Extract Comorbidities are common in chronic obstructive pulmonary disease (COPD), and clusters of co-occurring conditions (i.e. phenotypes) have been described 1, 2. These phenotypes capture clinical profiles but do not explain the underlying biological endotypes. Biomarker studies can link phenotypes to endotypes, identify drivers of disease progression, and suggest targets for intervention 3. Systemic inflammation is often proposed as a shared driver of COPD and its comorbidities 1, 4, but direct evidence remains elusive. Systemic processes beyond inflammation may also contribute. Biomarkers of tissue remodelling and injury, including extracellular matrix (ECM) fragments and markers of neutrophil activity and epithelial damage, have been proposed useful in COPD 5, 6, yet their relationship with comorbidities is largely unexplored.
Egerod et al. (Thu,) studied this question.