Airway hyperresponsiveness in chronic obstructive pulmonary disease: A marker of asthma-chronic obstructive pulmonary disease overlap syndrome?

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• 作者：Ruzena Tkacova ; MD ; PhD^a ; ^b ; Darlene L.Y. Dai ; MSc^a ; ^c ; Judith M. Vonk ; PhD^d ; ^e ; Janice M. Leung ; MD^a ; ^f ; Pieter S. Hiemstra ; PhD^g ; Maarten van den Berge ; MD ; PhD^e ; ^h ; Lisette Kunz ; MD^g ; Zsuzsanna Hollander ; PhD^a ; ^c ; Donald Tashkin ; MDⁱ ; Robert Wise ; MD^j ; John Connett ; PhD^k ; Raymond Ng ; PhD^a ; ^c ; ^l ; Bruce McManus ; MD ; PhD^a ; ^c ; ^m ; S.F. Paul Man ; MD^a ; ^f ; Dirkje S. Postma ; MD ; PhD^e ; ^h ; Don D. Sin ; MD^a ; ^f ; ^{don.sin@hli.ubc.ca}
• 关键词：Respiratory hypersensitivity ; airway obstruction ; lung function tests ; death rate
• 刊名：Journal of Allergy and Clinical Immunology
• 出版年：2016
• 出版时间：December 2016
• 年：2016
• 卷：138
• 期：6
• 页码：1571-1579.e10
• 全文大小：959 K
• 卷排序：138

文摘

The impact of airway hyperreactivity (AHR) on respiratory mortality and systemic inflammation among patients with chronic obstructive pulmonary disease (COPD) is largely unknown. We used data from 2 large studies to determine the relationship between AHR and FEV1 decline, respiratory mortality, and systemic inflammation.ObjectivesWe sought to determine the relationship of AHR with FEV1 decline, respiratory mortality, and systemic inflammatory burden in patients with COPD in the Lung Health Study (LHS) and the Groningen Leiden Universities Corticosteroids in Obstructive Lung Disease (GLUCOLD) study.MethodsThe LHS enrolled current smokers with mild-to-moderate COPD (n = 5887), and the GLUCOLD study enrolled former and current smokers with moderate-to-severe COPD (n = 51). For the primary analysis, we defined AHR by a methacholine provocation concentration of 4 mg/mL or less, which led to a 20% reduction in FEV1 (PC20).ResultsThe primary outcomes were FEV1 decline, respiratory mortality, and biomarkers of systemic inflammation. Approximately 24% of LHS participants had AHR. Compared with patients without AHR, patients with AHR had a 2-fold increased risk of respiratory mortality (hazard ratio, 2.38; 95% CI, 1.38-4.11; P = .002) and experienced an accelerated FEV1 decline by 13.2 mL/y in the LHS (P = .007) and by 12.4 mL/y in the much smaller GLUCOLD study (P = .079). Patients with AHR had generally reduced burden of systemic inflammatory biomarkers than did those without AHR.ConclusionsAHR is common in patients with mild-to-moderate COPD, affecting 1 in 4 patients and identifies a distinct subset of patients who have increased risk of disease progression and mortality. AHR may represent a spectrum of the asthma-COPD overlap phenotype that urgently requires disease modification.