阻塞性睡眠呼吸暂停综合征患者血浆脂蛋白相关磷脂酶A_2含量的变化

目的观察阻塞性睡眠呼吸暂停综合征(OSAS)患者血浆脂蛋白相关磷脂酶A2(Lp-PLA2)水平的变化特点,探索OSAS相关性脑卒中的病理生理学机制,为临床抗栓治疗提供依据。方法经临床和辅助检查确诊的OSAS患者40例(OSAS组)、伴OSAS的急性脑梗死患者36例(OSAS伴脑梗死组)以及不伴OSAS的急性脑梗死患者38例(脑梗死组)纳入本研究,另选取年龄、性别匹配的36名健康者作为对照组。采用ELISA法检测各组血浆Lp-PLA2水平。结果发病24h时,OSAS组、OSAS伴脑梗死组以及脑梗死组患者血浆LpPLA2水平均显著高于对照组(均P0.01),且OSAS伴脑梗死组血浆Lp-PLA2水平高于OSAS组和脑梗死组(均P0.01)。至发病后21d,OSAS伴脑梗死组患者血浆Lp-PLA2含量仍高于脑梗死组和对照组(P0.01),而脑梗死组和对照组血浆Lp-PLA2水平比较差异无统计学意义(P0.05)。结论 OSAS患者血浆LpPLA2水平升高,提示其体内存在Lp-PLA2相关性炎性反应,LP-PLA2可作为一种理想的分子标记物用于判断OSAS患者体内炎性反应状态;OSAS伴脑梗死患者炎性反应明显且持续时间较长,可能为早期强化抗炎治疗提供理论依据。

Changes of plasma lipoprotein-associated phospholipase A2 levels in patients with obstructive sleep apnea syndrome

Objective To observe the changing characteristics of plasma lipoprotein-associated phospholipase A2 (Lp-PLA2 )levels in patients with obstructive sleep apnea syndrome (OSAS)and to explore the pathophysiological mechanisms of OSAS-associated stroke so as to provide basis for clinical antithrombotic therapy. Methods Forty patients who were diagnosed as OSAS by clinical and accessory examinations did not receive antithrombotic therapy. 36 patients who had OSAS-associated acute cerebral infarction and 38 patients who did not have OSAS-associated acute cerebral infarction were enrolled in the study.And 36 age-matched and sex-matched subjects were used as a control group.The levels of plasma Lp-PLA2 in each groups were measured by ElISA method. Results Within 24 hours after symptom onset,the plasma Lp-PLA2 levels in the OSAS-associated acute cerebral infarction group [(209.89±18.29)ng/mL],in the OSAS group [(195.73±18.98) ng/mL]and in the not OSAS-associated acute cerebral infarction group [(193.45 ± 19.54 )ng/mL]were significantly higher than the control group [(142.55 ± 19.15 )ng/mL] (P < 0.01 ). Twenty-one day after symptom onset,the plasma Lp-PLA2 levels in the OSAS-associated acute cerebral infarction group [(194.98± 17.65) ng/mL]were still higher than the control group [(142.55 ± 19.15 )ng/mL]and the not OSAS-associated acute cerebral infarction group [(146.54 ± 18.56)ng/mL](P <0.01 ). But the plasma Lp-PLA2 levels were no significant differences between the not OSAS-associated acute cerebral infarction group and the control group 21 day after symptom onset (P > 0.05 ). Conclusions The plasma Lp-PLA2 levels were significantly elevated in the OSAS group,the OSAS-associated acute cerebral infarction group or the not OSAS-associated acute cerebral infarction group.We suggest that Lp-PLA2 associated-inflammation may play an important role in the pathogenesis of thromboembolism in OSAS and the measurement of Lp-PLA2 reflects activation of inflammation in vivo and may be a useful marker for the diagnosis of thrombosis or prothrombotic states.Early intensive anti-inflammation therapy may be a good way for the OSAS-associated ischemic stroke.