摘要
目的观察艾地苯醌(IDE)对帕金森病患者的运动及非运动症状的改善情况,探讨IDE对帕金森病患者的神经保护作用。方法选取帕金森病患者200例随机分为IDE治疗组(常规治疗+IDE治疗)和常规治疗组(常规治疗),分别监测两组治疗前及治疗后3、6、9、12、15、18个月统一帕金森评分量表(UPDRS)-Ⅲ(开期、关期)、蒙特利尔认知评估量表(MOCA)、匹兹堡睡眠质量指数量表(PSQI)、帕金森非运动症状评价量表(NMSS)评分变化,监测治疗前及治疗后6、12、18个月血超氧化物歧化酶、血尿酸结果的变化。结果①IDE治疗组治疗后3、6、9、12、15、18个月UPDRS-Ⅲ(开期)评分分别为16.64±6.08、14.69±5.33、12.81±4.73、11.04±3.95、9.66±3.43、8.47±3.09,常规治疗组治疗后3、6、9、12、15、18个月UPDRS-Ⅲ(开期)评分分别为16.79±6.44、15.64±6.16、14.58±5.86、13.54±5.56、12.41±5.11、11.16±4.65;治疗后9、12、15、18个月UPDRS-Ⅲ(开期)评分同一时间点相比较,IDE治疗组低于常规治疗组,且差异有统计学意义(P<0.05);治疗后3、6个月两组UPDRS-Ⅲ(开期)评分相比较,差异无统计学意义(P>0.05)。②IDE治疗组治疗后3、6、9、12、15、18个月UPDRS-Ⅲ(关期)评分分别为23.09±8.63、21.10±7.13、19.30±6.24、17.39±5.37、15.65±4.78、14.05±4.25;常规治疗组治疗后3、6、9、12、15、18个月UPDRS-Ⅲ(关期)评分分别为19.85±7.20、19.63±6.85、19.13±6.57、18.32±6.28、17.35±5.97、16.10±5.64;两组治疗后15、18个月UPDRS-Ⅲ(关期)评分同一时间点比较,IDE治疗组低于常规治疗组,且差异有统计学意义(P<0.05);两组治疗后3、6、9、12个月UPDRS-Ⅲ(关期)评分同一时间相比较,差异无统计学意义(P>0.05)。③IDE治疗组在治疗后3、6、9、12、15、18个月MOCA评分分别为21.68±4.59、23.02±3.60、24.39±2.66、25.30±2.12、25.94±1.81、24.72±2.23;常规治疗组在治疗后3、6、9、12、15、18个月MOCA评分分别为22.13±4.64、22.69±4.23、23.40±3.69、24.20±3.18、25.17±2.66、24.27±2.94;治疗后9、12、15个月MOCA评分同一时间点相比较,IDE治疗组高于常规治疗组,且差异有统计学意义(P<0.05);两组治疗后3、6、18个月MOCA评分同一时间点相比较,差异无统计学意义(P>0.05)。④IDE治疗组在治疗后3、6、9、12、15、18个月PSQI评分别为6.36±4.26、5.33±3.84、4.59±3.45、3.32±2.92、2.71±2.38、2.20±2.02,常规治疗组在治疗后3、6、9、12、15、18个月PSQI评分为6.12±4.19、5.25±3.85、4.50±3.50、3.51±3.27、3.26±3.03、3.04±2.84,两组治疗后18个月PSQI评分同一时间点相比较,IDE治疗组优于常规治疗组,且差异有统计学意义(P<0.05);两组治疗后3、6、9、12、15个月PSQI评分同一时间点比较,差异无统计学意义(P>0.05)。⑤IDE治疗组在治疗后3、6、9、12、15、18个月NMSS评分分别为54.69±31.87、52.01±30.11、46.84±30.76、41.20±29.60、38.77±26.67、36.63±25.39;常规治疗组在治疗后3、6、9、12、15、18个月NMSS评分为54.56±33.26、52.42±32.02、50.38±30.65、46.97±28.05、43.18±24.65、41.03±23.48;两组在治疗后3、6、9、12、15、18个月NMSS评分同一时间相比较,差异无统计学意义(P>0.05)。⑥IDE治疗组在治疗后6、12、18个月血尿酸水平分别为(253.81±111.86)μmol/L、(272.56±111.04)μmol/L、(280.12±111.09)μmol/L,常规治疗组在治疗后6、12、18个月血尿酸水平分别为(217.82±103.24)μmol/L、(198.90±102.36)μmol/L、(191.97±101.81)μmol/L,两组治疗后6、12、18个月血尿酸水平同一时间点相比较,IDE治疗组优于常规治疗组,差异有统计学意义(P<0.05)。⑦IDE治疗组在治疗后6、12、18个月血超氧化物歧化酶水平分别为(154.45±39.96)U/mL、(162.45±42.08)U/mL、(172.90±41.78)U/mL,常规治疗组在治疗后6、12、18个月血超氧化物歧化酶水平分别为(126.47±41.30)U/mL、(119.36±39.71)U/mL、(112.17±37.17)U/mL,两组治疗后6、12、18个月血超氧化物歧化酶水平同一时间点相比较,IDE治疗组优于常规治疗组,差异有统计学意义(P<0.05)。结论 IDE能改善帕金森病患者的运动及部分非运动症状,延缓病情的进展,对帕金森病具有一定的神经保护作用。
Objective To investigate the effects of idebenone(IDE) on the motor and non-motor symptoms in patients with Parkinson's disease(PD) and to explore its neuroprotective effect. Methods A total of 200 PD patients were randomly divided into the IDE group(IDE+routine treatment) and routine group(routine treatment). The scores of Unified Parkinson's Disease Rating-III(on-stimulation), UPDRS-III(off-stimulation), Montreal Cognitive Assessment(MOCA), Pittsburgh Sleep Quality Index(PSQI), and Non-Motor Symptoms Scale for Parkinson's Disease(NMSS) were monitored before treatment and 3, 6, 9, 12, 15 and 18 months after treatment. Furthermore, changes of plasma superoxide dismutase(SOD) and uric acid were detected before treatment and 6, 12 and 18 months after treatment. Results ① In month 3, 6, 9, 12, 15 and 18 after treatment, the score of UPDRS-III(on-stimulation) in the IDE group versus that in the routine group was 16.64±6.08 vs 16.79±6.44, 14.69±5.33 vs 15.64±6.16, 12.81±4.73 vs 14.58±5.86, 11.04±3.95 vs 13.54±5.56, 9.664±3.43 vs 12.41±5.11 and 8.471±3.09 vs 11.16±4.65, respectively. In month 3 and 6, there was no difference between the two groups(P>0.05). In month 9, 12, 15 and 18, the score was significantly lower in the IDE group than in the routine group(P<0.05). ② In month 3, 6, 9, 12, 15 and 18 after treatment, the score of UPDRS-III(off-stimulation) in the IDE group versus that in the routine group was 23.09±8.63 vs 19.85±7.20, 21.10±7.13 vs 19.63±6.85, 19.30±6.24 vs 19.13±6.57, 17.39±5.37 vs 18.32±6.28, 15.65±4.78 vs 17.35±5.97 and 14.05±4.25 vs 16.10±5.64, respectively. In month 3, 6, 9 and 12, there was no difference between the two groups(P>0.05). In month 15 and 18, the score was significantly lower in the IDE group than in the routine group(P<0.05). ③ In month 3, 6, 9, 12, 15 and 18 after treatment, the MOCA score in the IDE group versus that in the routine group was 21.68±4.59 vs 22.13±4.64, 23.02±3.60 vs 22.69±4.23, 24.39±2.66 vs 23.40±3.69, 25.30±2.12 vs 24.20±3.18, 25.94±1.81 vs 25.17±2.66 and 24.72±2.23 vs 24.27±2.94, respectively. In month 3, 6 and 18, there was no significant difference between the two groups(P>0.05). In month 9, 12 and 15, the score was significantly higher in the IDE group than in the routine group(P<0.05). ④ In month 3, 6, 9, 12, 15 and 18 after treatment, the PSQI score in the IDE group versus that in the routine group was 6.36±4.26 vs 6.12±4.19, 5.33±3.84 vs 5.25±3.85, 4.59±3.45 vs 4.50±3.50, 3.32±2.92 vs 3.51±3.27, 2.71±2.38 vs 3.26±3.03 and 2.20±2.02 vs 3.04±2.84, respectively. In month 3, 6, 9, 12 and 15, there was no difference between the two groups(P>0.05). In month 18, the score was significantly lower in the IDE group than in the routine group(P<0.05). ⑤ In month 3, 6, 9, 12, 15 and 18 after treatment, the NMSS score in the IDE group versus that in the routine group was 54.6±31.87 vs 54.56±33.26, 52.01±30.11 vs 52.42±32.02, 46.84±30.76 vs 50.38±30.65, 41.20±29.60 vs 46.97±28.05, 38.77±26.67 vs 43.18±24.65, 36.63±25.39 vs 41.03±23.48, respectively. There was no significant difference between the two groups(P>0.05). ⑥ In month 6, 12 and 18 after treatment, the level of uric acid in the IDE group versus the routine group was(253.81±111.86) vs(217.82±103.24) μmol/L,(272.56±111.04) vs(198.90±102.36) μmol/L, and(280.12±111.09) μmol/L vs(191.97±101.81) μmol/L, respectively. The level of uric acid was significantly higher in the IDE group than in the routine group(P<0.05). ⑦ In month 6, 12 and 18, the SOD level in the IDE group versus that in the routine group was(154.45±39.96) vs(126.47±41.30) U/mL,(162.45±42.08) vs(119.36±39.71) U/mL, and(172.90±41.78) vs(112.17±37.17) U/mL, respectively. The SOD level was significantly higher in the IDE group than in the routine group(P<0.05). Conclusion IDE can improve the motor and non-motor symptoms in PD patients and slow down the progression of the disease. It has a certain neuroprotective effect on PD.
引文
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