摘要目的 观察OSAHS患者血脂、血液流变学的变化,探讨OSAHS与二者变化的相关性.方法 收集2006年8月至2009年4月上海交通大学附属瑞金医院睡眠呼吸疾病诊疗中心就诊的疑有OSAHS者231例,分为4组,确诊OSAHS者中肥胖OSAHS组89例,非肥胖OSAHS组62例;非OSAHS患者中,肥胖组40例,非OSAHS非肥胖组(对照组)40例,检测受试者血脂及血液流变学指标,比较各组间差异.结果 肥胖OSAHS组甘油三酯[(2.74±2.02)mmol/L]、总胆固醇[(5.14±0.96)mmoL/L]均显著高于非肥胖OSAHS组[(1.68±0.83)mmol/L、(4.58±0.93)mmol/L],差异有统计学意义(F=7.77,7.99,均P<0.01);高密度脂蛋白(HDL)[(1.13±0.36)mmol/L]、载脂蛋白A-Ⅰ(apoA-Ⅰ)[(1.20±0.20)mmol/L],显著低于非肥胖OSAHS组[(1.31±0.30)mmol/L、(1.26±0.18)mmol/L].肥胖OSAHS组全血黏度(高切、中切和低切)明显高于非肥胖OSAHS组,差异有统计学意义(F=8.81～11.99,P<0.05).非肥胖OSAHS全血黏度(高切、中切和低切)、红细胞压积(HCT)显著高于对照组(F=6.42～11.99,均P<0.05),组间血脂各项指标末见差异.肥胖OSAHS组全血黏度(高切、中切和低切)及HCT明显高于肥胖组,两组间血脂指标均无差异.非肥胖OSAHS组中轻、中、重度亚组与对照组比较,所有血脂指标差异均无统计学意义(F=0.41～2.23,P>0.05).肥胖OSAHS组中轻、中、重度亚组与肥胖组比较,血脂指标差异均无统计学意义(F=0.12～2.10,P>0.05).结论 OSAHS可能与血脂异常无显著相关,肥胖是导致OSAHS患者血脂代谢紊乱的重要因素;OSAHS与血液流变学异常变化密切相关.

abstractsObjective To investigate whether there was a correlation between lipid level, hemorheology and the obstructive sleep apnea hypopnea syndrome. Methods Two hundred and thirty-one subjects in our sleep respiratory disease center between 2006 and 2009 were included. Eighty nine were obese OSAHS subjects,62 were non-obese OSAHS subjects,40 were obese subjects without OSAHS (obese group) and 40 were non-obese subjects without OSAHS ( control group). We examined and compared the lipid profile and hemorheology in all subjects. Results In obese OSAHS group, the levels of triglyceride(TG) [ (2. 74 ±2. 02) mmol/L],cholesterol(TC) [ (5. 14 ±0. 96) mmol/L] were higher and HDL [ (1. 13 ± 0. 36) mmol/L] ,apoA- Ⅰ[ ( 1. 20 ±0. 20) mmol/L] were lower,compared to the non-obese OSAHS group (F= 7. 77,7. 99, all P < 0.01 ). The level of the whole blood viscosity in obese OSAHS group was significantly higher than that in non-obese OSAHS group ( F = 8. 81 - 11. 99, P < 0. 05 ). There was no significant difference in blood lipid levels among the 2 study groups: non-obese OSAHS and control group,obese OSAHS and obese group ( F = 6. 42 - 11. 99, P > 005 ). The levels of the whole blood viscosity and HCT were significantly higher in non-obese OSAHS group than in control group ( F = 0. 41 - 2. 23, P < 0. 05 ) ; obese OSAHS group were higher than obese group ( F = 0. 12 - 2. 10, P < 0. 05). No significant difference in blood lipid levels was noted among the 4 non-obese groups with different disease severity;similar result was also observed among obese OSAHS groups. Conclusions Obesity is responsible for dyslipidemia in OSAHS. OSAHS has no significant correlation with lipid abnormalities, but it significantly correlates with hemorheology disorder.