THE METHYL FOLATE TRAP A physiological response in man to prevent methyl group deficiency in kwashiorkor (methionine deficiency) and an explanation for folic-acid-induced exacerbation of subacute combined degeneration in pernicious anaemia

Scott, J. M.; Weir, D. G.

doi:10.1016/s0140-6736(81)90650-4

Cited by 237 publications

(95 citation statements)

References 31 publications

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“…The reason for the finding of low methionine is not clear. B 12 deficiency could be one explanation (64 ), but in samples with extremely low methionine (which consistently had increased folate), B 12 was in the high range and tHcy was within the reference interval. Nitrous oxide exposure, which inactivates methionine synthase and thereby leads to increased serum folate, low methionine, and increased tHcy (65 ), is yet another possibility.…”

Section: Relationship Between Methionine and Folatementioning

confidence: 99%

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Screening for Serum Total Homocysteine in Newborn Children

et al. 2004

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Results:The median (5th-95th percentile) tHcy concentration was 6.8 (4.2-12.8) mol/L. B 12 status, as determined by serum concentrations of B 12 , tHcy, and MMA, was moderately better in boys than in girls. tHcy concentrations between 10 and 20 mol/L were often associated with low B 12 , whereas tHcy >20 mol/L (n ‫؍‬ 43) was nearly always explained by increased methionine. tHcy did not differ according to folate concentrations or MTHFR 677C>T genotypes. None of the babies had definite CBS deficiencies, but heterozygosity led to low cystathionine, increased methionine, but normal tHcy concentrations.

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Section: Relationship Between Methionine and Folatementioning

confidence: 99%

“…Thus, the findings in these babies are not consistent with nitrous oxide exposure. A third possibility is a primary methionine deficiency (64 ). Methionine is low in preterm infants before they receive amino acid supplementation (67 ) and may be low in infants before they start nursing.…”

Section: Relationship Between Methionine and Folatementioning

confidence: 99%

Screening for Serum Total Homocysteine in Newborn Children

et al. 2004

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“…The observations that serum folate in infants (but not in older children) tended to be inversely associated with serum cobalamin and positively related to plasma MMA (Table 3) support this contention. However, long-term methylfolate trapping is expected to cause folate depletion (42 ), whereas these infants had high-normal whole-blood folate ( Table 2).…”

Section: Possible Mechanisms and Implications Of Increased Metabolitementioning

confidence: 99%

Cobalamin Status and Its Biochemical Markers Methylmalonic Acid and Homocysteine in Different Age Groups from 4 Days to 19 Years

Monsen¹,

Refsum

Markestad³

et al. 2003

Clinical Chemistry

115

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Background: Recent data indicate that cobalamin and folate status, including the metabolic markers methylmalonic acid (MMA) and total homocysteine (tHcy), undergo marked changes during childhood, particularly during the first year. Methods: Serum cobalamin, serum and whole-blood folate, and plasma MMA and tHcy were determined in a cross-sectional study of 700 children, ages 4 days to 19 years. Results: During the first 6 months, serum cobalamin was lower than and plasma MMA, tHcy, and serum folate were higher than the concentrations detected in the other age groups. In infants 6 weeks to 6 months of age, median MMA and tHcy concentrations were >0.78 and >75 mol/L, respectively. In older children (>6 months), serum cobalamin peaked at 3-7 years and then decreased, median plasma MMA remained low (<0.26 mol/L), median plasma tHcy was low (<6 mol/L) and increased from the age of 7 years on, and serum folate gradually decreased. Plasma MMA was inversely associated with cobalamin (r ‫؍‬ ؊0.4) in both age groups, but across the whole range of cobalamin concentrations, MMA was markedly higher in infants (<6 months) than in older children. Plasma tHcy showed a strong negative correlation to cobalamin (r ‫؍‬ ؊0.52) but not to serum folate in infants <6 months. In older children, tHcy showed the expected association with both cobalamin (r ‫؍‬ ؊0.48) and folate (r ‫؍‬ ؊0.51).

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“…L'altération de la synthèse de l'ADN entraîne un blocage de la maturation cellulaire touchant d'abord les cellules à multiplication rapide d'où les manifestations hé-matologiques et cutanéo-muqueuses [74]. L'altération de la synthèse de la méthionine à partir de l'homocystéine se traduit par un défaut de synthèse de la protéine de base de la myéline ; ce défaut de synthèse est responsable de l'apparition des anomalies de la conduction nerveuse [14,31,70,73]. Les troubles neurologiques peuvent aussi être expliqués par le rôle de cofacteur de la vitamine B12 dans la régulation de la synthèse et de l'activité de certaines cytokines à tropisme neurologique [70,72,77].…”

Section: Absorption De La Vitamine B12 (Fig 2)unclassified

Carence en vitamine B12 (1^repartie) : mise au point

Loup-Leuciuc

Loup

Lombardi

et al. 2011

Med Buccale Chir Buccale

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(Reçu le 12 mai 2011, accepté le 24 juin 2011) Mots clés : vitamine B12 / métabolisme / carence / manifestationsRésumé -Classiquement, la carence en vitamine B12 s'accompagne d'une anémie mégaloblastique, de manifestations neuropsychiatriques et d'une glossite de Hunter. En réalité, les manifestations sont protéiformes et chacune d'elles peut rester longtemps isolée. Les manifestations stomatologiques, souvent discrètes, peuvent précéder de plusieurs années les autres manifestations. Elles constituent parfois un signe d'appel pour le dépistage précoce de cette carence. Depuis une bonne dizaine d'années, la conception de la physiopathologie de la carence en vitamine B12 a beaucoup évolué : on a identifié le syndrome de non-dissociation de la vitamine B12 des protéines porteuses qui constitue maintenant la principale cause de carence en vitamine B12 et il a été démontré qu'on peut effectuer un traitement de la carence per os. Key words: vitamin B12 / metabolism / deficiency / manifestationsAbstract -Vitamin B12 deficency. Part 1: update and littérature review. Vitamin B12 deficiency is classically accompanied by a megaloblastic anemia, neuropsychiatric disorders and an Hunter glossitis. Clinical manifestations are indeed polymorphic and each may remain the only one for a long period of time. Stomatological manifestations, often mild, may precede the others of many years. They sometimes are the first sign to early diagnose this deficiency. Since the last ten years, the physiopathology of vitamin B12 deficiency has considerably changed. In fact, nowadays, the main cause is the syndrome of food cobalamin malabsorption. It has also been demonstrated that the deficiency may now treated by an oral cobalamin therapy.La vitamine B12 est une vitamine hydrosoluble qui a une structure chimique proche de celle de l'hème avec un atome central constitué par du cobalt, d'où le nom de cobalamine (Fig. 1).Elle existe sous plusieurs formes regroupées dans la famille des cobalamines : cyanocobalamine, hydroxocobalamine, mé-thylcobalamine et adénosylcobalamine. La cyanocobalamine et l'hydroxocobalamine sont les seules formes stables. On peut considérer que les recherches sur la vitamine B12 ont commencé au XIX e siècle avec la description d'une anémie mortelle, l'anémie pernicieuse, par Thomas Addison et Michael Anton Biermer. Vers 1920, George Whipple, George Minot et William Murphy, tous les trois Prix Nobel de médecine en 1934, ont démontré que des extraits de foie sous forme de compléments alimentaires étaient susceptibles de corriger certaines anémies. On en a conclu que les extraits de foie contenaient le facteur extrinsèque, en réalité de la vitamine

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THE METHYL FOLATE TRAP A physiological response in man to prevent methyl group deficiency in kwashiorkor (methionine deficiency) and an explanation for folic-acid-induced exacerbation of subacute combined degeneration in pernicious anaemia

Cited by 237 publications

References 31 publications

Screening for Serum Total Homocysteine in Newborn Children

Screening for Serum Total Homocysteine in Newborn Children

Cobalamin Status and Its Biochemical Markers Methylmalonic Acid and Homocysteine in Different Age Groups from 4 Days to 19 Years

Carence en vitamine B12 (1^repartie) : mise au point

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THE METHYL FOLATE TRAP A physiological response in man to prevent methyl group deficiency in kwashiorkor (methionine deficiency) and an explanation for folic-acid-induced exacerbation of subacute combined degeneration in pernicious anaemia

Cited by 237 publications

References 31 publications

Screening for Serum Total Homocysteine in Newborn Children

Screening for Serum Total Homocysteine in Newborn Children

Cobalamin Status and Its Biochemical Markers Methylmalonic Acid and Homocysteine in Different Age Groups from 4 Days to 19 Years

Carence en vitamine B12 (1repartie) : mise au point

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Carence en vitamine B12 (1^repartie) : mise au point