From Queen’s University and Kingston General Hospital.
Correspondence to: Denis E. O’Donnell, MD, FCCP, Queen’s University and Kingston General Hospital-Medicine, 102 Stuart St, Kingston, ON, K7L 2V6, Canada; e-mail: email@example.com
Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.
Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).
© 2012 American College of Chest Physicians
We thank Drs van den Bemt and Schermer for their thoughtful comments on our recent article in CHEST1 on the confounding influence of increased body mass on the diagnosis of COPD. Given the dramatic global increases in the prevalence of both obesity and COPD over the past decades, we can no longer neglect the impact of this combination on common pulmonary function measurements and their clinical interpretation. The interaction of COPD and obesity is complex and poorly understood, given the vast pathophysiologic heterogeneity of both conditions.
COPD essentially remains a clinical diagnosis based on the triad of smoking (or other noxious gas) exposure, the presence of persistent respiratory symptoms, and the objective demonstration of airflow obstruction that is not fully reversible. The definition of airway obstruction based on postbronchodilator fixed FEV1/FVC ratio <0.7 has been criticized because of the risk of overdiagnosis in the elderly and underdiagnosis in the young.2,3 Less attention has been given to the risk of underdiagnosis of COPD in obese smokers by fixed ratio criteria, given the documented exponential decline in thoracic gas volumes (the denominator) with increasing BMI.1,4
Diagnosis of COPD is further confounded in overweight individuals by uncertainty concerning the specific origin of their respiratory symptoms. Thus, activity-related dyspnea in the obese smoker could be explained by factors other than airflow obstruction: higher ventilatory demands as a result of higher metabolic requirements of the physical task, skeletal muscle deconditioning due to decreased activity, or increased mechanical loading of the respiratory muscles due to decreased respiratory system compliance.5
The solution to this complex diagnostic dilemma is not simple. Reliance on a lower limit of normal criteria for FEV1/FVC based on population norms (instead of fixed ratio criteria) may not be the answer because the prevalence of obesity may be underestimated in the existing reference populations from which normative data were derived. Moreover, predictive equations for plethysmographic lung volumes have accounted for the influence of age, height, and sex but not of BMI per se. Future prospective population studies are urgently required to better clarify how the presence of obesity affects the diagnosis of COPD.
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