Minoguchi Kenji, Tazaki Toshiyuki, Yokoe Takuya, Minoguchi Hideko, Watanabe Yoshio, Yamamoto Mayumi, Adachi Mitsuru
First Department of Internal Medicine, Showa University, School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142, Japan.
Chest. 2004 Nov;126(5):1473-9. doi: 10.1378/chest.126.5.1473.
Tumor necrosis factor (TNF)-alpha is involved in the pathogenesis of atherosclerosis. In the present study, we examined TNF-alpha production by monocytes, serum levels of TNF-alpha, and the effects of nasal continuous positive airway pressure (nCPAP) in patients with obstructive sleep apnea syndrome (OSAS).
Prospective observational study.
University hospital.
Twenty-four patients with OSAS, 15 obese control subjects, and 12 healthy subjects.
After polysomnography, venous blood was collected at 5 am. Spontaneous production of TNF-alpha by monocytes for 24 h and serum levels of TNF-alpha were investigated. In addition, patients with moderate-to-severe OSAS were treated with nCPAP for 1 month, and spontaneous production of TNF-alpha by monocytes and serum levels of TNF-alpha were also measured. Spontaneous production of TNF-alpha by monocytes was significantly higher in patients with moderate-to-severe OSAS than in patients with mild OSAS (p < 0.0001), obese control subjects (p < 0.0001), or healthy subjects (p < 0.0001). Serum levels of TNF-alpha were also significantly higher in patients with moderate-to-severe OSAS than in patients with mild OSAS (p < 0.03), obese control subjects (p < 0.0005), or healthy subjects (p < 0.0001). Duration of hypoxia during total sleep time was independently associated with spontaneous production of TNF-alpha by monocytes in patients with OSAS and healthy and obese control subjects. nCPAP significantly decreased spontaneous production of TNF-alpha by monocytes (p < 0.03) and serum levels of TNF-alpha (p < 0.05) in patients with moderate-to-severe OSAS.
Spontaneous production of TNF-alpha by monocytes and serum levels of TNF-alpha are elevated in patients with moderate-to-severe OSAS but are decreased by nCPAP.
肿瘤坏死因子(TNF)-α参与动脉粥样硬化的发病机制。在本研究中,我们检测了阻塞性睡眠呼吸暂停综合征(OSAS)患者单核细胞产生的TNF-α、血清TNF-α水平以及经鼻持续气道正压通气(nCPAP)的影响。
前瞻性观察研究。
大学医院。
24例OSAS患者、15例肥胖对照者和12例健康受试者。
多导睡眠图检查后,于凌晨5点采集静脉血。研究单核细胞24小时自发产生的TNF-α以及血清TNF-α水平。此外,对中重度OSAS患者进行nCPAP治疗1个月,并测量单核细胞自发产生的TNF-α和血清TNF-α水平。中重度OSAS患者单核细胞自发产生的TNF-α显著高于轻度OSAS患者(p<0.0001)、肥胖对照者(p<0.0001)或健康受试者(p<0.0001)。中重度OSAS患者的血清TNF-α水平也显著高于轻度OSAS患者(p<0.03)、肥胖对照者(p<0.0005)或健康受试者(p<0.0001)。在OSAS患者以及健康和肥胖对照者中,总睡眠时间内的缺氧持续时间与单核细胞自发产生的TNF-α独立相关。nCPAP显著降低了中重度OSAS患者单核细胞自发产生的TNF-α(p<0.03)和血清TNF-α水平(p<0.05)。
中重度OSAS患者单核细胞自发产生的TNF-α和血清TNF-α水平升高,但nCPAP可使其降低。