COPD: time to improve its taxonomy?

Abstract

Due to well-conducted epidemiological studies and advances in genetics, molecular biology, translational research, the advent of computed tomography of the lungs and bioinformatics, the diagnosis of chronic obstructive pulmonary disease (COPD) as a single entity caused by susceptibility to cigarette smoke is no longer tenable. Furthermore, the once-accepted concept that COPD results from a rapid and progressive loss of lung function over time is not true for a sizeable proportion of adults with the disease. Now we know that some genetic predisposition and/or different environmental interactions (nutritional, infectious, pollution and immunological) may negatively modulate post-natal lung development and lead to poorly reversible airflow limitation later in life, consistent with COPD. We believe it is time to rethink the taxonomy of this disease based on the evidence at hand. To do so, we have followed the principles outlined in the 1980s by J.D. Scadding who proposed that diseases can be defined by four key characteristics: 1) clinical description (syndrome), 2) disorder of structure (morbid anatomy), 3) disorder of function (pathophysiology) and 4) causation (aetiology). Here, we propose a pragmatic approach to the taxonomy of COPD based on different processes that result in a similar syndromic presentation. It can accommodate changes over time, as the pathobiology that may lead to COPD expands. We hope that stakeholders in the field may find it useful to better define the patients now boxed into one single entity, so that specific studies can be designed and conducted for each type of COPDs.

FIGURE 1

Proposed taxonomy of chronic obstructive pulmonary diseases (COPDs) using the principles of Scadding [5]. Different aetiologies can be responsible for the expression of COPDs with or without airflow limitation. See text for further details.

FIGURE 2

Specific therapeutic and prophylactic interventions to consider in different taxonomic groups of chronic obstructive pulmonary diseases (COPDs). Although separated for the predominant aetiology, some patients may have different mechanisms contributing to the final expression of the disease. AAT: α₁-antitrypsin; ICS: inhaled corticosteroid.