Angiopoietin-2 expression in patients with an acute exacerbation of idiopathic interstitial pneumonias
Angiopoietin-2 expression in patients with an acute exacerbation of idiopathic interstitial pneumonias
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DOI：
10.1016/j.rmed.2016.05.012
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发表时间：
2016-08-01
影响因子：
4.3
通讯作者：
Kadota, Junichi
中科院分区：
文献类型：
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作者：
Ando, Masaru;Miyazaki, Eishi;Kadota, Junichi
背景和目的：我们假设肺血管通透性增加可能在特发性间质性肺炎（AE-IIP）急性加重的发病机制中发挥作用。血管生成素-2 (Ang-2) 促进内皮细胞活化、不稳定和炎症。本研究的目的是探讨Ang-2表达是否与AE-IIPs的发病机制相关。方法：纳入23名AE-IIP患者、18名急性肺损伤/急性呼吸窘迫综合征（ALI/ARDS）患者、37名特发性肺纤维化（IPF）患者和33名健康志愿者（HV）。采用酶联免疫吸附法测定血清Ang-2水平。结果：AE-IIPs和ALI/ARDS患者血清Ang-2水平高于IPF患者和HV； BALF 中 Ang-2 的水平也高于 IPF 患者。 AE-IIP患者血清Ang-2水平与CRP呈正相关,而ALI/ARDS患者血清Ang-2水平与CRP或SOFA评分呈显着正相关。尽管基线Ang-2水平与生存无关，但治疗期间幸存者的Ang-2水平显着下降，而非幸存者的Ang-2水平没有变化。结论：Ang-2引起的肺血管通透性增加和炎症可能在AE-IIP的发病机制中发挥作用。 (C) 2016 Elsevier Ltd. 保留所有权利。
Background and objective: We hypothesized that increased pulmonary vascular permeability may play a role in the pathogenesis of an acute exacerbation of the idiopathic interstitial pneumonias (AE-IIPs). Angiopoietin-2 (Ang-2) promotes endothelial activation, destabilization, and inflammation. The purpose of this study was to examine whether Ang-2 expression was associated with the pathogenesis of AE-IIPs.Methods: Twenty-three patients with AE-IIP patients, 18 acute lung injury/acute respiratory distress syndrome (ALI/ARDS) patients, 37 idiopathic pulmonary fibrosis (IPF) patients, and 33 healthy volunteers (HVs) were enrolled. The serum level of Ang-2 was measured by an enzyme-linked immunosorbent assay.Results: The serum levels of Ang-2 were higher in AE-IIPs and ALI/ARDS patients than in IPF patients and HVs; the BALF levels of Ang-2 were also higher than in IPF patients. There was a positive correlation between the serum level of Ang-2 and the CRP in patients with AE-IIP patients, whereas a significant positive correlation was found between the serum Ang-2 level and the CRP or SOFA scores of the ALI/ARDS patients. Although the baseline Ang-2 level was not related to survival, the Ang-2 levels significantly declined in survivors during treatment, while they did not change in non-survivors.Conclusions: Increased pulmonary vascular permeability and inflammation due to Ang-2 may play a role in the pathogenesis of AE-IIPs. (C) 2016 Elsevier Ltd. All rights reserved.