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Pain—Acute
Published in Charles Theisler, Adjuvant Medical Care, 2023
Methylcobalamin (MeCb1) is an activated form of vitamin B12. It exerts its neuronal protection by promoting regeneration of injured nerves and antagonizing gluta-mate-induced neurotoxicity.6 Methylcobalamin has demonstrated significant positive effects on both neck and back pain.7, 8
Cobalamin C, D, F, G diseases; methylmalonic aciduria and variable homocystinuria
Published in William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop, Atlas of Inherited Metabolic Diseases, 2020
William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop
Patients with methylmalonic aciduria and homocystinuria have defective metabolism of cobalamin to both cofactors, methylcobalamin and deoxyadenoxylcobalamin [1–4]. Accordingly, the activities of methionine synthase and methylmalonyl CoA mutase are defective (see Figure 4.1). Patients with impaired synthesis of methylcobalamin and deoxyadenosylcobalamin fall into two distinct complementation groups designated Cbl C and Cbl D. Another group of patients designated Cbl F have defective transport of free cobalamin out of lysosomes. In Cbl G disease, defective activity of methionine synthase results from mutations in the methionine synthase gene [5]. The differential diagnosis of methylmalonic acidemia and homocystinuria is given in Table 4.1.
Megaloblastic Anemias
Published in Harold R. Schumacher, William A. Rock, Sanford A. Stass, Handbook of Hematologic Pathology, 2019
The formation of methionine is central to DNA synthesis and requires both vitamin B12 and folate. Methylcobalamin, a form of vitamin Bi2 is an essential cofactor for methyltransferase in the conversion of homocysteine to methionine (Fig. 1). N5-methyltetrahydrofolate acts as the original methyl donor in this reaction. The methyl group is first transferred from N5-methyltetrahydrofolate to the enzyme-bound cobalamin to form methylcobalamin; methylcobalamin then transfers the methyl group to homocysteine to generate methionine. The importance of this reaction is that it generates tetrahydrofolate. Tetrahydrofolate is required (through its derivative N5, 10-methyltetrahydrofolate) for the conversion of deoxyuridine monophosphate (dUMP) to deoxythymidine monophosphate (dUMP), an immediate precursor of DNA.
Sublingual methylcobalamin treatment is as effective as intramuscular and peroral cyanocobalamin in children age 0–3 years
Published in Hematology, 2021
Betül Orhan Kiliç, Serhat Kiliç, Elif Şahin Eroğlu, Eylem Gül, Fatma Burcu Belen Apak
The first study that is comparing sublingual therapy with intramuscular and peroral is recently published in children between 5–18 ages[11]. Kartal T et al compared the efficacy of sublingual and intramuscular administration of vitamin B12 in terms of normalizing serum cyanocobalamin levels aged 5–18 years[11]. Pre-treatment mean values of serum cyanocobalamin level were increased from 146.7 ± 40.5 ng/L to 565.5 ± 108.1 ng/L in the sublingual group. In conclusion, sublingual methylcobalamin treatment was observed to correct serum vitamin B12 levels similar to intramuscular and sublingual cyanocobalamin treatment. Our results were found to be consistent with this study. Our study also adds additional information to this one as we evaluated mainly breastfed infants as our study evaluated children between 0–3 years.
A blend containing docosahexaenoic acid, arachidonic acid, vitamin B12, vitamin B9, iron and sphingomyelin promotes myelination in an in vitro model
Published in Nutritional Neuroscience, 2020
Jonas Hauser, Sébastien Sultan, Andreas Rytz, Pascal Steiner, Nora Schneider
During early life, infants receive both vit B9 and B12 through breast milk, in which B vitamin content is strongly modulated by maternal nutrition. In addition, all B vitamins are actively transported through the BBB [41]. In our study, we used cyanocobalamin, the common form of vit B12 used for nutritional solutions. The exact cellular mechanisms mediating brain bioavailability of vit B12 are still unclear [42]. In our study, while vit B12 treatment resulted in an early reduction of NF wrapping by MAG, it increased the wrapping of NF by MBP at a later stage. The differential effects of vit B12 observed at 18 and 30 DIV could be mediated by a change in cyanocobalamin metabolism. Notably, cyanocobalamin is an inactive form of vit B12, and needs to be converted into methylcobalamin or 5′-deoxyadenosylcobalamin [43,44]. Therefore, it would be interesting to test whether treatment with methylcobalamin could yield a more beneficial effect compared to cyanocobalamin, as methylcobalamin is the main isoform measured in adult frontal cortex [42].
Emerging Drugs for the Treatment of Amyotrophic Lateral Sclerosis: A Focus on Recent Phase 2 Trials
Published in Expert Opinion on Emerging Drugs, 2020
Andrea Barp, Francesca Gerardi, Andrea Lizio, Valeria Ada Sansone, Christian Lunetta
High-dose methylcobalamin – an active form of vitamin B12 – has been suggested to have a protective effect against neurodegeneration in vitro and in vivo [202]. Clinical research reports have suggested that administration of high-dose methylcobalamin to patients with ALS could have clinically beneficial results [203]. In a recent study by Kaji et al [204] they found no significant differences in either primary endpoint (minimal p value = 0.087). However, post-hoc analyses of methylcobalamin-treated patients diagnosed and entered early (≤12 months’ duration) showed longer time intervals to the primary event (p < 0.025) and less decreases in the ALSFRS-R score (p < 0.025) than the placebo group. Therefore, the authors planned a new investigator-initiated trial ‘The Japan Early-stage Trial of high dose methylcobalamin for ALS (JETALS)’ to evaluate the efficacy and safety of E0302 for ALS patients within 12 months from onset that is ongoing and the follow-up is scheduled to end in March 2020. If the results are positive, we intend to apply for E0302 approval for methylcobalamin as a new drug for treating ALS [205].