Alvar Agusti, Rosa Faner

European Respiratory Journal 2023 62: 2301470; DOI: 10.1183/13993003.01470-2023

Extract

Traditionally, COPD has been understood to be a self-inflicted disease caused by tobacco smoking, occurring in old, “susceptible” males and characterised by an accelerated decline of lung function with age [1, 2]. Yet, our understanding of the pathogenesis of COPD has changed very significantly over the past few years [3–6] and, as a result, it is now defined as a heterogeneous condition that results from gene (G)–environment (E) interactions occurring over the lifetime (T) of the individual (GETomics) that can damage the lungs and/or alter their normal development/ageing process [7]. As a result of this new understanding, the Global Initiative for Chronic Obstructive Lung Disease (GOLD) recognises the existence of a pre-COPD condition that identifies “… individuals of any age, with respiratory symptoms and/or other detectable structural (e.g. emphysema) and/or functional abnormalities (e.g. hyperinflation, reduced lung diffusing capacity, or rapid [lung function] decline), in the absence of airflow obstruction on post-bronchodilator spirometry […]. These patients may (or not) develop persistent airflow obstruction (i.e. COPD) over time” [7]. GOLD 2023 also recognises the category of PRISm (Preserved Ratio (hence no airflow obstruction) with Impaired Spirometry) [8] which may (or may not) develop chronic airflow limitation (CAL) over time [7]. Understanding better which pre-COPD patients eventually develop CAL (or PRISm) may allow earlier and more effective preventive and management interventions [9–12].