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Late-onset asthma: current perspectives

Authors Hirano T, Matsunaga K

Received 15 August 2017

Accepted for publication 23 October 2017

Published 9 February 2018 Volume 2018:11 Pages 19—27

DOI https://doi.org/10.2147/JAA.S125948

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Colin Mak

Peer reviewer comments 2

Editor who approved publication: Dr Amrita Dosanjh


Tsunahiko Hirano, Kazuto Matsunaga

Department of Respiratory Medicine and Infectious Disease, Graduate School of Medicine, Yamaguchi University, Yamaguchi, Japan

Abstract: Because the pathophysiology of asthma has diverse characteristics, to manage the disease effectively, it is important for clinicians to distinguish among the clinical phenotypes. Among them, adult-onset asthma, that is, late-onset asthma (LOA), is increasing because of the aging of the population. The phenotype of LOA is largely divided into two types according to the presence or absence of eosinophilic inflammation, T-helper (Th)2- and non–Th2-associated LOA. Especially in Th2 LOA related to rhinosinusitis, as pulmonary function at onset is poor and asthma exacerbations occur frequently, it is important to detect this phenotype in the early phase by using a biomarker of Th2-type inflammation such as fractional exhaled nitric oxide (FENO). As non–Th2-LOA is often resistant to corticosteroids, this phenotype often requires another treatment strategy such as macrolide, diet, or smoking cessation. We often struggle with the management of LOA patients due to a lack of evidence; therefore, the elucidation of the mechanism of LOA contributes to increased efficiency of diagnosis and treatment of LOA. Age-related immune system and structural changes are thought to be associated with the pathophysiology of LOA. In the former case, changes in inflammatory cell function such as variations in the innate immune response and acquisition of autoimmunity or upregulation of oxidative stress are thought to be involved in the mechanism. Meanwhile, the latter can also become triggers or exacerbating factors of LOA via enhancement of airway hyperresponsiveness, decline in lung function, increased air trapping, and reduction in chest wall compliance. Therefore, appropriate individualized management in LOA may be possible through precisely assessing the pathophysiology based on age-related functional changes, including the immune and structural system.

Keywords: aging, immunosenescence, rhinosinusitis, obesity, phenotype, endotype
 

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