中性粒细胞与淋巴细胞比率(NLR)作为临床稳定型慢性阻塞性肺疾病的生物标志物:SPIROMICS队列。

IF 5.4
Daniel T Hoesterey, Hong Dang, Daniela Markovic, Russell G Buhr, Donald P Tashkin, R Graham Barr, John A Belperio, Russell P Bowler, Eugene R Bleecker, David J Couper, Gerard G Criner, Christopher B Cooper, Claire M Doerschuk, Mark T Dransfield, M Bradley Drummond, Ashraf Fawzy, Christine M Freeman, MeiLan K Han, Nadia N Hansel, Annette T Hastie, Eric A Hoffman, Yvonne J Huang, Robert J Kaner, Richard E Kanner, Victor Kim, Jerry A Krishnan, Fernando J Martinez, Wanda K O'Neal, Victor E Ortega, Robert Paine, Abhishek K Shrivastav, J Michael Wells, Prescott G Woodruff, Jeffrey L Curtis, Igor Barjaktarevic
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引用次数: 0

摘要

理由:炎症是慢性阻塞性肺疾病(COPD)发病机制的核心,但在COPD预后模型中不完全代表。中性粒细胞与淋巴细胞比率(NLR)是一种容易获得的炎症生物标志物。目的:探讨NLR与吸烟状况、慢性阻塞性肺病临床特征和未来不良结局的关系。方法:在SPIROMICS多中心观察性队列研究中,我们分析了从目前或以前吸烟的参与者(n = 2624)和tobacco-naïve对照组(n = 187)的全血细胞计数计算的NLR。我们评估了NLR在6周和1年的稳定性,与选定的血液生物标志物的关联,以及吸烟对NLR和细胞计数的影响。我们按NLR四分位数对参与者进行分层,比较入组时的横断面临床特征、1年前瞻性观察到的恶化情况和纵向随访期间的死亡率。结果:更高的NLR四分位数与更严重的COPD临床特征广泛相关。NLR值在6周(ICC=0.74)和1年(ICC=0.62)时可重复。吸烟对NLR的影响随气流限制的严重程度而变化,这是由吸烟、预测FEV1 %和中性粒细胞计数(而不是淋巴细胞计数)之间的相互作用介导的。与1-3分位数相比,最高NLR四分位数(>3.11)与1年内恶化风险增加(调整后OR=1.51 95%CI 1.18, 1.92)和死亡风险增加(调整后HR=1.41, 95%CI 1.20, 1.66)相关。结论:稳定期COPD患者NLR升高是一个广泛可用的与加重和死亡风险增加相关的生物标志物。吸烟对NLR的影响因疾病严重程度而异。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Neutrophil-to-Lymphocyte Ratio (NLR) as a Biomarker in Clinically Stable Chronic Obstructive Pulmonary Disease: SPIROMICS cohort.

Rationale: Inflammation is central to chronic obstructive pulmonary disease (COPD) pathogenesis but incompletely represented in COPD prognostic models. Neutrophil to lymphocyte ratio (NLR) is a readily available inflammatory biomarker.

Objectives: To explore the associations of NLR with smoking status, clinical features of COPD, and future adverse outcomes.

Methods: We analyzed NLR calculated from the complete blood count of participants who currently or formerly smoked (n = 2,624) and tobacco-naïve controls (n = 187) in the SPIROMICS multicenter observational cohort study. We assessed the stability of NLR at 6 weeks and 1 year, the association with select blood biomarkers, and the impact of smoking on NLR and cell counts. We stratified participants by NLR quartiles to compare cross-sectional clinical features at enrollment, prospectively observed exacerbations at 1 year, and mortality during longitudinal follow-up.

Results: Higher NLR quartiles were broadly associated with more severe clinical features of COPD. NLR values were repeatable at 6 weeks (ICC=0.74) and 1 year (ICC=0.62). The impact of smoking on NLR varied with the severity of airflow limitation, mediated by an interaction between smoking, FEV1 % predicted, and neutrophil counts but not lymphocyte counts. The highest NLR quartile (>3.11) was associated with an increased risk of exacerbation over 1-year (adjusted OR=1.51 95%CI 1.18, 1.92) and increased risk of mortality (adjusted HR=1.41, 95%CI 1.20, 1.66) compared to quartiles 1-3.

Conclusions: Elevated NLR in stable COPD is a widely available biomarker associated with increased risk for exacerbation and death. The impact of cigarette smoking on NLR varies with disease severity.

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