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Neurological disorders in vitamin B12 deficiency.
Ter Arkh. 2019 May 16; 91(4):122-129.TA

Abstract

The review discusses thesteps of vitamin B12 metabolism and its role in maintaining of neurological functions. The term "vitamin B12 (cobalamin)" refers to several substances (cobalamins) of a very similar structure. Cobalamin enters the body with animal products. On the peripherу cobalamin circulates only in binding with proteins transcobalamin I and II (complex cobalamin-transcobalamin II is designated as "holotranscobalamin"). Holotranscobalamin is absorbed by different cells, whereas transcobalamin I-binded vitamin B12 - only by liver and kidneys. Two forms of cobalamin were identified as coenzymes of cellular reactions which are methylcobalamin (in cytoplasm) and hydroxyadenosylcobalamin (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 B12 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 B12 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 B12 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 be investigated besides carefully analysis of clinical manifestations.

Authors+Show Affiliations

I.M. Sechenov First Moscow State Medical University of the Ministry of Health of the Russian Federation (Sechenov University), Moscow, Russia.I.M. Sechenov First Moscow State Medical University of the Ministry of Health of the Russian Federation (Sechenov University), Moscow, Russia.I.M. Sechenov First Moscow State Medical University of the Ministry of Health of the Russian Federation (Sechenov University), Moscow, Russia.I.M. Sechenov First Moscow State Medical University of the Ministry of Health of the Russian Federation (Sechenov University), Moscow, Russia.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

31094486

Citation

Pavlov, Ch S., et al. "Neurological Disorders in Vitamin B12 Deficiency." Terapevticheskii Arkhiv, vol. 91, no. 4, 2019, pp. 122-129.
Pavlov CS, Damulin IV, Shulpekova YO, et al. Neurological disorders in vitamin B12 deficiency. Ter Arkh. 2019;91(4):122-129.
Pavlov, C. S., Damulin, I. V., Shulpekova, Y. O., & Andreev, E. A. (2019). Neurological disorders in vitamin B12 deficiency. Terapevticheskii Arkhiv, 91(4), 122-129. https://doi.org/10.26442/00403660.2019.04.000116
Pavlov CS, et al. Neurological Disorders in Vitamin B12 Deficiency. Ter Arkh. 2019 May 16;91(4):122-129. PubMed PMID: 31094486.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Neurological disorders in vitamin B12 deficiency. AU - Pavlov,Ch S, AU - Damulin,I V, AU - Shulpekova,Yu O, AU - Andreev,E A, PY - 2019/5/17/entrez PY - 2019/5/17/pubmed PY - 2019/7/2/medline KW - cobalamin KW - neurologic manifestations of cobalamin deficiency KW - vitamin B12 SP - 122 EP - 129 JF - Terapevticheskii arkhiv JO - Ter Arkh VL - 91 IS - 4 N2 - The review discusses thesteps of vitamin B12 metabolism and its role in maintaining of neurological functions. The term "vitamin B12 (cobalamin)" refers to several substances (cobalamins) of a very similar structure. Cobalamin enters the body with animal products. On the peripherу cobalamin circulates only in binding with proteins transcobalamin I and II (complex cobalamin-transcobalamin II is designated as "holotranscobalamin"). Holotranscobalamin is absorbed by different cells, whereas transcobalamin I-binded vitamin B12 - only by liver and kidneys. Two forms of cobalamin were identified as coenzymes of cellular reactions which are methylcobalamin (in cytoplasm) and hydroxyadenosylcobalamin (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 B12 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 B12 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 B12 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 be investigated besides carefully analysis of clinical manifestations. SN - 0040-3660 UR - https://www.unboundmedicine.com/medline/citation/31094486/Neurological_disorders_in_vitamin_B12_deficiency_ L2 - https://medlineplus.gov/bvitamins.html DB - PRIME DP - Unbound Medicine ER -