COPD as a small airways disease. Do we have a new pharmacotherapy target?

Alberto Fantin, Alessandra Manco, Annalisa Frizzelli, Ernesto Crisafulli


Chronic obstructive pulmonary disease (COPD) is characterized by a chronic airflow limitation caused by both small airways disease and parenchymal destruction [1]. The involvement of small airways is related to the progression of disease, with the accumulation of inflammatory mucous exudates in the lumen and infiltration of the wall as an innate and adaptive response [2] [3]; these changes are coupled to a remodeling process causing a thickness of the walls of airways [2] [3]. Structural changes affecting the terminal bronchioles precede emphysematous destruction [3]. The small airways, defined by an internal diameter ≤ 2 millimeters [1-4], represent in COPD patients the functional major site of airflow obstruction [1][2]; for this reason the term of small airways dysfunction (SAD) is often used to characterize it [1][2]. Due to discrepancy between the extensive damage of SAD and the occurrence of any symptom, the small airways are defined as a “silent zone” [1][2][5].

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