Turnbull Chris D, Stradling John R, Petousi Nayia, Lassalle Philippe
Oxford Centre for Respiratory Medicine, Oxford University Hospitals NHS, Foundation Trust, Oxford, UK.
Nuffield Department of Medicine, University of Oxford, Oxford, UK.
Sleep Breath. 2024 Dec;28(6):2509-2514. doi: 10.1007/s11325-024-03120-2. Epub 2024 Sep 6.
Endocan is a biomarker of endothelial dysfunction, which is a precursor to cardiovascular disease. Obstructive sleep apnoea (OSA) is associated with elevated endocan levels but the effects of treatment on endocan levels in OSA are not fully established. We aimed to determine whether endocan levels could be detected by immunoassay and to determine the effect of supplemental oxygen during continuous positive airway pressure (CPAP) withdrawal on circulating endocan levels.
We conducted an exploratory analysis from a randomised controlled crossover study which included participants with OSA. Participants stopped their CPAP therapy and were randomised to receive either supplemental oxygen or sham for 14 nights before crossing over. Supplemental oxygen blocked the rise in blood pressure seen in the sham group. We analysed plasma endocan levels by immunoassay at baseline and after 14 nights of intervention in both groups.
Twenty-five participants were included, with a total of 100 samples. Endocan levels were detectable at all time points in 22 participants (88%), and in 93 (93%) samples. Supplemental oxygen had no effect on endocan levels compared to sham (+ 0.52 ng/ml, 95%CI -0.21 to + 1.25, p = 0.16), and there was no significant difference in endocan levels from baseline to follow-up in either the sham (-0.30 ng/ml, 95%CI -0.89 to + 0.30, p = 0.31) or supplemental oxygen (+ 0.22 ng/ml, 95%CI 0.00 to + 0.44, p = 0.05) arm.
We have shown that endocan levels are detectable before and after CPAP withdrawal. However, we found no effect of supplemental oxygen following CPAP withdrawal on circulating endocan levels.
ISRCTN 17,987,510 19/02/2015.
内脂素是内皮功能障碍的生物标志物，而内皮功能障碍是心血管疾病的先兆。阻塞性睡眠呼吸暂停（OSA）与内脂素水平升高有关，但治疗对OSA患者内脂素水平的影响尚未完全明确。我们旨在确定免疫测定法能否检测到内脂素水平，并确定在持续气道正压通气（CPAP）撤机期间补充氧气对循环内脂素水平的影响。
我们对一项随机对照交叉研究进行了探索性分析，该研究纳入了OSA患者。参与者停止CPAP治疗，并被随机分为两组，分别接受14晚的补充氧气或安慰剂治疗，之后进行交叉。补充氧气可阻止安慰剂组出现的血压升高。我们在两组的基线期和干预14晚后通过免疫测定法分析血浆内脂素水平。
纳入25名参与者，共100份样本。22名参与者（88%）在所有时间点的内脂素水平均可检测到，93份样本（93%）也是如此。与安慰剂相比，补充氧气对内脂素水平无影响（+0.52 ng/ml，95%CI -0.21至+1.25，p = 0.16），安慰剂组（-0.30 ng/ml，CI 95% -0.89至+0.30，p = 0.31）或补充氧气组（+0.22 ng/ml，95%CI 0.00至+0.44，p = 0.05）从基线到随访的内脂素水平均无显著差异。
我们已证明在CPAP撤机前后内脂素水平均可检测到。然而，我们发现CPAP撤机后补充氧气对循环内脂素水平没有影响。
ISRCTN 17,987,510 2015年2月19日。
