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COPD Phenotypes: The Answers are in the Noise

While the classification of COPD into subsets of disease pathophysiology and severity has always been of interest to the medical community, never before have these issues been as important as we attempt to unravel the biochemical mechanisms and genetic variations manifesting in various subtypes of disease. Despite a common etiologic agent, tobacco smoke, the individual variation in the manifestation of disease may be quite remarkable. It is likely that variations in phenotypic presentation result from differences in basic molecular‐cellular pathogenic cascades due to genetic variations in the response to environmental agents. The comprehensive discussion by Dr. Friedlander and colleagues describes the remarkable variability in patients who share the simple label of “COPD”; for example, subjects sharing similar decrements in FEV1, the traditional metric of disease severity, may in fact vary greatly with respect to the extent and distribution of parenchymal emphysema and airway involvement (1). Additionally, the systemic pathology associated with COPD, including myopathy, malnutrition, coronary artery disease, osteoporosis and depression may vary greatly between individuals. It is likely that better characterization of these physiological, anatomical and clinical phenotypic subsets and their associations with specific pathogenic mechanisms will lead to earlier disease detection, better determination of prognosis, identification of unique therapeutic targets, and determination of short term surrogates of meaningful clinical response. The traditional approach of basic scientists in testing a hypothesis is to introduce or alter a single condition in eugenic mice such that any variation or “noise” in the experimental