26 Jul Asthma-COPD Overlap
Most clinicians can easily distinguish asthma and COPD. Asthma usually has an early onset with intermittent symptoms, a good response to inhaled therapy, and is often associated with other allergic diseases, whereas COPD is of late onset, slowly progressive symptoms, poor response to inhaled therapy, and is usually associated with long-term smoking. However, patients can sometimes have features of both diseases, and this condition has been termed asthma-COPD overlap (ACO). Some overlap may be predicted because asthma and COPD are both common, and there is no evidence that one disease protects against the other.
ACO includes different phenotypes, such as patients with COPD and eosinophilic inflammation, patients with asthma and severe disease or who smoke in whom there is predominantly neutrophilic inflammation, and patients with asthma who have largely irreversible airway obstruction due to structural changes. Therefore it is important to recognise whether a patient has ACO because this determination may influence the clinical course, long-term outlook, and response to therapy.
There is general agreement from several studies that 10% to 20% of patients with COPD have features of asthma, with most studies reporting these patients having a worse prognosis, in terms of more frequent and severe exacerbations, more frequent symptoms, worse quality of life, more comorbidities, and less emphysema as noted on CT scans.
COPD patients with asthma may have infiltration of eosinophils in the airways, and this may be driven by type 2 innate lymphoid cells, which secrete IL-5 but are not activated by allergens. There is an increased concentration of IL-5 in the sputum of patients with COPD who have increased eosinophils, and both are reduced by oral prednisolone. By contrast, patients with asthma and features of COPD may have predominantly neutrophilic inflammation or no increase in inflammatory cells.
Some studies suggest that patients with COPD and increased eosinophil counts may benefit from triple therapy with the addition of an inhaled corticosteroid to long-acting β2-agonist and anticholinergic inhalers. Similarly, asthmatic patients with COPD features may benefit from the addition of a long-acting anticholinergic agent to an inhaled corticosteroid/long-acting β2-agonist combination.
ACO is a clinical reality and is important to identify, with diagnosis currently done by clinical assessment, including history, exposure, and bronchodilator reversibility, which are imprecise. Airway eosinophilia may be measured by using sputum eosinophil counts or fractional exhaled nitric oxide. Blood eosinophil counts are easy to perform and may reflect airway eosinophilia and predict corticosteroid responsiveness. Sputum neutrophilia is not reflected by circulating neutrophils and can only be detected by examination of induced sputum, however. A formal trial of oral corticosteroids (prednisolone or prednisone 30 mg daily for 2 weeks) may be useful for identifying an asthmatic component in patients with COPD (with improvement in FEV1 > 15% or 200 mL).
Peter J. Barnes, Master FCCP. CHEST, January 2016, Volume 149, Issue 1, Pages 7–8