Circulating KL-6, a biomarker of lung injury, in obstructive sleep apnoea
Circulating KL-6, a biomarker of lung injury, in obstructive sleep apnoea
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DOI：
10.1183/09031936.00150708
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发表时间：
2009-04-01
影响因子：
24.3
通讯作者：
Bhattacharya, J.
中科院分区：
文献类型：
--
作者：
Lederer, D. J.;Jelic, S.;Bhattacharya, J.
在阻塞性睡眠呼吸暂停(OSA)中，氧化应激导致外周循环内皮细胞功能障碍。在肺部，氧化应激可导致肺泡损伤。11名OSA患者和10名对照组的睡眠特征、肱动脉血流介导的扩张和血浆KL-6水平分别为317(232-506)um L(-1)和226(179-257)u m L(-1)，OSA患者的中位(四分位数范围)血浆KL-6水平高于对照组。较高的血浆KL-6水平与睡眠中氧合血红蛋白饱和度为4%的较长睡眠时间和较低的臂动脉血流介导的扩张相关。调整最低点饱和度或血流介导的扩张可减弱血浆KL-6水平与OSA之间的关联。在一些阻塞性睡眠呼吸暂停患者中，循环KL-6水平升高，可能反映了肺泡壁通透性增加。
In obstructive sleep apnoea (OSA), oxidative stress contributes to endothelial dysfunction In the peripheral circulation. In the lung, oxidative stress can lead to alveolar injury. The present authors hypothesised that patients with OSA would have biomarker evidence of Increased alveolar wall permeability.Sleep characteristics, brachial artery flow-mediated dilation and plasma KL-6 levels were observed In 11 otherwise healthy patients with OSA and 10 controls.Median (interquartile range) plasma KL-6 levels were higher In patients with OSA compared with controls: 317 (232-506) U.mL(-1) versus 226 (179-257) U.mL(-1), respectively. Higher plasma KL-6 levels were associated with greater time spent asleep with an oxyhaemoglobin saturation 4% during sleep and lower brachial artery flow-mediated dilation. Adjustment for nadir saturation or flow-mediated dilation attenuated the association between plasma KL-6 levels and OSA.Circulating KL-6 levels are elevated In some patients with obstructive sleep apnoea, possibly reflecting Increased alveolar wall permeability.