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不同治疗方案下帕金森病患者周围神经病变的患病率及特征。

Prevalence and features of peripheral neuropathy in Parkinson's disease patients under different therapeutic regimens.

机构信息

Parkinson's Disease and Movement Disorders Centre, Neurology Unit, San Pio X Clinic, Fondazione Opera San Camillo, Milan, Italy.

Parkinson's Disease and Movement Disorders Centre, Department of Neurology, University of Eastern Piedmont "Amedeo Avogadro", Novara, Italy.

出版信息

Parkinsonism Relat Disord. 2014 Jan;20(1):27-31. doi: 10.1016/j.parkreldis.2013.09.007. Epub 2013 Sep 25.

DOI:10.1016/j.parkreldis.2013.09.007
PMID:24099722
Abstract

BACKGROUND

Recent reports suggest increased frequency of peripheral neuropathy (PN) in Parkinson's disease (PD) patients on levodopa compared with age-matched controls particularly during continuous levodopa delivery by intestinal infusion (CLDII). The aim of this study is to compare frequency, clinical features, and outcome of PN in PD patients undergoing different therapeutic regimens.

METHODS

Three groups of consecutive PD patients, 50 on intestinal levodopa (CLDII), 50 on oral levodopa (O-LD) and 50 on other dopaminergic treatment (ODT), were enrolled in this study to assess frequency of PN using clinical and neurophysiological parameters. A biochemical study of all PN patients was performed.

RESULTS

Frequency of PN of no evident cause was 28% in CLDII, 20% in O-LD, and 6% in ODT patients. Clinically, 71% of CLDII patients and all O-LD and ODT PN patients displayed a subacute sensory PN. In contrast, 29% of CLDII patients presented acute motor PN. Levodopa daily dose, vitamin B12 (VB12) and homocysteine (hcy) levels differed significantly in patients with PN compared to patients without PN.

CONCLUSIONS

Our findings support the relationship between levodopa and PN and confirm that an imbalance in VB12/hcy may be a key pathogenic factor. We suggest two different, possibly overlapping mechanisms of PN in patients on CDLII: axonal degeneration due to vitamin deficiency and inflammatory damage. Whether inflammatory damage is triggered by vitamin deficiency and/or by modifications in the intestinal micro-environment should be further explored. Proper vitamin supplementation may prevent peripheral damage in most cases.

摘要

背景

最近的报告表明,与年龄匹配的对照组相比,接受左旋多巴治疗的帕金森病(PD)患者周围神经病变(PN)的频率增加,尤其是在肠道输注(CLDII)持续给予左旋多巴时。本研究的目的是比较不同治疗方案的 PD 患者 PN 的频率、临床特征和结局。

方法

本研究纳入了三组连续的 PD 患者,50 例接受肠道左旋多巴(CLDII)治疗,50 例接受口服左旋多巴(O-LD)治疗,50 例接受其他多巴胺能治疗(ODT)。使用临床和神经生理参数评估 PN 的频率。对所有 PN 患者进行生化研究。

结果

CLDII、O-LD 和 ODT 患者无明显病因的 PN 发生率分别为 28%、20%和 6%。临床方面,71%的 CLDII 患者和所有 O-LD 和 ODT PN 患者表现为亚急性感觉性 PN。相比之下,29%的 CLDII 患者表现为急性运动性 PN。与无 PN 患者相比,PN 患者的左旋多巴日剂量、维生素 B12(VB12)和同型半胱氨酸(hcy)水平差异显著。

结论

我们的发现支持左旋多巴与 PN 之间的关系,并证实 VB12/hcy 失衡可能是一个关键的致病因素。我们提出了 CLDII 患者 PN 的两种不同的、可能重叠的机制:维生素缺乏导致的轴突变性和炎症损伤。炎症损伤是否由维生素缺乏和/或肠道微环境的改变引发,应进一步探讨。适当的维生素补充可能预防大多数情况下的外周损伤。

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