维生素B12缺乏和帕金森病

Z. Zalyalova, E. V. Ekusheva
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引用次数: 0

摘要

帕金森病(PD)是一种具有多种临床表现的进行性神经退行性疾病,其起源并不总是以多巴胺缺乏来解释。长期服用左旋多巴(特别是经十二指肠内给药),以及临床表现为多神经病变、认知缺陷、门冻结性体位障碍、REM睡眠行为障碍,多与维生素B12缺乏症相关。讨论了这种联系的几个原因及其发展机制。早期发现PD患者,特别是高危人群的钴胺素缺乏症,可以及时制止这种病理状态,防止不可逆的变化。高剂量(1000 μ g)口服维生素B12的现代使用数据显示,与静脉注射形式相比,在使用方便和避免不良注射后反应方面具有相当的临床疗效和显着优势。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Vitamin B12 deficiency and Parkinson’s disease
Parkinson’s disease (PD) is a progressive neurodegenerative disease with various clinical manifestations, its origin not always can be explained only by dopamine deficiency. Long-term treatment with levodopa (especially its intraduodenal administration), as well as clinical manifestations of polyneuropathy, cognitive deficits, postural disorders with freezing of gate, REM sleep behavioral disorders, are more often associated with vitamin B12 deficiency. Several reasons for this association and mechanisms of their development are discussed. Early detection of cobalamin deficiency in PD, especially in patients from high-risk groups, makes it possible to stop this pathological condition timely and prevent irreversible changes. Modern data on the use of high-dose (1000 μ g) oral vitamin B12 are presented, it has comparable clinical efficacy and significant advantages, compared with the parenteral form, in terms of the ease of use and the ability to avoid undesirable postinjection reactions.
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