Abstract
Asthma and chronic obstructive pulmonary disease (COPD) are now recognized to be able to co-exist as asthma–COPD overlap (ACO). It is clinically relevant to evaluate whether patients with COPD concurrently have components of asthma in primary care. This is because: (i) ACO is a relatively common condition among asthma (over 40 years of age) or COPD irrespective of its diagnosis criteria; (ii) patients with ACO can have higher frequency of exacerbation and more rapid decline in lung function than those with asthma or COPD; and (iii) asthmatic features such as eosinophilic airway inflammation are promising indicators for prediction of inhaled corticosteroid-responsiveness in COPD. The aim of this review to evaluate diagnostic markers for ACO. We searched PubMed for articles related to ACO published until 2020. Articles associated with diagnostic biomarkers were included. We identified a total of 25 studies, some of which have revealed that a combination of biomarkers such as fractional exhaled nitric oxide and serum immunoglobulin E is useful to discern type 2 inflammation in the airways of COPD. Here, we review the current understanding of the clinical characteristics, biomarkers and molecular pathophysiology of ACO in the context of how ACO can be differentiated from COPD.
Highlights
We found that the sensitivity was 1.0 and the specificity was 0.56 for the subjects who had reversibility of airway obstruction by 12-week-inhalation therapy of fluticasone propionate (FP)/Salmeterol (SAL) when
There are important problems yet to be addressed in clinical practice for asthma–COPD overlap (ACO) and chronic obstructive pulmonary disease (COPD): Why should we have a diagnostic term of ACO? How can we distinguish between
We reported that excessive nitrosative stress and lower antioxidant capability were observed in neutrophils and macrophages collected from the airways of patients with ACO [136]
Summary
Asthma is a heterogenous and inflammatory disease affecting large and small respiratory tracts but not the lung parenchyma, and contains clusters of demographical, clinical and pathophysiological characteristics underpinned by different pathophysiological processes [5]. This heterogeneity may be explained by the complexity of dysregulated innate and adaptive inflammatory responses to exogenous allergens and proteases leading to the spectrum of abnormal tissue remodeling, where type 2 cytokines such as interleukin (IL)-4, IL-13 and IL-5 primarily promote airway eosinophil infiltration, mucus hypersecretion, bronchial hyperresponsiveness and mast cell activation [6]. In line with this translational study, accumulated evidence from randomized control trials have revealed the importance of ICS usage from the early steps of asthma treatment because clinical studies have shown that ICS robustly reduced the risk of symptoms, exacerbations, hospitalization and mortality from asthma [8,9,10]
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