Do asthma and COPD share enough characteristics such as reduced rate of airflow resulting from increased inflammation, along with similar responses to some forms of treatment, reduce the importance of differential diagnosis?
As noted by Barbara Yawn, MD, in “Differential Assessment and Management of Asthma vs Chronic Obstructive Pulmonary Disease,” asthma and chronic obstructive pulmonary disease (COPD) “are prevalent respiratory conditions with overlapping disease characteristics. Differentiation between asthma and COPD is important because several aspects of the guideline-recommended management strategies differ for these conditions.” However, despite that fact that there are differences between these conditions “in terms of age at onset, prevalence in relation to age and sex, potential for reversibility of airway obstruction, pathophysiology, and typical symptom presentation,” is it possible that these differences do not make much difference when it comes to treatment decisions?
The 2014 Annual Meeting of the American Academy of Allergy, Asthma & Immunology, held February 28 — March 4, 2014, in San Diego, CA, featured a “pro vs. con” debate between two clinicians that addressed this issue, with the presenters describing how COPD and asthma can be differentiated, and comparing and contrasting treatment options and treatment expectations for the two conditions.
For the debate, Stephen P. Peters, MD, PhD, Wake Forest Baptist Medical Center, Winston-Salem, NC, argued in favor of the proposition that the diagnosis of asthma versus COPD does not greatly affect treatment decisions. Nicola A. Hanania, MD, Associate Professor of Medicine at Baylor College of Medicine, Houston, TX, argued that despite sharing several overlapping characteristics, the differences between asthma and COPD are such that clinicians must distinguish between the two when making therapeutic decisions.
Peters began by pointing out that the two diseases share many common features, particularly airflow obstruction. Both are characterized by bronchial hyper-responsiveness and are typically treated with bronchodilators and inhaled corticosteroids (ICS).
To underscore his assertion that the two conditions are more alike than not, he referred to a recent paper by Moore and colleagues in the Journal of Allergy and Clinical Immunology that “identified five asthma subphenotypes that represent the severity spectrum of early-onset allergic asthma, late-onset severe asthma, and severe asthma with chronic obstructive pulmonary disease characteristics.”
Peters said this indicates a continuum of features that could usefully be covered by the term “chronic nonspecific lung disease” (CNSLD), adopted by proponents of the Dutch Hypothesis floated by Opie in 1961, which states that these diseases all result from a common genetic root and should be considered as one disease.
Peters implied that classification of diseases like COPD “can get out of hand,” and cited the American Thoracic Society guidelines published in the American Journal of Respiratory and Critical Care Medicine as an example.
Noting that asthma and COPD appear to be similar with respect to responsiveness to newer agents such as tioproprium, Peters cited the study by Kerstjens et al in the New England Journal of Medicine on the use of tiotropium to treat poorly controlled asthma, and as study by Hanania and colleagues, published in Respiratory Medicine, showing that combination treatment with fluticasone/salmeterol and tiotropium in patients with COPD “significantly improves lung function without increasing the risk of adverse events.”
Peters’ argument rested on the similarities in symptoms, physical characteristics such as airway obstruction, and response to therapy, whether traditional (bronchodilators and inhaled corticosteroids) or newer agents like tiotropium. He underscored his position by insisting that the placing of one or another label on a patient was not helpful in the clinic. “Treat the individual patient,” was his mantra.
In reply, Hanania was quick to seize on Peters’ seeming dependence on several outmoded concepts dating back to the 1960s. He insisted that the wealth of information about asthma and COPD since that time has revealed distinct pathophysiologies and responses to treatment, not to mention genetic susceptibilities and environmental factors. However, he did concede that there was some overlap in the characteristics of the two disorders.
Hanania proceeded to hammer out all the pertinent developments in our knowledge of asthma and COPD, referring to a schematic in an article on the multifaceted mechanisms in COPD published in the European Respiratory Journal in 2008, and a paper on bronchodilator response in patients with COPD also published in the European Respiratory Journal.
He mentioned various diagnostic procedures now in the armamentarium (including bronchodilator response, elastic recoil, diffusion capacity, lung volume, and exhaled nitric oxide) that allow clinicians to make diagnostic distinctions leading to more effective choices for therapy.
Furthermore, Hanania pointed out, the genotypes are not the same for asthma and COPD and the disease courses differ. COPD is invariably progressive while asthma tends to be episodic with acute exacerbations and remissions.
In conclusion, Hanania said the preponderance of evidence supports the position that asthma and COPD require different approaches to treatment.