To the Editor:
We read with great interest the recent article published in CHEST by Awan et al.1 The study presents convincing evidence that radiomic texture features from CT scans are linked to markers of systemic inflammation and increased death risk in individuals with COPD. This work marks an important step forward in the use of imaging biomarkers to improve clinical risk assessment and patient treatment.
Interestingly, this study found no significant association between blood eosinophil levels and CT scan texture features. This finding stands in contrast to prior observations from large COPD cohorts, such as COPDGene and SPIROMICS, where blood eosinophil counts have been linked to specific imaging phenotypes, which includes airway remodeling and emphysema patterns.2,3 This difference raises important questions about how eosinophilic COPD presents on imaging and highlights the heterogeneity within this disease. The discrepancy underscores the complexity of COPD inflammatory endotypes and suggests that eosinophilic inflammation may lead to structural changes that are not captured fully by current texture-based radiomic methods. Given that newer biologic therapies that target eosinophilic inflammation, such as anti-IL-5 and anti-IL-13 treatments, are now available and show promise in managing eosinophilic COPD, further exploration into how these biologics interact with imaging features could lead to more tailored and effective treatment strategies for this subset of patients.4
Additionally, this study does not address specifically the potential impact of autoimmune diseases on plasma biomarkers. Although the authors focus on associations between CT scan texture features, systemic inflammation, and death in COPD, it is not clear whether comorbid autoimmune conditions, which are known to influence inflammatory biomarkers, were accounted for. Autoimmune diseases can elevate markers such as C reactive protein, IL-6, and tumor necrosis factor-α independently of COPD, and their presence might confound interpretations of systemic inflammation.5 It would be valuable to know whether these factors were considered or adjusted for in the analysis. Future research would benefit from explicitly accounting for autoimmune comorbidities to enhance the specificity of biomarker-based risk stratification in COPD.
Financial/Nonfinancial Disclosures
None declared.
References
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