Muñoz-Lucas Maria Ángeles, Jareño-Esteban Javier, Gutiérrez-Ortega Carlos, López-Guijarro Pablo, Collado-Yurrita Luis, Quintana-Díaz Manuel, Callol-Sánchez Luis
Unidad de Apoyo a la Investigación, Jefatura de Docencia e Investigación, Hospital Central de la Defensa, Madrid, Spain.
Servicio de Neumología, Hospital Central de la Defensa, Universidad de Alcalá de Henares (Madrid), Spain.
Arch Bronconeumol. 2020 Dec;56(12):801-805. doi: 10.1016/j.arbr.2020.10.004. Epub 2020 Nov 5.
The etiology of lung cancer is multifactorial. Exposure to tobacco smoke and the role played by the carcinogenic compounds that it contains would explain the common association between lung cancer and chronic obstructive pulmonary disease (COPD), which is closely linked to tobacco use. In both diseases, sustained inflammation is caused by increased oxidative stress (for example, lipid peroxidation). This generates low molecular weight substances called volatile organic compounds (VOC) that are excreted during breathing. VOC metabolomics provides an indirect measure of oxidative stress.
The aim of this study was to establish the relative influence of COPD on the VOC profile in patients with non-small cell lung cancer (NSCLC), by first studying the possible variation of VOC associated with lung cancer histology.
Exhaled air was tested in 107 NSCLC patients, who were divided into 2 groups: NSCLC with COPD and non-COPD with NSCLC. The exhaled air sample was obtained with the BIOVOC® sampler, and transferred to desorption tubes for later analysis by thermal desorption-gas chromatography-mass spectrometry. The VOC analysis showed lineal aldehydes and carboxylic acids.
No statistically significant differences were found in VOC associated with histology. NSCLC and COPD patients present a 1.7-fold (1.1-2.7) greater probability of detection of propionic acid (95% CI: 1.22-6.2) than patients without COPD or NSCLC (p = 0.013).
肺癌的病因是多因素的。接触烟草烟雾及其所含致癌化合物所起的作用可以解释肺癌与慢性阻塞性肺疾病（COPD）之间的常见关联，而COPD与烟草使用密切相关。在这两种疾病中，持续的炎症是由氧化应激增加（例如脂质过氧化）引起的。这会产生称为挥发性有机化合物（VOC）的低分子量物质，这些物质在呼吸过程中排出体外。VOC代谢组学提供了氧化应激的间接测量方法。
本研究的目的是通过首先研究与肺癌组织学相关的VOC的可能变化，确定COPD对非小细胞肺癌（NSCLC）患者VOC谱的相对影响。
对107例NSCLC患者的呼出气体进行检测，这些患者分为两组：合并COPD的NSCLC患者和不合并COPD的NSCLC患者。使用BIOVOC®采样器获取呼出气体样本，并转移至解吸管中，以便稍后通过热解吸-气相色谱-质谱法进行分析。VOC分析显示了直链醛和羧酸。
与组织学相关的VOC未发现统计学上的显著差异。与无COPD或NSCLC的患者相比，NSCLC和COPD患者检测到丙酸的可能性高1.7倍（1.1-2.7）（95%CI：1.22-6.2）（p=0.013）。
