摘要
BackgroundObstructive 睡觉呼吸暂停(OSA ) 是抵抗高血压的最普通的原因，它被建议了源于 renin-angiotensin-aldosterone 系统(RAAS ) 的激活。我们分析元 RAAS components.MethodsFull 文章研究的血浆层次上的 OSA 的效果在与 OSA 在成年人分析至少一个 RAAS 部件的 fasting 血浆层次与或没有高血压的 MEDLINE 和 EMBASE 上出版了。OSA 作为一个呼吸暂停呼吸过慢过浅索引或呼吸骚乱索引 ≥ 被诊断；5。学习质量用纽卡斯尔渥太华规模被评估，并且异质用 I <sup>2</sup> 统计数值被估计。从单个研究的结果用反的变化被综合并且分享了使用一个随机效果的模型。亚群分析，敏感分析，和元回归被执行，并且出版偏爱的风险是包括的 assessed.ResultsThe 元分析 13 研究， 10 在高血压蛋白原酶上报导了结果( n = 470 个案例和控制)， 7 在血管收缩素 II 上( AngII ， n = 384 )，并且 9 在醛固酮上( n = 439 )。AngII 层次比在控制在 OSA 是显著地更高的[吝啬的差别 = 3.39 ng/L， 95% CI：2.00-4.79， P <；0.00001 ] 当醛固酮层次比 OSA 然而并非与高血压在有高血压的 OSA 是显著地更高的时(吝啬的差别 = 1.32 ng/dL， 95% CI：0.58-2.07， P = 0.0005 ) 。所有研究的元分析没在醛固酮在之间建议重要差别 OSA 和控制，而是一个重要分享的平均数 1.35 ng/mL 的差别(95% CI：0.88-1.82， P <；0.00001 ) 出现在排除一小样品的研究以后。出版偏爱的重要风险都没在所有包括的 studies.ConclusionsOSA 之中被检测与更高的 AngII 和醛固酮层次被联系，特别在高血压的病人。OSA 可以引起高血压，至少部分地，由刺激 RAAS 活动。
Background Obstructive sleep apnea （OSA） is the most common cause of resistant hypertension, which has been proposed to result from activation of the renin-angiotensin-aldosterone system （RAAS）. We meta-analyzed the effects of OSA on plasma levels of RAAS components. Methods Full-text studies published on MEDL1NE and EMBASE analyzing fasting plasma levels of at least one RAAS component in adults with OSA with or without hypertension. OSA was diagnosed as an apnea-hypopnea index or respiratory disturbance index 〉 5. Study quality was evaluated using the Newcastle-Ottawa Scale, and heterogeneity was assessed using the 12 statistic. Results from individual studies were synthesized using inverse variance and pooled using a random-effects model. Subgroup analysis, sensitivity analysis, and meta-regression were performed, and risk of publication bias was assessed. Results The meta-analysis included 13 studies, of which 10 reported results on renin （n = 470 cases and controls）, 7 on angiotensin II （AnglI, n = 384）, and 9 on aldosterone （n = 439）. AnglI levels were significantly higher in OSA than in controls [mean differences = 3.39 ng/L, 95% CI： 2.00-4.79, P 〈 0.00001], while aldosterone levels were significantly higher in OSA with hypertension than OSA but not with hypertension （mean differences = 1.32 ng/dL, 95% CI： 0.58-2.07, P = 0.0005）. Meta-analysis of all studies suggested no significant differences in aldosterone between OSA and controls, but a significant pooled mean difference of 1.35 ng/mL （95% CI： 0.88-1.82, P 〈 0.00001） emerged after excluding one small-sample study. No significant risk of publication bias was detected among all included studies. Conelusions OSA is associated with higher AnglI and aldosterone levels, espe- cially in hypertensive patients. OSA may cause hypertension, at least in part, by stimulating RAAS activity.
