Asthma/Obstructive Pulmonary Disease Overlap

Update on Definition, Biomarkers, and Therapeutics

August Generoso; John Oppenheimer

Disclosures

Curr Opin Allergy Clin Immunol. 2020;20(1):43-47. 

In This Article

Disease Mechanism

Likely, the overlap seen clinically in ACO is related to the overlap in the underlying inflammatory pathophysiologic mechanisms of both asthma and COPD.[3] Traditionally, the inflammation associated with asthma is considered to be mediated by T2 high cytokines. However, some patients (who often have the most severe or recalcitrant disease) do not respond to T2 high-targeted therapeutics. These patients are instead thought to have neutrophilic or pauci-granulocytic pattern of inflammation.

Meanwhile, the inflammation associated with COPD is generally considered to be mediated by neutrophils. However, increasing evidence suggests that some COPD patients have T2 high phenotype. Eosinophils (in sputum, bronchoalveolar lavage, and lung tissue) have been reported in 15–40% of patients with stable COPD.[10–12]

Furthermore, a cluster analysis by Ghebre et al.[13] examining sputum from patients with obstructive lung disease found three clusters: asthma predominant (eosinophilic), COPD predominant (mixed eosinophilic and neutrophilic), and ACO (neutrophilic). Such findings further highlight the need to study the inflammatory milieu present in ACO.

The heterogeneity in mucosal inflammation in asthma and COPD described above likely manifests as the various phenotypes observed clinically in both diseases.

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