Researchers Pinpoint Catalyst Behind Asthma-COPD Overlap Syndrome

A medical phenomenon called asthma-COPD overlap syndrome (ACOS) — is closer to being understood by researchers.

Among nonsmokers with chronic asthma, ACOS occurs when the patient suffers from a loss of lung elasticity and airflow limitation—symptoms mimicking COPD. However, recent evidence indicated this condition occurred because of large and small airway reconstruction.

“The mechanism(s) responsible for loss of lung elastic recoil and persistent expiratory airflow limitation in nonsmokers with chronic asthma consistent with ACOS remain unknown in the absence of structure-function studies,” the authors wrote in the August issue of CHEST.

For their study, Arthur Gelb, MD, FCCP of the Geffen School of Medicine at University of California, Los Angeles (UCLA) Medical Center, and his colleagues observed ten asthma patients who didn’t smoke, but suffered from constant airflow obstruction despite “partial reversibility.”

From this analysis, the team found certain people with asthma were susceptible for COPD development due to pro-inflammatory and proteolytic cascade, which could trigger the degradation of lung tissue breakdown and unsuspected diffuse. The investigators claimed this mechanism leads to the mild centrilobular emphysema, which was not detected until the autopsy.

“All 10 patients with asthma had a significant decrease in lung elastic recoil, and unsuspected, microscopic mild centrilobular emphysema was noted in all three autopsies obtained although it was not easily identified on lung CT scan,” they pointed out.

Though airflow obstruction is a symptom typical to smokers, how this process—along with lung elastic recoil and persistent expiratory airflow limitation—occurs in nonsmokers still isn’t clear. Why is is unclear is due to the lack of structure-function studies on ACOS, which investigators believe will provide more insight into ACOS development, according to a statement released by the American College of Chest Physicians.

“These sentinel pathophysiologic observations need to be confirmed to further unravel the epiphenomenon of ACOS. The pro-inflammatory and proteolytic mechanism(s) leading to lung tissue breakdown need to be further investigated,” the researchers concluded.