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呼吸功能障碍和抑郁是高2型重度哮喘的核心肺外和行为/危险因素特征

2025/04/30

    摘要
    背景:肥胖和吸烟是低2型(T2)哮喘的核心可治疗特征(TT),有助于其病理生理学。相比之下,高T2哮喘的核心肺外和行为/危险因素特征尚不清楚。
    目的:本研究旨在确定T2高哮喘的核心肺外和行为/危险因素特征。
    方法:对187名(年龄≥18岁)重度哮喘患者进行横断面研究,他们完成了多维评估。高T2哮喘定义为血液嗜酸性粒细胞≥150个细胞/μl和/或FeNO≥20 ppb。使用哮喘控制问卷得分、哮喘生活质量问卷得分、加重频率和肺功能的网络分析和显性分析,在9个肺外特征和4个行为/危险因素特征中确定了高T2哮喘的核心TT。在高T2哮喘的参与者中检查了所确定的核心TT和生物标志物之间的关联。
    结果:187名参与者中,151名(80.7%)患有高T2重度哮喘。功能失调性呼吸功能障碍和抑郁的节点强度值高于其他TT,这是高T2哮喘患者哮喘症状加重、生活质量下降和频繁恶化的主要原因。高T2哮喘的这些情况与全身炎症升高有关,包括血液中性粒细胞、中性粒细胞淋巴细胞比率和血清高敏C反应蛋白,与肥胖、口服皮质类固醇剂量和焦虑无关。
    结论:高T2重度哮喘的核心肺外和行为/危险因素特征是功能失调性呼吸功能障碍和抑郁,导致哮喘预后恶化,这表明哮喘炎症表型之间的核心TT可能不同。全身炎症升高可能有助于识别高T2重度哮喘中呼吸功能障碍和抑郁的存在。

(中日友好医院呼吸与危重症医学科 李红雯 摘译 林江涛 审校)
(J Allergy Clin Immunol Pract. 2025 Mar 20:S2213-2198(25)00267-3. doi: 10.1016/j.jaip.2025.03.017.)

Dysfunctional breathing and depression are core extrapulmonary and behavior/risk factor traits in type 2-high severe asthma
Yuto Hamada, Peter G Gibson, Vanessa L Clark, Hayley Lewthwaite, Michael Fricker, Dennis Thomas, Vanessa M McDonald
Abstract
Background: Obesity and smoking are core treatable traits (TTs) in type 2 (T2)-low asthma, contributing to its pathophysiology. In contrast, core extrapulmonary and behavior/risk factor traits remain unclear in T2-high asthma.
Objective: This study aimed to identify core extrapulmonary and behavior/risk factor traits for T2-high asthma.
Methods: A cross-sectional study was conducted on 187 people (aged ≥18 years) with severe asthma who completed a multidimensional assessment. T2-high asthma was defined as blood eosinophils ≥150 cells/μl and/or FeNO ≥20 ppb. Core TTs in T2-high asthma were identified among nine extrapulmonary traits and four behavior/risk factor traits, using network analysis and dominance analysis for the Asthma Control Questionnaire scores, the Asthma Quality of Life Questionnaire scores, exacerbation frequency, and lung function. Associations between the identified core TTs and biomarkers were examined in participants with T2-high asthma.
Results: Of 187 participants, 151 (80.7%) had T2-high severe asthma. Dysfunctional breathing and depression had higher values of node strength than other TTs, contributing most to worse asthma symptoms, poorer quality of life, and frequent exacerbations in T2-high asthma. These conditions in T2-high asthma were associated with elevated systemic inflammation, including blood neutrophils, neutrophil-lymphocyte ratio, and serum high-sensitivity C-reactive protein, independent of obesity, oral corticosteroid dose, and anxiety.
Conclusion: Core extrapulmonary and behavior/risk factor traits in T2-high severe asthma were dysfunctional breathing and depression, contributing to worse asthma outcomes, suggesting that core TTs may differ between asthma inflammatory phenotypes. Elevated systemic inflammation may help in recognizing the presence of dysfunctional breathing and depression in T2-high severe asthma.


 


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