerbations or more severe disease.
Currently, blood eosinophils remain the most accessible and practical biomarker for identifying type 2 inflammation in COPD. Additional markers such as sputum eosinophils and IgE may be informative but are less commonly used in routine clinical practice. Peripheral neutrophil counts, despite being easily obtained, have limited utility in reflecting airway inflammation or guiding treatment decisions in COPD. Ongoing research aims to better understand the heterogeneity of inflammation in COPD and to develop more targeted therapies for both eosinophilic and non-eosinophilic phenotypes. Until then, eosinophil counts offer a valuable tool for recognizing and managing the subset of patients with COPD with type 2 inflammatory features.
