|
|
Clinical effect of Levodopa and Benserazide Hydrochloride combined with Entacapone in the treatment of Parkinson disease |
WANG Zhiqing YAN Yan▲ |
Department of Pharmacy, Nanjing Brain Hospital, Jiangsu Province, Nanjing 210029, China |
|
|
Abstract Objective To investigate the effect of Levodopa and Benserazide Hydrochloride combined with Entacapone in the treatment of Parkinson disease. Methods One hundred and two patients with Parkinson disease treated in Nanjing Brain Hospital (“our hospital” for short) from January 2014 to June 2016 were selected and randomly divided into combined group and monotherapy group, with 51 cases in each group. Another 51 healthy persons taken body examination in our hospital were selected as control group. The monotherapy group was given conventional Levodopa and Benserazide Hydrochloride, on basis of which, the combined group was added with Entacapone, both groups were treated for 12 weeks. The efficacy and the scores of unified Parkinson disease rating scale Ⅲ (UPDRSⅢ) and activities of daily living (ADL) before and after treatment in the two groups were compared. The motor evoked potential (MEP) of the two groups was detected before and after treatment, including relaxed motor threshold (RMT), cortical latency (CL), cortical silent period (CSP); the levels of plasma homocysteine (Hcy), serum superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and reduced glutathione (GSH) of the two groups were observed before and after treatment, which were compared with control group; the peak concentration of Levodopa and average daily dosage of Levodopa and Benserazide Hydrochloride of the two groups were compared; the conditions of adverse reactions of the two groups were recorded after treatment for half years. Results After treatment, the scores of UPDRSⅢ, ADL in combined group were lower than those before treatment, while RMT, CL, CSR were increased compared with those before treatment (P < 0.05); after treatment, the scores of UPDRSⅢ in monotherapy group were lower than those before treatment, while CL, CSR were increased (P < 0.05); after treatment, the scores of UPDRSⅢ, ADL in combined group were lower than those of monotherapy group, while RMT, CL, CSR were all higher than those of control group (P < 0.05). After treatment, the plasma Hcy in monotherapy group was higher than those of combined group and control group (P < 0.05), while combined group was higher than control group (P < 0.05); the levels of SOD, GSH and GSH-Px in monotherapy group were all lower than those of combined group and control group (P < 0.05), while combined group was lower than control group (P < 0.05). The peak concentration of LD in combined group was higher than that of monotherapy group, while average daily dosage of Levodopa and Benserazide Hydrochloride was lower than that of monotherapy group, the differences were all statistically significant (P < 0.05). At the same time, the total effective rate in combined group (84.3%) was higher than that of monotherapy group (62.7%) (P < 0.05), but the incidence of adverse reactions between combined group (19.6%) and monotherapy group (23.5%) had no statistically significant difference (P > 0.05). Conclusion Levodopa and Benserazide Hydrochloride combined with Entacapone in the treatment of Parkinson disease can make the bioavailability of LD in vivo higher, inhibit the abnormal increase of plasma Hcy, relieve the damage of oxygen free radicals at the same time, with significant effects, which is worthy of promotion.
|
|
|
|
|
[1] 吴艳,杜娟.美多芭联合恩他卡朋对帕金森患者抗氧化应激的研究[J].药学与临床研究,2017,25(1):6-8,38.
[2] Mages L. Management of levodopa for residents with Parkinson's disease [J]. Nursing Older People,2016,28(9):23.
[3] Radford JR. Gut microbiota dysbiosis motor deficits and neuroinflammation in a model of Parkinson's Disease [J]. Br Dent J,2016,221(12):772.
[4] 赵鹏,杨俊峰,刘崴,等.恩他卡朋对左旋多巴治疗的帕金森病患者血浆同型半胱氨酸的影响[J].中华医学杂志,2013,93(7):512-515.
[5] 中华医学会神经病学分会帕金森病及运动障碍学组.中国帕金森病治疗指南(第二版)[J].中华神经科杂志,2009, 42(5):352-355.
[6] 张俊,袁虎.恩他卡朋与金刚烷胺治疗帕金森异动症的临床效果分析[J].河南医学研究,2016,25(6):1017-1018.
[7] Yan MH,Wang X,Zhu X. Mitochondrial defects and oxidative stress in Alzheimer disease and Parkinson disease [J]. Free Radic Biol Med,2013,62(9):90-101.
[8] Mullin S,Schapira AH. Pathogenic Mechanisms of Neurodegeneration in Parkinson Disease [J]. Neurol Clin,2015, 33(1):1-17.
[9] Curtze C,Nutt JG,Carlson-Kuhta P,et al. Objective Gait and Balance Impairments Relate to Balance Confidence and Perceived Mobility in People With Parkinson′s Disease [J].Phys Ther Res,2016,96(11):1734-1743.
[10] Phani S,Loike JD,Przedborski S. Neurodegeneration and Inflammation in Parkinson's disease [J]. Parkinsonism Relat Disord,2012,18(Suppl 1):S207.
[11] 李建,陈侃,高芸,等.左旋多巴治疗对帕金森病患者血浆同型半胱氨酸水平的影响[J].临床神经病学杂志,2014,27(5):399-400.
[12] 解建国,王妍妮.左旋多巴联合恩他卡朋对帕金森病患者血清IL-1β及Cys-C的影响[J].西部医学,2017,29(6):791-794.
[13] 罗娟.恩他卡朋联合复方左旋多巴治疗帕金森病58例疗效及安全性观察[J].中国药业,2014,23(20):43-45.
[14] 张丽,孙萍,谷莹丽,等.血浆同型半胱氨酸与帕金森病临床关系的研究[J].现代生物医学进展,2015,15(19):3660-3663.
[15] Gorgone G,Curro M,Ferlazzo N,et al. Coenzyme Q10,hyperhomocysteinemia and MTHFR C677T polymorphism in levodopa-treated Parkinson′s disease patients [J]. Neuromolecular Med,2012,14(1):84-90.
[16] Abbruzzese G,Barone P,Bonuccelli U,et al. Continuous intestinal infusion of levodopa/carbidopa in advanced Parkinson′s disease:efficacy,safety and patient selection [J]. Funct Neurol,2012,27(3):147.
[17] 史肖锦,屈洪党.脂多糖联合MPTP诱导的小鼠慢性帕金森病模型的评价[J].中国实验动物学报,2015,23(5):513-516.
[18] 崔晓瑞,李名鹏.恩他卡朋与吡贝地尔治疗帕金森病异动症效果的对比研究[J].中国医学创新,2017,14(6):95-97.
[19] 戴毅,吴玉泉,成军,等.普拉克索联合恩他卡朋治疗对帕金森病非运动症状的临床疗效及安全性评价[J].中国临床药理学杂志,2015,31(20):1996-1998.
[20] 李伟英.多巴丝肼联合盐酸普拉克索对老年中晚期PD患者血清中Hcy浓度的影响及其临床意义[J].中国现代医生,2015,53(13):16-18,22.
[21] 吴艳,杜娟,任义胜.美多芭联合恩他卡朋治疗对帕金森病患者血浆同型半胱氨酸水平的影响[J].临床神经病学杂志,2016,29(5):333-335.
[22] 俱西驰,王伟,屈秋民,等.高同型半胱氨酸血症与帕金森病认知功能障碍的关系?[J].成都医学院学报,2015, 10(5):525-527.
[23] 吴艳,杜娟,任义胜,等.美多芭联合恩他卡朋对中晚期帕金森患者的临床疗效研究[J].药学与临床研究,2017, 25(2):121-123.
[24] 江振华,刘晶晶,王恩铭,等.盐酸普拉克索改善帕金森病非运动症状效果评价[J].中国现代医生,2015,53(27):92-94.
[25] 袁永胜,张克忠.帕金森病发病机制的研究进展[J].临床神经病学杂志,2013,26(4):313-315.
[26] 闻公灵,温昌明,王彦平,等.左旋多巴联合恩他卡朋治疗帕金森病的临床研究[J].中国临床药理学杂志,2016, 32(14):1289-1292. |
|
|
|