阻塞性睡眠呼吸暂停患者呼出气中一氧化碳水平。

Exhaled carbon monoxide levels in obstructive sleep apnoea.

机构信息

Department of Pulmonology, Semmelweis University, 1/C Dios arok, 1125, Budapest, Hungary.

出版信息

J Breath Res. 2019 Jun 7;13(3):036012. doi: 10.1088/1752-7163/ab231d.

DOI:10.1088/1752-7163/ab231d

PMID:31108481

Abstract

BACKGROUND

Obstructive sleep apnoea (OSA) is characterised by chronic intermittent hypoxia, which enhances airway inflammation and oxidative stress. Exhaled carbon monoxide (eCO), a marker for oxidative stress, has been investigated in OSA. However, previous studies could be biased as they did not differentiate patients with OSA based on smoking history, a known factor influencing eCO levels. The aim of this study to investigate eCO levels in patients with OSA and non-OSA controls and compare evening to morning results.

METHODS

Exhaled carbon monoxide concentration was measured in the evening and in the morning following an in-hospital cardiorespiratory polygraphy in 60 never-smoker OSA patients, 14 ex-smoker OSA patients, 39 current-smoker OSA patients, 10 never-smoker asthmatic patients with OSA, 16 COPD patients with OSA and 20 never-smoker non-OSA controls. OSA was diagnosed based on the apnoea-hypopnoea index (AHI > 5/h).

RESULTS

There was no difference between the never-smoker controls and never-smoker patients with OSA either in the evening (1.98 ± 1.00 ppm versus 1.95 ± 1.28 ppm, p = 0.57, OSA versus controls, respectively) or morning (1.95 ± 0.96 ppm versus 1.80 ± 0.95 ppm, p = 0.42), however there was a weak correlation between eCO and AHI in the evening (r = 0.31, p = 0.01). Accordingly, patients with severe OSA had higher eCO levels in the evening (2.43 ± 1.12 ppm) compared to mild OSA patients (1.57 ± 0.87 ppm, p < 0.01). Ex-smoker (3.07 ± 2.23 ppm), current-smoker (13.13 ± 11.35 ppm), asthmatic (2.70 ± 1.16 ppm) and COPD (18.25 ± 18.60 ppm) patients with OSA had higher levels of eCO compared to the non-smoker OSA group.

CONCLUSION

Exhaled carbon monoxide is elevated only in severe never-smoker OSA suggesting accelerated oxidative stress. Previous smoking history is a major influencing factor which may explain differences between our findings and those of previous studies. Although our results show some impact of OSA on eCO measurements, the bias is small, and it does not significantly affect the clinical utility of eCO to monitor smoking cessation.

摘要

背景

阻塞性睡眠呼吸暂停（OSA）的特征是慢性间歇性低氧，这会增强气道炎症和氧化应激。呼气一氧化碳（eCO）是氧化应激的标志物，已在 OSA 中进行了研究。然而，以前的研究可能存在偏差，因为它们没有根据吸烟史对 OSA 患者进行区分，而吸烟史是影响 eCO 水平的已知因素。本研究旨在调查 OSA 患者和非 OSA 对照组中的 eCO 水平，并比较早晚结果。

方法

对 60 名从不吸烟的 OSA 患者、14 名曾吸烟的 OSA 患者、39 名当前吸烟的 OSA 患者、10 名从不吸烟的伴有 OSA 的哮喘患者、16 名伴有 OSA 的 COPD 患者和 20 名从不吸烟的非 OSA 对照组患者进行了院内心肺多导睡眠图检查后，分别在晚上和早上测量呼气一氧化碳浓度。OSA 是根据呼吸暂停-低通气指数（AHI＞5/h）诊断的。

结果

从不吸烟的对照组和从不吸烟的 OSA 患者在晚上（分别为 1.98±1.00 ppm 和 1.95±1.28 ppm，p=0.57，OSA 与对照组相比）或早上（分别为 1.95±0.96 ppm 和 1.80±0.95 ppm，p=0.42）时，eCO 没有差异，但晚上时 eCO 与 AHI 之间存在弱相关性（r=0.31，p=0.01）。因此，患有严重 OSA 的患者在晚上的 eCO 水平较高（2.43±1.12 ppm），而轻度 OSA 患者（1.57±0.87 ppm，p＜0.01）。曾吸烟（3.07±2.23 ppm）、当前吸烟（13.13±11.35 ppm）、哮喘（2.70±1.16 ppm）和 COPD（18.25±18.60 ppm）伴有 OSA 的患者的 eCO 水平高于非吸烟的 OSA 组。