The epidemiological impasse.

We read with interest the letter of QUANJER et al. [1] persuading the Global Initiative for Chronic Obstructive Lung Disease (GOLD) committee to abandon the fixed ratio of forced expiratory volume in 1 s (FEV1)/forced vital capacity (FVC) ,0.70 in favour of the lower limit of normal (LLN). We feel that, in the current debate, some basic epidemiological principles have been overlooked. We will briefly address these principles in an attempt to clear up the discussion. QUANJER et al. [1] point out that numerous studies have reported a higher prevalence of chronic obstructive pulmonary disease (COPD) when using the fixed FEV1/FVC ,0.70 criterion when compared with the LLN. They interpret this as an ''over-diagnosis'' of COPD [2]. However, this neither implies nor ascertains that the LLN is the superior diagnostic. Conversely, one can state that the LLN leads to ''underdiagnosis'' of COPD. As long as either the fixed criterion or the LLN are not compared with a gold standard of COPD (when possible, a test with specificity and sensitivity approaching 100%), one should rea-lise that it is impossible to label either criterion as superior. The only valid conclusion of comparative studies lacking that gold standard is that both criteria differ. How then to solve the issue? COPD is and remains a clinical diagnosis and therefore a panel decision on its absence or presence by taking into account all relevant clinical factors, such as age, respiratory complaints, smoking history, etc., is the classical approach. The fixed FEV1/FVC ,0.70 criterion and the LLN should subsequently be compared with that panel diagnosis of COPD and the sensitivity/specificity evaluated. Unfortunately, we are unaware of any such studies and, in the mean time, any discussion and debate about the superiority/inferiority of a particular spirometric threshold will remain unproductive. In conclusion, with the currently available literature it is impossible to label either threshold as superior or suitable. 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 under-taken 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 tomo-graphy (CT) scans and …