2/20/2024 0 Comments Sandra teen model waterfall set![]() We propose that structural and functional changes in lung parenchymal tissue are just as (if not more) important than airway remodeling in causing persistent lung function decline in asthma with FAO. In this Perspective we draw upon what is known thus far on the pathophysiological mechanisms contributing to FAO in asthma. There is now a large body of evidence showing that loss of lung elasticity and even alveolar destruction, which results in mild alveolar dilation and reduced radial traction and mechanical support of airways, is an important mechanism causing FAO. Our group and others have recently shown that in asthma with FAO, there are also critical and substantial structural and functional changes to the lung parenchyma and its lung elastic properties. The heavy focus on airway remodeling as the cause of FAO in asthma overlooks the potentially important contributions from disease-related changes in the mechanical properties of the lung parenchyma. In many however, standard treatment does not prevent FAO from developing suggesting other mechanisms may play a role in the pathophysiology of this condition. Treatment with standard asthma therapy, such as inhaled corticosteroids and bronchodilators, likely prevents excessive lung function loss in some patients, although there is little specific evidence to support this, likely due to difficulty in long term studies with a primary outcome of FEV1 decline. ![]() ![]() The current paradigm is that FAO in asthma is due to airway remodeling driven by persistent eosinophilic inflammation. There is no current treatment to reverse or prevent excessive lung function decline in these severe asthmatics with FAO, due to a lack of understanding the underlying pathophysiology. ![]() The prevalence of FAO is higher in those patients with severe asthma, being most frequent in older patients with long standing history of the condition ( Lee et al., 2007). Asthma with FAO is often (mis)labelled as chronic obstructive pulmonary disease (COPD) yet may develop despite nil-to-negligible smoking history or exposure to noxious agents. We believe this paradigm of FAO should be considered when developing novel treatments.Īsthma with irreversible or fixed airflow obstruction (FAO) is a clinical phenotype that is underappreciated and, subsequently, undertreated because our understanding of this phenotype is limited. We propose the view that structural and functional changes in parenchymal tissue, are just as (if not more) important than airway remodeling in causing persistent lung function decline in asthma. In this Perspective we draw upon what is known thus far on the pathophysiological mechanisms contributing to FAO in asthma, and focus on recent advances and future directions. However, emerging evidence indicates significant and critical structural and functional changes to the lung parenchyma and its lung elastic properties in asthma with FAO, suggesting that FAO is a ‘whole lung’ problem and not just of the airways. The current paradigm is that FAO in asthma is due to airway remodeling driven by chronic inflammation. There are no current treatments to reverse or prevent this excessive decline in lung function in these patients, due to a lack of understanding of the underlying pathophysiology.
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