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Neurological disorders in vitamin B-12 deficiency

机译:维生素B-12缺乏的神经障碍

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摘要

The review discusses thesteps of vitamin B-12 metabolism and its role in maintaining of neurological functions. The term "vitamin B-12 (cobalamin)" refers to several substances (cobalamins) of a very similar structure. Cobalamin enters the body with animal products. On the periphery cobalamin circulates only in binding with proteins transcobalamin I and II (complex cobalamin-transcobalamin II is designated as "hobotranscobalamin"). Holotranscobalamin is absorbed by different cells, whereas transcobalamin I-binded vitamin B-12- only by liver and kidneys. Two forms of cobalamin were identified as coenzymes of cellular reactions which are methylcobalamin (in cytoplasm) and hydroxy-adenosylcobalamin (in mitochondria). The main causes of cobalamin deficiency are related to inadequate intake of animal products, autoimmune gastritis, pancreatic insufficiency, terminal ileum disease, syndrome of intestinal bacterial overgrowth. Relative deficiency may be seen in excessive binding of vitamin B-12 to transcobalamin I. Cobalamin deficiency most significantly affects functions of blood, nervous system and inflammatory response. Anemia occurs in 13-15% of cases; macrocytosis is an early sign. The average size of neutrophils and monocytes is the most sensitive marker of megaloblastic hematopoiesis. The demands in vitamin B-12 are particularly high in nervous tissue. Hypovitaminosis is accompanied by pathological lesions both in white and gray brain matter. Several types of neurological manifestations are described: subacute combined degeneration of spinal cord (funicular myelinosis), sensomotor polyneuropathy, optic nerve neuropathy, cognitive disorders. The whole range of neuropsychiatric disorders with vitamin B-12 deficiency has not been studied well enough. Due to certain diagnostic difficulties they are often regarded as "cryptogenic", "reactive", "vascular" origin. Normal or decreased total plasma cobalamin level could not a reliable marker of vitamin deficiency. In difficult cases the content of holotranscobalamin, methylmalonic acid/homocysteine, and folate in the blood serum should he investigated besides carefully analysis of clinical manifestations.
机译:审查讨论了维生素B-12代谢的味觉及其在维持神经功能方面的作用。术语“维生素B-12(Cobalamin)”是指非常相似的结构的几种物质(钴胺蛋白)。 Cobalamin用动物产品进入身体。在外周钴胺蛋白仅与蛋白质转基质I和II的结合循环(复杂的钴胺蛋白 - 转基状II被指定为“Hobotranscobalamin”)。 Holotranscobalamin被不同的细胞吸收,而转基质素I结合的维生素B-12-仅由肝脏和肾脏。将两种形式的钴胺蛋白鉴定为细胞反应的辅酶,其是甲基丙二醇蛋白(在细胞质中)和羟基 - 腺苷(Mitochondria)中的级联。钴胺素缺乏的主要原因与动物产品的摄入不足,自身免疫性胃炎,胰腺功能不全,肠胃病,肠道细菌过度生长综合症。维生素B-12的过度结合可以看出相对缺乏,以转基钴胺I.钴胺素缺乏最大程度地影响血液,神经系统和炎症反应的功能。贫血在13-15%的病例中发生;宏细胞症是早期标志。中性粒细胞和单核细胞的平均尺寸是MegaloBolas弹性造血的最敏感的标志物。维生素B-12的要求在神经组织中特别高。下钙胺素伴随着白色和灰色脑中的病理病变。描述了几种类型的神经系统表现:椎间脊髓(鼠髓鞘),患者多肌病,视神经神经病变,认知障碍的亚急性联合退化。含有维生素B-12缺乏的全系列神经精神障碍尚未得到足够的研究。由于某些诊断困难,它们通常被视为“加密”,“反应性”,“血管”起源。正常或降低总血浆钴胺水平不能是维生素缺乏的可靠标志物。在困难的情况下,除了仔细分析临床表现之外,他应该研究血清菌霉素,甲基丙酸/同型半胱氨酸和血清中叶酸的含量。

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