Lung elasticity linked to airflow obstruction


By Mardi Chapman

15 Oct 2019

Increased lung compliance and loss of lung elastic recoil has been observed in older people with asthma and fixed airflow obstruction (FAO).

However the association appears to be independent of likely contributing factors such as age or asthma duration.

The small Australian study comprised 18 non-smoking patients with a median age of 64 years, asthma duration of 39 years and receiving optimal asthma treatment.

Most had moderate airflow obstruction defined as FEV1/FVC ratio z-score < 1.64 which was unchanged after two months of treatment.

Nine of 18 subjects had increased lung compliance and 5 of 18 had reduced elastic recoil pressure.

“Furthermore, reduced spirometric ratio was predicted by both increased lung compliance (K) and lower BMI, with lung compliance as the sole predictor on multiple linear regression, suggesting that obesity may exert its effects via increased elastic recoil.”

“Finally, FAO as measured by Rrs5 [respiratory system resistance] was predicted by loss of elastic recoil (B/A). Together, these data suggest that there are structural changes in lung tissue in older asthmatic subjects, which increase lung compliance and reduce lung elastic recoil pressure, thereby reducing FEV1/FVC ratio and increasing Rrs, respectively.”

They suggested that lung tissue abnormalities make a large contribution to airflow obstruction in older asthmatic subjects, in addition to the contribution of airway remodelling.

First author Dr Katrina Tonga, from Royal North Shore Hospital and the Woolcock Institute, told the limbic it was surprising that, statistically, age didn’t appear to play a part in the loss of lung elastic recoil.

“I think we probably need more numbers and also to look at younger people with asthma,” she said.

“We’ve shown previously in our group that younger people with asthma also have a loss of elastic recoil or changes in the lungs’ elastic properties compared to healthy controls.”

She said it might be that some patients with asthma also had changes in the lung tissue that physiologically look like they have emphysema in that they don’t respond to bronchodilators.

And there is evidence from postmortem studies that patients can have microscopic emphysema, which is not evident on CT scan.

“So we wonder whether these people have proteolytic enzymes that are causing some change to the lung tissue that results in microscopic emphysema or something that changes their elastic properties.”

She said some people probably have a combination of airway remodeling and microscopic emphysema.

“Not all people with asthma have this. I don’t think everyone with asthma has changes to the lung tissue. There will be some that do and some that don’t.”

“We’re targeting all their airways with the puffers, and there are the biologics given systemically, but maybe if we find there are proteolytic enzymes, targeting them might help.”

The study concluded that further research in a larger cohort was required to examine relationships with lung ageing and asthma duration, as well as the underlying cellular and molecular mechanisms that cause loss of lung elasticity.

“These future studies may lead to identification of new targets for intervention for FAO that is steroid unresponsive,” the study said.


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