From the authors:
We admire the extensive chronic obstructive pulmonary disease (COPD) collaborative project COPACETIC, (COPD Pathology: Addressing Critical gaps, Early Treatment and diagnosis and Innovative Concepts) [1] currently being undertaken by F.A.A. Mohamed Hoesein and co-investigators, and appreciate their letter that highlights the difficulties in defining early COPD. It is now recognised that several distinct COPD phenotypes exist in genetically susceptible adult smokers [2]. The COPACETIC study recognises two of these phenotypes: airway obstruction (detected by spirometry) and emphysema (detected by low lung tissue density from computed tomography (CT) scans and low diffusing capacity). The statistical power of studies like COPACETIC to successfully demonstrate associations between COPD phenotypes and the genetic variants that increase the risk for each phenotype will be greatly enhanced by minimising the misclassification rate for each phenotype in study participants. Misclassification of the airway obstruction phenotype for research studies and when considering a diagnosis of COPD in individual patients in clinical settings will be greatly reduced by using the fifth percentile lower limits of the normal range for both forced expiratory volume in 1 s (FEV1)/forced vital capacity and for FEV1, as recommended by our open letter to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) committee [3].
In 1959, the Ciba Symposium coined the term “chronic nonspecific lung disease” (CNSLD) as an umbrella term grouping chronic bronchitis, asthma, emphysema and irreversible or persistent obstructive lung disease. This term was superseded by COPD, emphasising “a consistent use of asthma, emphysema, and [COPD], but restricts the use of chronic bronchitis to those patients with chronic bronchial hypersecretion without chronic airways obstruction” [4]. The vast majority of current evidence regarding the diagnosis, clinical course and treatment of COPD is based on the severe airway obstruction phenotype with a FEV1 <60% predicted. A vast evidence gap exists in the definition of mild or early COPD. Therefore, we risk mistreatment of individual patients when we attempt to treat mild COPD, because even in smokers with respiratory symptoms and airway obstruction on post-bronchodilator spirometry, but with an FEV1 >60% pred, we have a low degree of confidence that they belong to the 10–15% group of genetically susceptible smokers who will rapidly lose lung function if they continue smoking [5]. Hopefully, the COPACETIC study will follow the cohort members longitudinally to discover the baseline factors that will eventually allow clinicians to confidently predict which young adult smokers will develop clinically important COPD.
Meanwhile, we do not think that assembling a panel of clinicians to attempt a consensus about the diagnosis of COPD in a number of cases will be useful. Establishing a diagnosis is a means to an end: intervention. Apart from smoking cessation, which is effective at any level of FEV1, the cost-effectiveness of COPD interventions when FEV1 is >60% pred remains very poor, and, thus, screening or case-finding for early COPD should not currently be performed [6]. We are especially concerned for older persons who are classified as having COPD stage I, as such a designation may lead to inappropriate pharmacotherapy and delays in the consideration of other diagnoses, such as heart failure, which is common in older smokers [7].
Footnotes
Statement of Interest
Statements of interest for all authors of this manuscript can be found at www.erj.ersjournals.com/site/misc/statements.xhtml
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