New Treatment Approaches and Prognostic Biomarkers for Advanced Chronic Obstructive Pulmonary Disease and Potential Associated Cardiovascular Risks.
New Treatment Approaches and Prognostic Biomarkers for Advanced Chronic Obstructive Pulmonary Disease and Potential Associated Cardiovascular Risks.
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晚期慢性阻塞性肺疾病和潜在相关心血管风险的新治疗方法和预后生物标志物。
DOI：
10.1164/rccm.201804-0659rr
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发表时间：
2019
影响因子：
24.7
通讯作者：
Sankari,Abdulghani
中科院分区：
文献类型：
--
作者：
Khorfan,Omar;Alsamman,Samer;Abbas,Hawazin;Sankari,Abdulghani
慢性阻塞性肺疾病（COPD）的传统特征是中性粒细胞、巨噬细胞、蛋白酶、IL-6和8以及t辅助细胞1型细胞因子浓度升高，而哮喘的特征是嗜酸性粒细胞和t辅助细胞2型细胞因子浓度升高(1)。近年来，这种模式发生了变化，COPD和哮喘在症状、生理和治疗反应方面被视为异质。这促使研究人员确定具有特定表型的患者亚群，可以为其量身定制治疗。ECLIPSE （COPD纵向评估以确定预测替代终点）研究报道，在COPD中，痰中性粒细胞浓度与肺功能和健康状况弱相关，但与加重、肺气肿或全身炎症无关(2)。其他COPD研究报道，血液和痰中嗜酸性粒细胞增加与呼吸恶化和更严重的恶性通货膨胀有关（3,4）。针对慢性阻塞性肺病患者的嗜酸性粒细胞的试验表明，它们在慢性阻塞性肺病的发病机制中起着重要但尚未完全了解的作用（5,6）。
Chronic obstructive pulmonary disease (COPD) has been traditionally characterized by increased concentrations of neutrophils, macrophages, proteases, IL-6 and-8, and T-helper cell type 1 cytokines, whereas asthma has been characterized by increased concentrations of eosinophils and T-helper cell type 2 cytokines (1). This paradigm has shifted in recent years, and COPD and asthma are now viewed as heterogeneous with respect to symptoms, physiology, and response to treatments. This has driven investigators to identify subpopulations of patients with specific phenotypes for which treatment can be tailored. The ECLIPSE (Evaluation of COPD Longitudinally to Identify Predictive Surrogate End-points) study reported that in COPD, sputum neutrophil concentrations were weakly associated with lung function and health status but not associated with exacerbations, emphysema, or systemic inflammation (2). Other COPD studies have reported that increased eosinophils in both blood and sputum are associated with respiratory exacerbations and greater hyperinflation (3, 4). Trials aimed at targeting eosinophils in patients with COPD have shown that they play an important yet not completely understood the role in the pathogenesis of COPD (5, 6).