Vitamin B12 Unit Converter
Vitamin B12 Unit Converter
Convert serum vitamin B12 between pg/mL, ng/L and pmol/L, and see why a normal result does not exclude deficiency.
Vitamin B12 converter
Mass ⇄ molarSerum vitamin B12 350 pg/mL
Formula and conversion factor
pg/mL = pmol/L ÷ 0.7378
ng/L = pg/mL (numerically identical)
- 0.7378
- derived from the molecular weight of cyanocobalamin, 1355.37 Da
- ng/L
- the same number as pg/mL — 1 ng/L is 1 pg/mL, so no arithmetic is needed between them
- holoTC
- holotranscobalamin, the fraction bound to transcobalamin and available to cells; it is a separate assay and is not what a total B12 reports
Worked example
Serum vitamin B12 350 pg/mL
350 × 0.7378 = 258 pmol/L
= 350 ng/L, since ng/L and pg/mL are numerically identical
Within the 200–900 pg/mL interval shown here, and just above the 150–250 pmol/L grey zone in which functional testing changes management
Common decision points in both units
| pg/mL (ng/L) | pmol/L | Interpretation |
|---|---|---|
| < 200 | < 148 | Below a widely used lower limit — investigate the cause of deficiency |
| 200 – 340 | 148 – 250 | Grey zone; a functional marker changes management here more often than anywhere else |
| 350 | 258 | Worked example — inside the interval and just above the grey zone |
| > 900 | > 664 | Above the interval; usually supplementation, otherwise consider liver or myeloproliferative disease |
What moves the result without changing B12 status
| Direction | Cause | Mechanism |
|---|---|---|
| Falsely raised | Liver disease, myeloproliferative disease, recent supplement or injection | Released or increased circulating binding proteins, or the administered dose itself |
| Falsely lowered | Pregnancy, combined oral contraceptives | Fall in haptocorrin and transcobalamin without a fall in tissue B12 |
| Falsely lowered | Folate deficiency, multiple myeloma | Reduced binding protein concentration |
| Falsely normal or raised | Intrinsic factor antibodies on some competitive-binding assays | Antibody interferes with the assay’s intrinsic factor binder |
Why a serum B12 inside the interval does not exclude deficiency
Serum B12 in pg/mL is converted to pmol/L by multiplying by 0.7378, a factor that follows from the molecular weight of cyanocobalamin, 1355.37 Da. Results reported in ng/L need no conversion at all, since ng/L and pg/mL are numerically identical. The interval shown here, 200–900 pg/mL or roughly 148–664 pmol/L, is a widely used example rather than a universal figure; platforms differ, and the interval printed on the report is the one that applies.
The assay reports the total circulating pool, and most of that pool is bound to haptocorrin and is not available to cells. Only the holotranscobalamin fraction, roughly a fifth of the total, is delivered to tissue. A serum B12 inside the reference interval therefore does not exclude tissue deficiency. Methylmalonic acid and homocysteine are the functional markers, and both rise before serum B12 falls, which is why they resolve the clinical question in a way a borderline total B12 cannot. The grey zone between roughly 150 and 250 pmol/L is where that functional testing most often changes management.
Several conditions move the number without moving B12 status. Results are falsely raised in liver disease and in myeloproliferative disease, where circulating binding proteins are increased or released, and after recent supplementation or an injection, which measures the dose rather than the stores. Results are falsely low in pregnancy and with combined oral contraceptive use, both of which lower the binding proteins without lowering tissue B12, and also in folate deficiency and in multiple myeloma. A single total B12 taken out of that context is a weak test.
The most dangerous failure mode is analytical. Intrinsic factor antibodies can interfere with the intrinsic factor binder used in some competitive-binding assays and produce a spuriously normal or high result in exactly the patients who have pernicious anaemia. A convincing clinical picture — macrocytosis, glossitis, neuropathy, subacute combined degeneration — should not be abandoned because the B12 came back normal. Measure methylmalonic acid, request intrinsic factor antibodies, and if necessary ask the laboratory to repeat the assay on a different platform.
Frequently asked questions
How do I convert vitamin B12 from pg/mL to pmol/L?
Multiply by 0.7378, a factor derived from the molecular weight of cyanocobalamin, 1355.37 Da. A B12 of 350 pg/mL is 258 pmol/L. Results in ng/L are numerically the same as pg/mL.
Does a normal serum B12 exclude deficiency?
No. The assay measures the total circulating pool, most of which is bound to haptocorrin and unavailable to cells; only the holotranscobalamin fraction is delivered to tissue. Methylmalonic acid and homocysteine are the functional markers and both rise before serum B12 falls.
What can make a B12 result falsely high or low?
It is falsely raised in liver disease, myeloproliferative disease and after recent supplementation, and falsely low in pregnancy, with combined oral contraceptives, in folate deficiency and in multiple myeloma. Most of these act by changing the circulating binding proteins.
Can pernicious anaemia give a normal B12?
Yes, and this is the assay’s most dangerous failure mode. Intrinsic factor antibodies can interfere with the intrinsic factor binder in some competitive-binding assays and produce a spuriously normal or high result in the very patients who have pernicious anaemia.
What is the B12 grey zone?
Roughly 150 to 250 pmol/L, about 200 to 340 pg/mL. Within this band neither deficiency nor sufficiency is established by the total B12 alone, and measuring methylmalonic acid or homocysteine is what changes management.
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References
- Devalia V, Hamilton MS, Molloy AM; British Committee for Standards in Haematology. Guidelines for the diagnosis and treatment of cobalamin and folate disorders. Br J Haematol. 2014;166(4):496–513.
- Carmel R. Biomarkers of cobalamin (vitamin B-12) status in the epidemiologic setting. Am J Clin Nutr. 2011;94(1):348S–358S.
- Hoffbrand AV, Higgs DR, Keeling DM, Mehta AB, eds. Postgraduate Haematology. 7th ed. Wiley-Blackwell; 2016.