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Age-Related Clinical Characteristics, Inflammatory Features, Phenotypes, and Treatment Response in Asthma

医学 哮喘 优势比 过敏性 内科学 前瞻性队列研究 人口 儿科 免疫学 环境卫生
作者
Ji Wang,Xin Zhang,Li Zhang,Ying Liu,Gang Wang,Hong Ping Zhang,Gang Wang,De Ying Kang,Brian G. Oliver,Hua Wan,Vanessa M. McDonald,Alan Hsu,Dan Liu,Wei Min Li,Surinder S. Birring,Gang Wang
出处
期刊:The Journal of Allergy and Clinical Immunology: In Practice [Elsevier BV]
卷期号:11 (1): 210-219.e3 被引量:56
标识
DOI:10.1016/j.jaip.2022.09.029
摘要

Background Emerging evidence suggests that aging affects asthma outcomes, but the mechanism remains largely unexplored. Objective To explore age-related clinical characteristics, inflammatory features, phenotypes, and treatment response in asthma. Methods This was a prospective cohort study of asthmatic patients with a 12-month follow-up in a real-world setting. Clinical inflammatory and phenotypic characteristics, future risk for exacerbations, and treatment response were assessed across different age groups (young was defined as age 18 to 39 years; middle-aged, 40 to 64 years; and elderly, 65 years or older). Results Compared with young (n = 106) and middle-aged (n = 179) asthmatic patients, elderly patients (n = 55) had worse airway obstruction, more comorbidities including chronic obstructive pulmonary disease and diabetes, less atopy, and lower levels of IgE and FeNO, and were more likely to have late-onset and fixed airflow obstruction asthma and a reduced risk for having type 2 profile asthma. Levels of IFN-gamma, IL-17A, and IL-8 in induced sputum were significantly increased in elderly asthmatic patients (all P < .05). Path analysis indicated that age directly and significantly led to future exacerbations in asthma, partially mediated by an upregulation of airway IFN-gamma. Moreover, elderly patients with asthma had a reduced treatment response (improvement in FEV1 of 12% or greater, or 200 mL, and a reduction in Borg scores of 1 or greater) (adjusted odds ratio = 0.11; 95% CI, 0.02-0.52; and adjusted odds ratio = 0.12; 95% CI, 0.03-0.49, respectively). Conclusions This study confirms that asthma in the elderly population represents a specific phenotype and indicates that aging can influence asthma in terms of clinical characteristics, inflammatory features, exacerbations, and treatment response. Emerging evidence suggests that aging affects asthma outcomes, but the mechanism remains largely unexplored. To explore age-related clinical characteristics, inflammatory features, phenotypes, and treatment response in asthma. This was a prospective cohort study of asthmatic patients with a 12-month follow-up in a real-world setting. Clinical inflammatory and phenotypic characteristics, future risk for exacerbations, and treatment response were assessed across different age groups (young was defined as age 18 to 39 years; middle-aged, 40 to 64 years; and elderly, 65 years or older). Compared with young (n = 106) and middle-aged (n = 179) asthmatic patients, elderly patients (n = 55) had worse airway obstruction, more comorbidities including chronic obstructive pulmonary disease and diabetes, less atopy, and lower levels of IgE and FeNO, and were more likely to have late-onset and fixed airflow obstruction asthma and a reduced risk for having type 2 profile asthma. Levels of IFN-gamma, IL-17A, and IL-8 in induced sputum were significantly increased in elderly asthmatic patients (all P < .05). Path analysis indicated that age directly and significantly led to future exacerbations in asthma, partially mediated by an upregulation of airway IFN-gamma. Moreover, elderly patients with asthma had a reduced treatment response (improvement in FEV1 of 12% or greater, or 200 mL, and a reduction in Borg scores of 1 or greater) (adjusted odds ratio = 0.11; 95% CI, 0.02-0.52; and adjusted odds ratio = 0.12; 95% CI, 0.03-0.49, respectively). This study confirms that asthma in the elderly population represents a specific phenotype and indicates that aging can influence asthma in terms of clinical characteristics, inflammatory features, exacerbations, and treatment response.
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