恩他卡朋添加治疗症状波动的帕金森病的自身对照临床研究

目的:探讨添加恩他卡朋治疗帕金森病患者剂末现象的疗效及安全性。方法:17例伴有剂末现象的帕金森病患者进行添加服用恩他卡朋前后对照。根据患者日记记录的“开”“关”时间、UPDRSⅡ/Ⅲ评分、左旋多巴每天剂量来综合评估。结果:12周观察显示恩他卡朋添加治疗帕金森病剂末现象能够显著延长“开”时间、缩短“关”时间、降低UPDRSⅡ/Ⅲ评分,没有发现严重不良事件及实验室的异常改变。结论:帕金森病伴有剂末现象患者添加恩他卡朋治疗有效、安全。     

恩他卡朋添加治疗症状波动的帕金森病的随机、双盲、安慰剂对照临床研究

目的:探讨添加恩他卡朋治疗PD患者剂末现象的疗效和安全性。方法:40例伴有剂末现象的PD患者进行随机、双盲、安慰剂、平行分组临床对照试验。根据患者日记记录的"开"、"关"期时间、UPDRS各部分评分、研究者总体评估变化量表和左旋多巴每日剂量来评定疗效。结果:恩他卡朋治疗12周时能显著延长"开"期时间、缩短"关"期时间,降低UPDRS评分,减少每日左旋多巴用量,研究者主观感觉65%的患者病情好转,与安慰剂组相比差异有显著意义。不良事件的发生率与安慰剂组相比差异无显著意义。结论:添加恩他卡朋治疗伴有剂末现象的PD患者安全、有效。     

恩他卡朋治疗帕金森病剂末现象的临床观察

目的探讨恩他卡朋对PD患者剂末现象影响。方法选择40例出现剂末现象的PD患者进行相关资料分析,根据不同治疗方案分为普拉克索组和恩他卡朋组,入选患者治疗8周,分析恩他卡朋对PD剂末现象的疗效。结果恩他卡朋组疗效(90%)高于普拉克索组(60%),UPDRSⅡ评分低于普拉克索组,关期时间短于普拉克索组;恩他卡朋组异动症时间(2.3±0.6)h,低于普拉克索组的(2.7±1.0)h,差异均有统计学意义(P0.05)。结论恩他卡朋能够延长患者开期时间,缩短关期时间,改善剂末现象开期运动症状。     

金刚烷胺治疗帕金森病异动症的疗效观察

目的探讨金刚烷胺治疗帕金森病(PD)左旋多巴诱导异动症(LID)的临床疗效。方法将42例帕金森病患者随机分为金刚烷胺组与恩托卡朋组,每组21例,每组均应用美多巴和普拉克索作为帕金森病基础治疗。经12 w联合用药治疗后,以统一帕金森病评定量表(UPDRS)各部分评分相对于基线(治疗前评分)的变化为指标评估疗效。同时监测血压,观察患者不良反应,比较两组治疗方案的安全性。结果经12 w治疗后金刚烷胺组UPDRS.IV(治疗的并发症)评分相对基线有显著下降.差异有统计学意义(P<0.05)。金刚烷胺组UPDRS.IV(治疗的并发症)评分较恩托卡朋组评分下降更多,差异有统计学意义(P<0.05)。金刚烷胺组临床总有效率为86%,恩托卡朋组临床总有效率为32%,差异有显著统计学意义(P<0.05)。两组药品不良反应发生率分别为19%和23%。差异无统计学意义(P>0.05)。结论金刚烷胺治疗左旋多巴诱导的帕金森病异动症可获得较显著的近期疗效。     

恩他卡朋治疗帕金森病的疗效观察

目的观察恩他卡朋辅助复方多巴制剂对帕金森病患者运动症状的影响。方法原发性帕金森病患者28例,均服用复方多巴制剂并在出现症状加重或运动波动时加用恩他卡朋。服药前、后定期行统一帕金森病评分量表(unified parkinson disease rating scale,UPDRS)Ⅱ与Ⅲ评分,观察其副作用,记录每剂复方多巴制剂的起效时间及药效维持时间。结果UPDRSⅡ与Ⅲ评分在服药前分别为15.1±5.1、22.2±8.1,服药1个月后(10.9±2.8;16.4±4.5)、服药3个月后(12.2±3.5;18.8±5.2)均降低(P<0.01)。服药后每剂药物起效时间不变,药效维持时间延长(1.3±0.6)h(P<0.05)。结论恩他卡朋可改善帕金森病患者的运动功能,副作用少,服用安全。     

帕金森病患者脑脊液胆碱水平减少

作者测定了16例原发性帕金森病患者脑脊液(CSF)乙酰胆碱酯酶(AchE)活性和胆碱水平,从9例相应年龄的正常男性作对照,并以卡方检验作统计学分析。结果表明:8例未经治疗的帕金森病患者其CAF胆碱水平为1.131±0.29nmol/ml,4例接受卡别多巴100mg/日、左旋多巴1000mg/日治疗20±3月的为1.00±0.29umol/ml,4例接受卡别多巴110mg/日、左旋多巴1100mg/日,28±18月及金刚脘胺200mg/日,16±8月治疗的为1.26±0.19nmol/ml,正常组CSF胆碱水平为2.97±0.79nmol/ml,与正常组相比,未治的及治疗的帕金森病患者     

恩他卡朋对帕金森病大鼠的疗效

目的:观察恩他卡朋与左旋多巴/苄丝肼(美多芭)联用对帕金森病大鼠的治疗作用。方法:6-羟多巴(6-OHDA)毁损内侧前脑束(MFB)建立SD大鼠PD模型。成模大鼠腹腔注射不同剂量的美多芭与恩他卡朋,观测大鼠旋转圈数和持续时间。结果:单用恩他卡朋不能诱导PD大鼠旋转。采用美多芭(6.25、12.5mg·kg-1)和不同剂量的恩他卡朋(10、5、0mg·kg-1)联用的PD大鼠,旋转圈数明显增加、旋转时间也明显延长;恩他卡朋的剂量越大,旋转运动的持续时间越长,但出现旋转反应高峰的时间向后推迟。结论:足量的恩他卡朋可以加强左旋多巴的疗效,半量的恩他卡朋疗效欠佳。     

左旋多巴联合恩他卡朋治疗帕金森病疗效观察

目的研究左旋多巴联合恩他卡朋治疗帕金森病(PD)的疗效及对炎症因子、氧化应激指标水平的影响。方法选取132例PD患者为研究对象,随机数字表法分成治疗组和对照组各66例。治疗组给予左旋多巴联合恩他卡朋治疗,对照组给予左旋多巴治疗。3个月后采用帕金森统一评分量表(UPDRS)比较2组临床疗效,记录其治疗前后血清炎症因子[白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)]、血浆氧化应激指标[超氧化物歧化酶(SOD)、谷胱甘肽(GSH)、丙二醛(MDA)水平变化情况。结果 2组治疗后UPDRS评分和IL-1β、IL-6、MDA水平均较治疗前显著降低(P0.05),SOD、GSH水平则较治疗前显著升高(P0.05),且治疗组变化幅度大于对照组(P0.05);治疗组总有效率优于对照组(P0.05)。结论左旋多巴联合恩他卡朋方案对PD患者体内炎症因子和氧化应激指标水平有一定调节作用,疗效确切,于病情转归有利。     

恩他卡朋添加治疗帕金森病症状波动的系统评价

目的 系统评价恩他卡朋治疗帕金森病(PD)症状波动的疗效.方法 采用Pubmed、Embase、Cochrane Database及其他互联网公共搜索引擎作为检索工具,检索国内外1966-2007年6月已发表的有关恩他卡朋对照、安慰剂治疗PD症状波动的临床研究资料.由2位研究者独立评价研究质量.使用Revman 4.2.10进行统计学处理.结果 共纳入10项随机对照临床试验(RCT)研究(共2212例患者),结果 表明恩他卡朋治疗PD伴症状波动的患者有延长"开"期、缩短"关"期、减少每日左旋多巴剂量(WMD=-1.41,95%CI-2.09～-0.72)和改善"开"期运动症状及生活质量的趋势,然而与安慰剂比,恩他卡朋可以增加异动症的发生率(OR=2.00,95%CI 1.55～2.58).结论恩他卡朋可以改善PD症状波动,同时也需要更多设有相同判效指标的大样本高质量RCT研究进一步证实.     

恩他卡朋添加治疗对药效减退的帕金森病患者的疗效观察

目的 探讨恩他卡朋添加治疗对药效减退的帕金森病(PD)患者的疗效及安全性.方法 对4l例服用美多芭疗效减退的PD患者添加恩他卡朋治疗.在添加恩他卡朋治疗前和治疗后第1个月、2个月、3个月分别进行"统一PD评定量表(UPDRS)"评分及运动诱发电位(MEP)检查,比较各时间点美多芭的每日服用总量,并观察其不良反应.结果 添加恩他卡朋治疗后第1个月、2个月、3个月UPDRSⅡ和UPDRSⅢ评分均较添加治疗前明显下降,差异有统计学意义(均P＜0.05),美多芭每日服用总量也明显减少,与添加治疗前比较有统计学意义(均P＜0.05);MEP静息阈值(RMT)在治疗后第3个月明显升高(P＜0.05),潜伏期(CL)及皮质静息期(CSP)明显延长(均P＜0.05);无严重不良反应.结论 恩他卡朋添加治疗能有效改善美多芭药效减退PD患者的运动功能,且安全.     

Customer, Client, Consumer, Recipient, or Patient

Since the arrival of managed care, there has been a trend toward changing the basic terminology used to address clinicians and patients. Instead of the term patient, third party payors frequently use terms such as customer, client, consumer or recipient. One study demonstrated that patients prefer to be called patients. To investigate the preferred term to refer to patients and to be referred to by patients, we mailed a questionnaire to 100 physicians in four medical specialties each and to 100 psychologists. The overall response rate was 61%. Physicians overwhelmingly preferred to refer to patients by the patient's last name, their second preference was the patient's first name. Psychologists preferred to refer to the patients by first name, their second preference was the patient's last name. No group favored using terms such as client, customer, consumer, or recipient. Most physicians and psychologists preferred being referred to as doctors and nobody favored the term provider.     

Fasciitis, perimyositis, myositis, polymyositis, and eosinophilia

Several groups of cases of fasciitis and myositis with eosinophilia are reported. The common features are inflammation into fascia and/or perimysium, and/or muscle fibers; eosinophilia in blood and/or in muscle biopsy. The following classification of 24 cases is suggested: at one end of the spectrum are fasciitis with eosinophilia: diffuse fasciitis (Shulman syndrome): 10 cases (3 with hematological complications); 2 cases of diffuse fasciitis with muscle atrophy; 3 cases of restricted fasciitis. Relapsing perimyositis with eosinophilia belong to the same spectrum, either diffuse (5 cases) with myalgias, or localized (2 cases). Other cases are focal myositis or multiple myositis, polymyositis with eosinophilia. The relationship among these cases is discussed. There is a continuum among the different groups. The pathophysiology remains unknown.     

高海拔地区缺血性卒中患者单核 细胞/HDL-C比值与脑动脉粥样硬化性狭窄的相关性

目的 研究高海拔地区缺血性卒中患者单核细胞/HDL-C比值（monocyte/HDL-C ratio,MHR）与颅内动脉粥样硬化性狭窄（intracranial atherosclerotic stenosis,ICSA）程度的相关性。 方法 回顾性连续纳入2017年6月-2021年6月在青海省人民医院住院治疗的高海拔地区（海拔2260～4080?m）的急性缺血性卒中患者,依据DSA上脑血管狭窄程度（以狭窄最严重的动脉为准）分为无狭窄组、轻度狭窄（狭窄率≤50%）组、中度狭窄（狭窄率50%～70%）组、重度狭窄（狭窄率≥70%）组及闭塞（100%）组。比较5组患者的临床资料、实验室检查指标和MHR,并采用logistic回归模型计算不同程度血管狭窄的独立危险因素。 结果 共纳入349例患者,其中无狭窄组69例、轻度狭窄组78例、中度狭窄组41例、重度狭窄组84例、闭塞组77例。5组中年龄、性别分布、吸烟、饮酒、高血压、糖尿病比例方面差异均有统计学意义,实验室检查中白细胞、单核细胞、中性粒细胞、血小板计数以及血红蛋白、HDL-C水平和MHR差异也有统计学意义。多因素logistic回归分析显示,相对于无动脉狭窄,高龄为脑血管轻度狭窄（OR?1.061,95%CI?1.027～1.097,P＜0.001）,中度狭窄（OR?1.057,95%CI?1.017～1.099,P＝0.005）,重度狭窄（OR?1.096,95%CI?1.057～1.137,P＜0.001）,闭塞（OR?1.036,95%CI?1.001～1.072,P＝0.046）的独立危险因素;相对于无动脉狭窄,高MHR为轻度狭窄（OR?1.041,95%CI?1.009～1.074,P＝0.011）,中度狭窄（OR?1.082,95%CI?1.045～1.119,P＜0.001）,重度狭窄（OR?1.096,95%CI?1.062～1.131,P＜0.001）,闭塞（OR?1.101,95%CI?1.067～1.136,P＜0.001）的独立危险因素;相对于无动脉狭窄,单核细胞计数升高是中度狭窄（OR?1.684,95%CI?1.569～2.725,P=0.027）、重度狭窄（OR?3.529,95%CI?1.541～5.766,P=0.002 ）和闭塞（OR?5.446,95%CI?4.453～6.917,P=0.002）的独立危险因素。 结论 高龄、高MHR和单核细胞计数升高在高海拔地区对急性缺血性卒中患者的脑动脉粥样硬化性狭窄程度具有一定预测价值。     

Pregabalin effect on steady-state pharmacokinetics of carbamazepine, lamotrigine, phenobarbital, phenytoin, topiramate, valproate, and tiagabine

By reducing neuronal excitability through selective binding to the α(2)δ subunit of voltage-dependent calcium channels, pregabalin effectively treats epilepsy, chronic pain, and anxiety disorders. To evaluate if pregabalin coadministration affects pharmacokinetics of other antiepileptic drugs, population pharmacokinetic analyses using NONMEM software were performed on data from three epilepsy trials involving seven antiepileptic drugs with pregabalin as add-on therapy. Results demonstrated that pregabalin did not alter the steady-state plasma concentrations of carbamazepine, lamotrigine, phenobarbital, phenytoin, tiagabine, topiramate, and valproate. Furthermore, the small percent change in the population estimate of antiepileptic drug plasma clearance values (-2% to +7%) suggests that pregabalin coadministration exerted no significant effect on the pharmacokinetics of these antiepileptic drugs, with the possible exception of tiagabine (+34.9%). These findings are in agreement with those of previously published reports. A further clarification study is necessary for tiagabine. In conclusion, it appears that pregabalin can be coadministered with other antiepileptic drugs without concern for significantly altering their pharmacokinetic profiles.     

Clobazam, Oxcarbazepine, Tiagabine, Topiramate, and Other New Antiepileptic Drugs

Summary: Clinical investigators recently have studied at least 21 new antiepileptic drugs (AEDs) in people with epilepsy. This review briefly examines 15 of these new AEDs: clobazam (CLB), dezinamide, flunarizine (FNR), loreclezole, milacemide (MLM), MK-801, nafimidone, ORG-6370, oxcarbazepine (OCBZ), progabide (PGB), ralitoline, stiripentol, tiagabine (TGB), topiramate (TPM), and zonisamide (ZNS). CLB, PGB, and TGB represent agents that act on the GABA system, and MLM acts on the glycine system. MK-801 and ZNS (in part) are excitatory amino acid antagonists, and FNR is a calcium-channel antagonist. OCBZ is a keto analogue of carbam-azepine, which is not metabolized to the epoxide and may have fewer side effects. The remaining agents are novel compounds with a variety of suspected mechanisms. TPM appears especially effective for intractable partial seizures but has a high incidence of cognitive side effects. None of these new AEDs is useful for all patients with inadequate seizure control or ongoing toxicity. The role of each will require further clinical study and experience.     

Consecutive Gas Chromatographic Determination of Phenytoin, Phenobarbital, Primidone, Phenylethylmalondiamide, Carbamazepine, Trimethadione, Dimethadione, Ethosuximide, and Valproate from the Same Serum Specimen

A quantitative gas-liquid chromatographic procedure is described for the consecutive determination of phenytoin, phenobarbital, primidone, phenylethylmalondiamide, carbamazepine, trimethadione, dimethadione, ethosuximide and valproate from a single serum specimen of 1.2 ml. After extraction from serum by two different procedures, the anticonvulsants are chromatographed without further purification on a 3% OV 17 column either with or without derivative formation by means of "on-column" methylation. Multiple internal standards are employed in order to enhance the reproducibility of drug-concentration measurement.