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731.
732.
Heinz Reichmann 《European journal of neurology》2023,30(Z2):15-20
An important aim in long-term levodopa therapy is to prolong the duration of symptomatic efficacy of each dose without increasing peak plasma concentrations above the threshold for the emergence of dyskinesias. One strategy is to enhance levodopa delivery to the brain by co-administering it with inhibitors of peripheral dopa-decarboxylase and catechol-O-methyltransferase (COMT). Levodopa, carbidopa and entacapone (LCE), available in a range of fixed-dose combinations as the branded formulation Stalevo® (Orion Pharma), has been developed to address this requirement and has been in general use for 20 years, having first been evaluated in randomized controlled trials. Experience with LCE has established that improved levodopa pharmacokinetics achieved with dual-enzyme inhibition are translated into improved clinical efficacy, including the possibility of reducing total levodopa dosage with no loss of therapeutic effect. The ease and tolerability of switching to LCE has been affirmed in the SIMCOM trial and by personal experience detailed in this review. Some 300,000 patient-years of safety data are available for LCE, including trial data for up to 5 years. Most adverse effects associated with LCE are attributable to the levodopa component rather than the enzyme inhibitors. The hepatotoxicity observed with the class comparator tolcapone has not been observed with entacapone, the COMT inhibitor in LCE, and there is no formal requirement to monitor liver function during LCE therapy. Other common side effects include diarrhoea, which is one of the more prominent non-dopaminergic adverse events, and urine discolouration, which is harmless but about which patients may require reassurance. 相似文献
733.
Stefanie T. Jost PhD Marie-Ann Kaldenbach Angelo Antonini MD PhD Pablo Martinez-Martin MD PhD Lars Timmermann MD Per Odin MD PhD Regina Katzenschlager MD Rupam Borgohain MD PhD Alfonso Fasano MD PhD Fabrizio Stocchi MD PhD Nobutaka Hattori MD PhD Prashanth Lingappa Kukkle MD PhD Mayela Rodríguez-Violante MD PhD Cristian Falup-Pecurariu MD PhD Sebastian Schade MD Jan Niklas Petry-Schmelzer MD Vinod Metta MD PhD Daniel Weintraub MD PhD Guenther Deuschl MD Alberto J. Espay MD PhD Eng-King Tan MD PhD Roongroj Bhidayasiri MD PhD Victor S.C. Fung MD PhD Francisco Cardoso MD PhD Claudia Trenkwalder MD Peter Jenner PhD DSc K. Ray Chaudhuri MD PhD Haidar S. Dafsari MD the International Parkinson Movement Disorders Society Non-Motor Parkinson Disease Study Group 《Movement disorders》2023,38(7):1236-1252
Background
To compare drug regimens across clinical trials in Parkinson's disease (PD) conversion formulae between antiparkinsonian drugs have been developed. These are reported in relation to levodopa as the benchmark drug in PD pharmacotherapy as ‘levodopa equivalent dose’ (LED). Currently, the LED conversion formulae proposed in 2010 by Tomlinson et al. based on a systematic review are predominantly used. However, new drugs with established and novel mechanisms of action and novel formulations of longstanding drugs have been developed since 2010. Therefore, consensus proposals for updated LED conversion formulae are needed.Objectives
To update LED conversion formulae based on a systematic review.Methods
The MEDLINE, CENTRAL, and Embase databases were searched from January 2010 to July 2021. Additionally, in a standardized process according to the GRADE grid method, consensus proposals were issued for drugs with scarce data on levodopa dose equivalency.Results
The systematic database search yielded 3076 articles of which 682 were eligible for inclusion in the systematic review. Based on these data and the standardized consensus process, we present proposals for LED conversion formulae for a wide range of drugs that are currently available for the pharmacotherapy of PD or are expected to be introduced soon.Conclusions
The LED conversion formulae issued in this Position Paper will serve as a research tool to compare the equivalence of antiparkinsonian medication across PD study cohorts and facilitate research on the clinical efficacy of pharmacological and surgical treatments as well as other non-pharmacological interventions in PD. © 2023 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society. 相似文献734.
Valentina Leta Lisa Klingelhoefer Katherine Longardner Marta Campagnolo Hafize Çotur Levent Federico Aureli Vinod Metta Roongroj Bhidayasiri Guy Chung-Faye Cristian Falup-Pecurariu Fabrizio Stocchi Peter Jenner Tobias Warnecke K. Ray Chaudhuri International Parkinson Movement Disorders Society Non-Motor Parkinson's Disease Study Group 《European journal of neurology》2023,30(5):1465-1480
Levodopa is the gold standard for the symptomatic treatment of Parkinson's disease (PD). There are well documented motor and non-motor fluctuations, however, that occur almost inevitably once levodopa is started after a variable period in people with PD. Whilst brain neurodegenerative processes play a part in the pathogenesis of these fluctuations, a range of barriers across the gastrointestinal (GI) tract can alter levodopa pharmacokinetics, ultimately contributing to non-optimal levodopa response and symptoms fluctuations. GI barriers to levodopa transport and absorption include dysphagia, delayed gastric emptying, constipation, Helicobacter pylori infection, small intestinal bacterial overgrowth and gut dysbiosis. In addition, a protein-rich diet and concomitant medication intake can further alter levodopa pharmacokinetics. This can result in unpredictable or sub-optimal levodopa response, ‘delayed on’ or ‘no on’ phenomena. In this narrative review, we provided an overview on the plethora of GI obstacles to levodopa transport and absorption in PD and their implications on levodopa pharmacokinetics and development of motor fluctuations. In addition, management strategies to address GI dysfunction in PD are highlighted, including use of non-oral therapies to bypass the GI tract. 相似文献
735.
Rui Yan Huihui Cai Yusha Cui Dongning Su Guoen Cai Fabin Lin Tao Feng 《European journal of neurology》2023,30(4):1118-1134
736.
目的:探讨补肾养肝方药对长期服用左旋多巴帕金森病大鼠黑质纹状体系统功能的影响。方法:建立6-羟基多巴胺(6-OHDA)帕金森病大鼠模型,随机分为4组:假手术组、模型组、左旋多巴组、左旋多巴加补肾养肝组,每组10只。各组药物处理每日1次,12周后处死取材。结果:(1)模型组纹状体多巴胺(DA)、多巴克(DOPAC)、高香草酸(HVA)含量及DOPAC/DA、HVA/DA显著低于假手术组(P<0.05),降低幅度约为90%;左旋多巴组DA、DOPAC、HVA含量及DOPAC/DA、HVA/DA明显高于假手术组;左旋多巴加补肾养肝组DA、DPOAC、HVA含量及DOPAC/DA、HVA/DA显著低于左旋多巴组(P<0.05),接近假手术组水平(P>0.05)。(2)模型组纹状体酪氨酸羟化酶(TH)活性显著低于假手术组,左旋多巴组较模型组显著降低,左旋多巴加补肾养肝组纹状体TH活性显著高于左旋多巴组(P<0.05)。(3)左旋多巴加补肾养肝组中脑THmRNA表达明显高于左旋多巴组。结论:补肾养肝方药能有效改善长期服用左旋多巴造成的不良反应。 相似文献