血清同型半胱氨酸与阻塞性睡眠呼吸暂停低通气综合征患者氧化应激的关系

目的：探讨不同疾病程度的阻塞性睡眠呼吸暂停低通气综合征（OSAHS）患者血清同型半胱氨酸（Hcy）和丙二醛（MDA）及谷胱甘肽（GSH）水平的变化。方法选取2008年6月～2013年12月就诊于苏州大学附属第一医院睡眠中心的患者行多导睡眠监测，依据多导睡眠图（PSG）监测结果确诊为OSAHS的117例患者被分成3组：轻度OSAHS、中度OSAHS、重度OSAHS，选取同期经PSG监测呼吸暂停低通气指数（AHI）＜5次/h的33名健康者为对照组，所有受试者均被记录睡眠呼吸监测相关指标和晨起采取空腹肘静脉血4 mL，采用循环酶法测定Hcy,紫外分光光度比色法测定MDA、GSH。结果血清MDA水平：重度组显著高于对照组、轻度组、中度组[（7.33±1.04）比（4.55±0.87）、（5.39±1.28）、（6.77±0.66）μmol/L]（均P＜0.05）。血清GSH水平：轻、中度组均显著高于对照组[（6.49±2.10）、（7.52±1.50）比（4.21±1.39）mg/L]（均P＜0.05），但重度组[（4.62±1.40）mg/L]与对照组差异无统计学意义（P＞0.05）。血清Hcy水平：轻、中度组均显著高于对照组[（10.30±1.98）、（13.31±2.63）比（8.72±0.68）μmol/L]（P＜0.05），但重度组[（9.53±1.84）μmol/L]与对照组差异无统计学意义（P＞0.05）。结论氧化应激损伤水平与抗氧化水平在OSAHS患者疾病的不同阶段，变化不完全一致。Hcy的改变与抗氧化水平GSH改变同步，与疾病的严重程度不同步。氧化应激的作用可能是OSAHS患者血清Hcy水平改变的内在机制。

Association Between Serum Homocysteine Level and Oxidative Stress in Patients with Obstructive Sleep Apnea/Hypopnea Syndrome

Objective To investigate the changes of serum homocysteine （Hcy）, malonaldehyde （MDA） and glutathione （GSH） in patients with obstructive sleep apnea/hypopnea syndrome （OSAHS） at different stages of disease. Methods Patients who were submitted to overnight full polysomnography （PSG） study were selected from the Sleep Disorders Center in the First Affiliated Hospital of Soochow University between June 2008 and December 2013. 117 patients with OSAHS recruited and divided into three patients groups （mild OSAHS, moderate OSAHS and severe OSAHS） were compared with the 33 normal people （controls）. All subjects were recorded PSG variables and the contents of Hcy, MDA and GSH which were detected after sleep. Serum Hcy was measured by cyclophorase. MDA and GSH were measured by spectrophotometer. Results The concentrations of MDA in severe group were higher than those in the other three groups （[7.33±1.04 vs 4.55±0.87, 5.39±1.28, 6.77±0.66] μmol/L, all P〈0.05）. The concentrations of GSH in the mild and moderate groups were both higher than the controls （[6.49±2.10, 7.52±1.50 vs 4.21±1.39] mg/L, all P〈0.05）, but there was no significant difference in the severe group[（4.62±1.40） mg/L] and controls （P〉0.05）. The Hcy level in the mild and moderate groups were both higher than the controls （[10.30±1.98, 13.31±2.63 vs 8.72±0.68]μmol/L, all P〈0.05）, but there was no significant difference in the severe group （[9.53±1.84]μmol/L） and controls （P〉0.05）. Conclusion The change of marker levels in oxidative stress is not entirely consistent with the antioxidant levels in the OSAHS patients at different stages of disease. The change of Hcy levels is proportional to GSH levels, but not proportional to the severity in OSAHS patients. The mechanism of serum Hcy change in patients with OSAHS might be oxidative stress.