Researchers may be closer to finding the mechanism responsible for loss of lung elastic recoil and airflow limitation in nonsmokers with chronic asthma.
The study published today in the journal CHEST Unraveling the Pathophysiology of the Asthma-COPD Overlap Syndrome reported that both nonsmokers and smokers with chronic asthma share features of COPD. This conundrum, often referred to as asthma-COPD overlap syndrome (ACOS), has been assumed to be due to large and especially small airway remodeling.
The study found that many patients with asthma are at risk for COPD due to a proinflammatory and proteolytic cascade. This may lead to lung tissue breakdown and unsuspected diffuse, mild centrilobular emphysema that is not easily detected clinically.
While these characteristics of airflow obstruction are common in smokers, the mechanisms responsible for lung elastic recoil and persistent expiratory airflow limitation in nonsmokers remains unknown. Current knowledge about ACOS lack structure-function studies, which researchers believe may help to better unravel the mechanisms of ACOS.