Endo-phenotyping of COPD patients

Chronic obstructive pulmonary disease (COPD) is a heterogeneous syndrome and may comprise several different phenotypes that are driven by different molecular mechanisms (endotypes). Several different clinical, genetic, and inflammatory phenotypes of COPD have been recognized and this may lead to more precise effective therapies.

The different clinical phenotypes, including smoking versus nonsmoking COPD, small airway disease versus emphysema, non-exacerbators versus frequent exacerbators are discussed. Rare genetic endotypes (alpha₁-antitrypsin deficiency, telomerase polymorphisms), and inflammatory phenotypes (eosinophilic versus neutrophilic) are also recognized in stable and exacerbating patients and have implications for the choice of therapy.

Clinical phenotypes have so far not proved to be very useful in selecting more personalized therapy for COPD. Even with genetic endotypes, this has not led to improved therapy. More promising is the recognition that COPD patients who have increased sputum or blood eosinophils tend to have more frequent exacerbations and inhaled corticosteroids are more effective in preventing exacerbation. Increased blood eosinophils have proved to be a useful biomarker now used to target ICS more effectively. Furthermore, COPD patients with low eosinophils are more likely to get pneumonia with ICS and to have lower airway bacterial colonization.