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Laboratory assessment of vitamin B12 status.
J Clin Pathol. 2017 Feb; 70(2):168-173.JC

Abstract

The detection and correction of vitamin B12 (B12) deficiency prevents megaloblastic anaemia and potentially irreversible neuropathy and neuropsychiatric changes. B12 status is commonly estimated using the abundance of the vitamin in serum, with ∼148 pmol/L (200 ng/L) typically set as the threshold for diagnosing deficiency. Serum B12 assays measure the sum of haptocorrin-bound and transcobalamin-bound (known as holotranscobalamin) B12 It is only holotranscobalamin that is taken up by cells to meet metabolic demand. Although receiver operator characteristic curves show holotranscobalamin measurement to be a moderately more reliable marker of B12 status than serum B12, both assays have an indeterminate range. Biochemical evidence of metabolic abnormalities consistent with B12 insufficiency is frequently detected despite an apparently sufficient abundance of the vitamin. Laboratory B12 status markers that reflect cellular utilisation rather than abundance are available. Two forms of B12 act as coenzymes for two different reactions. Methionine synthase requires methylcobalamin for the remethylation of methionine from homocysteine. A homocysteine concentration >20 µmol/L may suggest B12 deficiency in folate-replete patients. In the second B12-dependent reaction, methylmalonyl-CoA mutase uses adenosylcobalamin to convert methylmalonyl-CoA to succinyl-CoA. In B12 deficiency excess methylmalonyl-CoA is hydrolysed to methylmalonic acid. A serum concentration >280 nmol/L may suggest suboptimal status in young patients with normal renal function. No single laboratory marker is suitable for the assessment of B12 status in all patients. Sequential assay selection algorithms or the combination of multiple markers into a single diagnostic indicator are both approaches that can be used to mitigate inherent limitations of each marker when used independently.

Authors+Show Affiliations

The Nutristasis Unit, St Thomas' Hospital NHS Foundation Trust, London, UK. Division of Women's Health, School of Medicine, King's College London, London, UK.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

27169753

Citation

Harrington, Dominic J.. "Laboratory Assessment of Vitamin B12 Status." Journal of Clinical Pathology, vol. 70, no. 2, 2017, pp. 168-173.
Harrington DJ. Laboratory assessment of vitamin B12 status. J Clin Pathol. 2017;70(2):168-173.
Harrington, D. J. (2017). Laboratory assessment of vitamin B12 status. Journal of Clinical Pathology, 70(2), 168-173. https://doi.org/10.1136/jclinpath-2015-203502
Harrington DJ. Laboratory Assessment of Vitamin B12 Status. J Clin Pathol. 2017;70(2):168-173. PubMed PMID: 27169753.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Laboratory assessment of vitamin B12 status. A1 - Harrington,Dominic J, Y1 - 2016/05/11/ PY - 2016/01/08/received PY - 2016/04/19/revised PY - 2016/04/20/accepted PY - 2016/5/14/pubmed PY - 2017/2/7/medline PY - 2016/5/13/entrez KW - B12 KW - COBALAMIN KW - DIAGNOSIS KW - LABORATORY TESTS SP - 168 EP - 173 JF - Journal of clinical pathology JO - J Clin Pathol VL - 70 IS - 2 N2 - The detection and correction of vitamin B12 (B12) deficiency prevents megaloblastic anaemia and potentially irreversible neuropathy and neuropsychiatric changes. B12 status is commonly estimated using the abundance of the vitamin in serum, with ∼148 pmol/L (200 ng/L) typically set as the threshold for diagnosing deficiency. Serum B12 assays measure the sum of haptocorrin-bound and transcobalamin-bound (known as holotranscobalamin) B12 It is only holotranscobalamin that is taken up by cells to meet metabolic demand. Although receiver operator characteristic curves show holotranscobalamin measurement to be a moderately more reliable marker of B12 status than serum B12, both assays have an indeterminate range. Biochemical evidence of metabolic abnormalities consistent with B12 insufficiency is frequently detected despite an apparently sufficient abundance of the vitamin. Laboratory B12 status markers that reflect cellular utilisation rather than abundance are available. Two forms of B12 act as coenzymes for two different reactions. Methionine synthase requires methylcobalamin for the remethylation of methionine from homocysteine. A homocysteine concentration >20 µmol/L may suggest B12 deficiency in folate-replete patients. In the second B12-dependent reaction, methylmalonyl-CoA mutase uses adenosylcobalamin to convert methylmalonyl-CoA to succinyl-CoA. In B12 deficiency excess methylmalonyl-CoA is hydrolysed to methylmalonic acid. A serum concentration >280 nmol/L may suggest suboptimal status in young patients with normal renal function. No single laboratory marker is suitable for the assessment of B12 status in all patients. Sequential assay selection algorithms or the combination of multiple markers into a single diagnostic indicator are both approaches that can be used to mitigate inherent limitations of each marker when used independently. SN - 1472-4146 UR - https://www.unboundmedicine.com/medline/citation/27169753/Laboratory_assessment_of_vitamin_B12_status_ L2 - https://jcp.bmj.com/lookup/pmidlookup?view=long&pmid=27169753 DB - PRIME DP - Unbound Medicine ER -
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