Vitamin B12 deficiency

Hunt, Alesia Abigael; Harrington, Dominic J.; Robinson, S.

doi:10.1136/bmj.g5226

Cited by 352 publications

(383 citation statements)

References 21 publications

Supporting

Mentioning

360

Contrasting

Unclassified

Order By: Relevance

“…The classic manifestation of overt vitamin B-12 deficiency, subacute combined degeneration of the spinal cord, involves demyelination of the posterior and lateral tracts of the spinal cord (6,7). Neurologic disturbances associated with B-12 deficiency can affect peripheral motor and sensory systems and include ataxia, gait disturbance, symmetric paresthesia, numbness, impaired vibration or position sensation, abnormal balance, reflexes, and weakness (3,6,7).…”

Section: Introductionmentioning

confidence: 99%

Vitamin B-12 status and neurologic function in older people: a cross-sectional analysis of baseline trial data from the Older People and Enhanced Neurological Function (OPEN) study,

Miles

Allen

Mills

et al. 2016

The American Journal of Clinical Nutrition

View full text Add to dashboard Cite

Background: Aging is associated with a progressive decline in vitamin B-12 status. Overt vitamin B-12 deficiency causes neurologic disturbances in peripheral and central motor and sensory systems, but the public health impact for neurologic disease of moderately low vitamin B-12 status in older people is unclear. Evidence from observational studies is limited by heterogeneity in the definition of vitamin B-12 status and imprecise measures of nerve function. Objective: We aimed to determine whether vitamin B-12 status is associated with electrophysiologic indexes of peripheral or central neurologic function in asymptomatic older people with moderately low vitamin B-12 status. Design: We used a cross-sectional analysis of baseline data from the Older People and Enhanced Neurological Function study conducted in Southeast England. This trial investigated the effectiveness of vitamin B-12 supplementation on electrophysiologic indexes of neurologic function in asymptomatic older people (mean age: 80 y) with moderately low vitamin B-12 status (serum vitamin B-12 concentrations $107 and ,210 pmol/L without anemia, n = 201). Vitamin B-12 status was assessed with the use of total vitamin B-12, holotranscobalamin, and a composite indicator of vitamin B-12 status (cB-12). Electrophysiologic measures of sensory and motor components of peripheral and central nerve function were assessed in all participants by a single observer. Results: In multivariate models, there was no evidence of an association of vitamin B-12, holotranscobalamin, or cB-12 with any nerve conduction outcome. There was also no evidence of an association of vitamin B-12 status with clinical markers of neurologic function. Conclusion: This secondary analysis of high-quality trial data did not show any association of any measure of vitamin B-12 status with either peripheral or central neurologic function or any clinical markers of neurologic function in older people with moderately low vitamin B-12 status. The results of this study are unlikely to be generalizable to a less healthy older population with more severe vitamin B-12 deficiency. This trial was registered at www. controlled-trials.com as ISRCTN54195799.Am J Clin Nutr 2016;104:790-6.

show abstract

Section: Introductionmentioning

confidence: 99%

Vitamin B-12 status and neurologic function in older people: a cross-sectional analysis of baseline trial data from the Older People and Enhanced Neurological Function (OPEN) study,

Miles

Allen

Mills

et al. 2016

The American Journal of Clinical Nutrition

View full text Add to dashboard Cite

show abstract

“…В связи с этим развитие В 12 -дефицитного состояния и его последствий у пожилых людей, веге-тарианцев, а также лиц, страдающих хроническим алкоголизмом или хроническими заболеваниями же-лудочно-кишечного тракта, понятно и ожидаемо. На-стороженность в отношении дефицита витамина В 12 присутствует и при повышенной потребности в нем в период беременности, при приеме ряда препаратов (оральные контрацептивы, ингибиторы протонной пом-пы, антагонисты Н 2 -рецепторов, метформин, колхицин, холестирамин), а также при наличии генетичес кой предрасположенности (синдром Имерслунда-Грес бе-ка, ювенильная пернициозная анемия, врожденные нарушения метаболизма кобаламина) [1][2][3][4]. В то же вре-мя у относительно здоровых молодых людей, не имею-щих ограничений в питании, развитие неврологичес-ких осложнений, связанных с дефицитом витамина В 12 , приводит врача к замешательству.…”

unclassified

Chronic Intoxication With “Laughing Gas” (Nitrous Oxide) as a Cause of B12 Deficiency Myelopolyneuropathy in Young Adults

Супонева¹,

Гришина²,

Legostaeva³

et al. 2016

Neuromuscular Diseases

View full text Add to dashboard Cite

ВведениеОбщая распространенность клинически значимого дефицита витамина В 12 неизвестна, однако риск разви-тия симптомов недостаточности цианокобаламина значительно повышается, прежде всего при нехватке его поступления с пищей (диета, вегетарианство и др.), а также при снижении его всасывания в желудочно-кишечном тракте (хронический атрофический гастрит, воспалительные заболевания кишечника, последствия хирургических операций на желудочно-кишечном трак-те и др.). В связи с этим развитие В 12 -дефицитного состояния и его последствий у пожилых людей, веге-тарианцев, а также лиц, страдающих хроническим алкоголизмом или хроническими заболеваниями же-лудочно-кишечного тракта, понятно и ожидаемо. На-стороженность в отношении дефицита витамина В 12 присутствует и при повышенной потребности в нем в период беременности, при приеме ряда препаратов (оральные контрацептивы, ингибиторы протонной пом-пы, антагонисты Н 2 -рецепторов, метформин, колхицин, холестирамин), а также при наличии генетичес кой предрасположенности (синдром Имерслунда-Грес бе-ка, ювенильная пернициозная анемия, врожденные нарушения метаболизма кобаламина) [1][2][3][4]. В то же вре-мя у относительно здоровых молодых людей, не имею-щих ограничений в питании, развитие неврологичес-ких осложнений, связанных с дефицитом витамина В 12 , приводит врача к замешательству. В связи с этим важ-ным является информирование практикующих врачей (терапевтов, неврологов) о такой причине дефицита цианокобаламина, как хроническое злоупотребление закисью азота («веселящим газом») [5][6][7][8][9]. Ниже мы представляем 2 подобных клинических наблюдения.

show abstract

“…Vitamin B-12 deficiency is a common but serious condition (10). Results from the third NHANES from the US population have reported a prevalence of 3.2% of low serum vitamin B-12 concentrations (,148 pmol/L) for all adults, which reaches 4.4% in individuals aged .50 y (11).…”

Section: Introductionmentioning

confidence: 99%

Association of TCN2 rs1801198 c.776G>C polymorphism with markers of one-carbon metabolism and related diseases: a systematic review and meta-analysis of genetic association studies

Oussalah

Lévy

Filhine-Trésarrieu

et al. 2017

The American Journal of Clinical Nutrition

View full text Add to dashboard Cite

Background: Vitamin B-12 (cobalamin) deficiency may produce severe neurologic and hematologic manifestations. Approximately 20-25% of circulating cobalamin binds to transcobalamin 2 (TCN2), which is referred to as active vitamin B-12. The G allele of the TCN2 c.776G.C (rs1801198) polymorphism has been associated with a lower plasma concentration of holotranscobalamin. However, genotype association studies on rs1801198 have led to conflicting results regarding its influence on one-carbon metabolism (OCM) markers or its association with pathologic conditions. Objective: We assessed the association of rs1801198 genotypes with OCM marker concentrations and primary risks of congenital abnormalities, cancer, and Alzheimer disease. Design: We conducted a systematic review of the literature that was published from January 1966 to February 2017 and included all studies that assessed the association between rs1801198 and OCM markers or a pathologic condition. Results: Thirty-four studies met the inclusion criteria. Subjects with the rs1801198 GG genotype had significantly lower concentrations of holotranscobalamin [standardized mean difference (SMD): 20.445 (95% CI: 20.673, 20.217; P , 0.001); I 2 = 48.16% (95% CI: 0.00%, 78.10%; P = 0.07)] and higher concentrations of homocysteine (European descent only) [SMD: 0.070 (95% CI: 0.020, 0.120; P = 0.01); I 2 = 0.00% (95% CI: 0.00%, 49.59%; P = 0.73)] than did subjects with the rs1801198 CC genotype. The meta-analysis on the association between rs1801198 and methylmalonic acid (MMA) lacked statistical power. No significant difference was observed regarding cobalamin, folate, and red blood cell folate. No significant association was observed between rs1801198 and primary risks of congenital abnormalities, cancer, or Alzheimer disease. Conclusions: Meta-analysis results indicate an influence of rs1801198 on holotranscobalamin and homocysteine concentrations in Europeandescent subjects. In addition, well-designed and -powered studies should be conducted for assessing the association between rs1801198 and MMA and clinical manifestations that are linked to a decreased availability of cobalamin. This review was registered at www.crd.york.ac.uk/prospero as CRD42017058504.

show abstract

Vitamin B12 deficiency

Cited by 352 publications

References 21 publications

Vitamin B-12 status and neurologic function in older people: a cross-sectional analysis of baseline trial data from the Older People and Enhanced Neurological Function (OPEN) study,

Vitamin B-12 status and neurologic function in older people: a cross-sectional analysis of baseline trial data from the Older People and Enhanced Neurological Function (OPEN) study,

Chronic Intoxication With “Laughing Gas” (Nitrous Oxide) as a Cause of B12 Deficiency Myelopolyneuropathy in Young Adults

Association of TCN2 rs1801198 c.776G>C polymorphism with markers of one-carbon metabolism and related diseases: a systematic review and meta-analysis of genetic association studies

Contact Info

Product

Resources

About