Rosalind Franklin University of Medicine and Science, Chicago Medical School, North Chicago, IL, USA.
Pulmonary and Sleep Medicine, James A Lovell Federal Health Care Center, North Chicago, IL, USA ; James A. Lovell Federal Health Care Centre, 3001 Green Bay Road, North Chicago, IL, 60064, USA.
J Inflamm (Lond). 2013 Mar 22;10:13. doi: 10.1186/1476-9255-10-13. eCollection 2013.
Obstructive sleep apnea (OSA) is associated with coronary artery disease (CAD). Intermittent hypoxia associated with OSA increases sympathetic activity and may cause systemic inflammation, which may contribute to CAD in patients with OSA. Treatment with continuous positive airway pressure (CPAP) has been shown to change levels of inflammatory markers. We analyzed data from published studies by a systematic meta-analysis.
To asses if treatment for sleep apnea by CPAP will affect levels of inflammatory markers.
PubMed, Embase and Cochrane library.
Study eligibility criteria full text English studies of adult, human subjects, addressing values of at least one of the inflammatory markers before and after CPAP treatment. We used the definition of OSA as an apnea-hypopnea index (AHI) of ≥ 5/h, reported values in mean and standard deviation or median with range.
Adult, human.
CPAP treatment for OSA.
A total of 3835 studies were reviewed for inclusion, while 23 studies pooled for analysis. A total of 14 studies with 771 patients were pooled for C-reactive protein (CRP); 9 studies with 209 patients were pooled for tumor necrosis factor-alpha (TNF-α); and 8 studies with 165 patients were pooled for interleukin-6 (IL-6).
THE FOLLOWING INFLAMMATORY MARKERS WERE CHOSEN: CRP, TNF-α, and IL-6.
C-reactive protein: Study level means ranged from 0.18 to 0.85 mg/dl before CPAP treatment and 0.10 to 0.72 mg/dl after CPAP treatment. Mean differences, at a study level, ranged from -0.05 to 0.50. The pooled mean difference was 0.14 [95% confidence interval 0.08 to 0.20, p < 0.00001]. There was heterogeneity in this endpoint (df = 13, p < 0.00001, I(2) = 95%). Tumor necrosis factor-α: Study level means ranged from 1.40 to 50.24 pg/ml before CPAP treatment and 1.80 to 28.63 pg/ml after CPAP treatment. Mean differences, at a study level, ranged from -1.23 to 21.61. The pooled mean difference was 1.14 [95% confidence interval 0.12 to 2.15, p = 0.03]. There was heterogeneity in this endpoint (df = 8, p < 0.00001, I2 = 89%). Interleukin-6: Study level means ranged from 1.2 to 131.66 pg/ml before CPAP treatment and 0.45 to 66.04 pg/ml after CPAP treatment. Mean differences, at a study level, ranged from -0.40 to 65.62. The pooled mean difference was 1.01 [95% confidence interval -0.00 to 2.03, p = 0.05]. There was heterogeneity in this endpoint (df = 7, p < 0.00001, I(2) = 95%).
Only published data. Studies pooled were mainly small, non-randomized trials.
Sleep apnea treatment with CPAP improves levels of inflammatory markers.
阻塞性睡眠呼吸暂停（OSA）与冠状动脉疾病（CAD）有关。与 OSA 相关的间歇性低氧会增加交感神经活动，并可能导致全身炎症，这可能导致 OSA 患者的 CAD。持续气道正压通气（CPAP）治疗已被证明可以改变炎症标志物的水平。我们通过系统的荟萃分析分析了已发表研究的数据。
评估 CPAP 治疗睡眠呼吸暂停是否会影响炎症标志物的水平。
PubMed、Embase 和 Cochrane 图书馆。
研究入选标准为全文为英文的成年、人体研究，涉及 CPAP 治疗前后至少一种炎症标志物的值。我们使用呼吸暂停低通气指数（AHI）≥5/h 的 OSA 定义，报告均值和标准差或中位数及范围。
成年，人类。
CPAP 治疗 OSA。
共回顾了 3835 项研究纳入标准，其中 23 项研究进行了汇总分析。共纳入了 14 项研究 771 例患者用于 C 反应蛋白（CRP）分析；9 项研究 209 例患者用于肿瘤坏死因子-α（TNF-α）分析；8 项研究 165 例患者用于白细胞介素-6（IL-6）分析。
选择以下炎症标志物：CRP、TNF-α 和 IL-6。
C 反应蛋白：研究水平均值范围为 CPAP 治疗前 0.18 至 0.85mg/dl，CPAP 治疗后 0.10 至 0.72mg/dl。研究水平的平均差异范围为-0.05 至 0.50。汇总的平均差异为 0.14[95%置信区间 0.08 至 0.20，p<0.00001]。该终点存在异质性（df=13，p<0.00001，I²=95%）。肿瘤坏死因子-α：研究水平均值范围为 CPAP 治疗前 1.40 至 50.24pg/ml，CPAP 治疗后 1.80 至 28.63pg/ml。研究水平的平均差异范围为-1.23 至 21.61。汇总的平均差异为 1.14[95%置信区间 0.12 至 2.15，p=0.03]。该终点存在异质性（df=8，p<0.00001，I²=89%）。白细胞介素-6：研究水平均值范围为 CPAP 治疗前 1.2 至 131.66pg/ml，CPAP 治疗后 0.45 至 66.04pg/ml。研究水平的平均差异范围为-0.40 至 65.62。汇总的平均差异为 1.01[95%置信区间-0.00 至 2.03，p=0.05]。该终点存在异质性（df=7，p<0.00001，I²=95%）。
仅发表的数据。汇总的研究主要是小型、非随机试验。
CPAP 治疗睡眠呼吸暂停可改善炎症标志物水平。
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