Neutrophils, airway hyperresponsiveness and COPD: true, true and related?

O nce upon a time distinguishing between COPD and asthma in a smoking or ex-smoking patient was easy: a patient who smoked, had a low diffusing capacity of the lung for carbon monoxide or a hyperlucent radiogram, and no bronchodilator response was labelled as COPD; whereas a patient who, whether they smoked or not, had a bronchodilator response and airway hyperresponsiveness (AHR) was an asthmatic. Nothing could be simpler; that is until studies of asthmatics included measurements of inflammation and studies of patients with COPD included performing methacholine challenges. We now know that significant bronchodilator responses can be present in many patients with COPD [1] and, as discussed below, airway responsiveness is also not a stable feature of asthma. As determined by unbiased analysis, such as cluster or factor analysis, asthma [2, 3] and COPD [4] both have been shown to have distinctly different clinical phenotypes. While there is no doubt that these phenotype assignments will prove to be variable, irreproducible and effervescent, at least this clustering of patients’ characteristics provides a conceptual framework to advance the field. The clinical significance is that if a patient with airway disease is assigned a phenotype, then a targeted, effective treatment will be forthcoming, or at least that is the hope.