Vitamin K1 (Phylloquinone) Unit Converter
Vitamin K1 (Phylloquinone) Unit Converter
Convert serum vitamin K1 between ng/mL, µg/L and nmol/L — and read the result alongside a lipid profile, because phylloquinone travels on triglyceride-rich lipoproteins and a raised triglyceride inflates it.
Vitamin K1 (Phylloquinone) converter
Mass ⇄ molarFasting serum vitamin K1 0.8 ng/mL
The conversion
ng/mL = nmol/L ÷ 2.21877
because 2.21877 = 1 ng/mL ÷ 450.70 g/mol, the molecular weight of phylloquinone
- ng/mL = µg/L
- identical concentrations written two ways; no arithmetic is needed between them
- MW 450.70 — phylloquinone
- vitamin K1, C₃₁H₄₆O₂: the plant form, from green leafy vegetables and vegetable oils, and the form given as an injection or tablet. Menaquinones (vitamin K2) are different molecules of different chain lengths and are measured separately where they are measured at all
- the lipid problem
- phylloquinone is fat-soluble and circulates on triglyceride-rich lipoproteins. The measured concentration therefore tracks the triglyceride, and a hypertriglyceridaemic sample reads high without any more vitamin reaching the tissues. Some laboratories express the result per unit triglyceride for this reason. Read the K1 with a lipid profile
- light
- phylloquinone is photolabile. The specimen goes into an amber vial or is wrapped, the serum is separated within about two hours, and it is kept light-protected — an exposed sample is reported falsely low
Worked example
Fasting serum vitamin K1 0.8 ng/mL
0.8 ng/mL = 0.80 µg/L — the same number
0.8 × 2.21877 = 1.78 nmol/L
1.78 nmol/L sits inside Mayo's 0.10–2.20 ng/mL interval, which is 0.22–4.88 nmol/L
Going back: 1.78 ÷ 2.21877 = 0.80 ng/mL
Before reading it as vitamin K status, look at the triglyceride on the same sample. Phylloquinone rides on triglyceride-rich lipoproteins, so a fasting triglyceride of 4 mmol/L can carry a K1 into the upper part of the interval in someone whose tissues are no better supplied than anyone else's
Three ways of asking about vitamin K, and what each answers
| Measurement | What it reflects | Standing |
|---|---|---|
| Serum or plasma phylloquinone (this test) | Recent dietary intake, over roughly the last day or two, confounded by the triglyceride it travels on | A measure of circulating vitamin, not of function |
| PIVKA-II — undercarboxylated prothrombin, also called des-gamma-carboxy prothrombin | Whether hepatic vitamin K-dependent carboxylation is actually keeping up. Rises before the prothrombin time moves | The functional marker of hepatic vitamin K status, and the more informative test |
| Prothrombin time / INR | Gross failure of factor II, VII, IX and X carboxylation | Crude and late. It moves only once deficiency is substantial, and it is affected by liver disease and anticoagulants for reasons that have nothing to do with vitamin K intake |
| Undercarboxylated osteocalcin | Extrahepatic (bone) vitamin K status | Used in research on bone and vascular health — see the osteocalcin page |
What raises or lowers a measured phylloquinone, other than vitamin K intake
| Factor | Effect on the measured K1 |
|---|---|
| A non-fasting sample | Raises it, sometimes markedly — phylloquinone appears in chylomicrons within hours of a meal containing it |
| Raised triglycerides | Raises it, because the vitamin is carried on triglyceride-rich lipoproteins. This is the single commonest reason a K1 looks better than the patient’s status |
| Very low triglycerides, or fat malabsorption | Lowers it, both because less is absorbed and because there is less lipoprotein to carry it |
| Light exposure between collection and analysis | Lowers it — the vitamin is destroyed photochemically |
| Lipaemic specimen | May cause the sample to be rejected outright |
| Warfarin | Does not lower phylloquinone. Warfarin blocks the recycling of vitamin K, not its absorption, so a patient on warfarin can have a normal or high K1 with grossly undercarboxylated clotting factors |
Where vitamin K deficiency genuinely arises
| Setting | Mechanism |
|---|---|
| The newborn | Little placental transfer, low concentrations in breast milk and a sterile gut — which is why intramuscular vitamin K is given at birth to prevent vitamin K deficiency bleeding |
| Fat malabsorption: cholestasis, biliary obstruction, coeliac disease, cystic fibrosis, pancreatic insufficiency, short bowel | A fat-soluble vitamin needs bile salts and an intact absorptive surface |
| Prolonged broad-spectrum antibiotics with poor intake | Reduced menaquinone synthesis by colonic bacteria on top of a low dietary intake |
| Prolonged parenteral nutrition without adequate supplementation | No enteral source at all |
| Warfarin and other vitamin K antagonists | Not deficiency of the vitamin but blockade of its recycling — managed by INR monitoring, and reversed with vitamin K where needed |
A fat-soluble vitamin measured on the lipoproteins that carry it
Vitamin K1, phylloquinone, is the plant form of vitamin K: the form in green leafy vegetables and vegetable oils, and the form given therapeutically. Serum concentrations are reported in nanograms per millilitre, identical to micrograms per litre, or in nanomoles per litre, and the bridge is the molecular weight of 450.70 — one nanogram per millilitre is 2.21877 nanomoles per litre. The concentrations are low, which is why the numbers on this page sit below five in either unit.
Two properties of the molecule shape how the result has to be read. The first is that it is photolabile. Phylloquinone is destroyed by light, so the specimen is collected into an amber vial or wrapped, the serum is separated within about two hours, and it is kept light-protected until it is analysed. A sample that travelled in daylight is reported falsely low, and a falsely low vitamin K is a deficiency created by the transport arrangements rather than by the patient.
The second is that phylloquinone is fat-soluble and circulates bound to triglyceride-rich lipoproteins. The measured concentration therefore moves with the triglyceride: a hypertriglyceridaemic patient reads high without any more vitamin reaching their tissues, and a patient with very low triglycerides reads low for the same arithmetic reason. This is why a vitamin K1 is taken fasting — chylomicrons appear within hours of a meal containing the vitamin — why heavily lipaemic samples are rejected, and why some laboratories express the result per unit triglyceride. A K1 interpreted without a lipid profile beside it is being over-read.
Even correctly sampled, a plasma phylloquinone answers a narrow question: how much vitamin K has been eaten recently. It does not say whether vitamin K-dependent carboxylation is keeping up, which is what actually matters. The functional measure is PIVKA-II — undercarboxylated prothrombin, sometimes called des-gamma-carboxy prothrombin — which rises when hepatic carboxylation falls behind and does so before the clotting times move. The prothrombin time and INR are cruder still: they shift only once deficiency is substantial, and they are displaced by liver disease and anticoagulants for reasons unconnected with intake. Warfarin makes the point plainly. It inhibits vitamin K epoxide reductase, blocking the recycling of the vitamin rather than its absorption, so a patient on warfarin can have a perfectly normal phylloquinone alongside grossly undercarboxylated clotting factors — which is why warfarin is monitored by INR and not by this assay.
Frequently asked questions
How do you convert vitamin K1 from ng/mL to nmol/L?
Multiply by 2.21877, which is one nanogram per millilitre divided by phylloquinone’s molecular weight of 450.70 g/mol. A vitamin K1 of 0.8 ng/mL is 1.78 nmol/L. Divide by the same factor to go back, and note that ng/mL and µg/L are numerically identical.
Why do triglycerides affect a vitamin K1 result?
Because phylloquinone is fat-soluble and travels in the blood on triglyceride-rich lipoproteins. The measured concentration therefore rises and falls with the triglyceride independently of how much vitamin reaches the tissues — a hypertriglyceridaemic patient reads high, and someone with very low triglycerides or fat malabsorption reads low. That is why the sample is taken fasting, why lipaemic specimens are often rejected, and why a K1 should be interpreted alongside a lipid profile.
What is the best test of vitamin K status?
PIVKA-II, undercarboxylated prothrombin, is the functional marker: it rises when hepatic vitamin K-dependent carboxylation falls behind, and it does so before the prothrombin time changes. A plasma phylloquinone reflects recent intake rather than function. The prothrombin time or INR is a crude and late indicator, and is influenced by liver disease and anticoagulants for reasons unrelated to vitamin K intake.
Does the sample need protecting from light?
Yes. Phylloquinone is photolabile, so light exposure between collection and analysis destroys some of the vitamin and the result is reported falsely low. Laboratories ask for an amber vial or a wrapped tube, separation within about two hours, and light-protected storage. A 12-hour fast is also required for the reference interval to apply.
Does warfarin lower the vitamin K1 level?
No. Warfarin inhibits vitamin K epoxide reductase, which blocks the recycling of the vitamin after each carboxylation reaction; it does not stop the vitamin being absorbed. A patient on warfarin can therefore have a normal or even raised phylloquinone while their clotting factors are grossly undercarboxylated. That is why warfarin is monitored with the INR rather than with a vitamin K level.
Related calculators
References
- Mayo Clinic Laboratories. Test ID: VITK1 — Vitamin K1, Serum. Reference values: 18 years and over 0.10–2.20 ng/mL. Liquid chromatography tandem mass spectrometry; 12-hour fast required; ship in amber vial protected from light.
- Card DJ, Gorska R, Harrington DJ. Laboratory assessment of vitamin K status. J Clin Pathol. 2020;73(2):70–75. doi:10.1136/jclinpath-2019-205997
- Shearer MJ, Fu X, Booth SL. Vitamin K nutrition, metabolism, and requirements: current concepts and future research. Adv Nutr. 2012;3(2):182–195. doi:10.3945/an.111.001800
- Institute of Medicine. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. Washington DC: National Academies Press; 2001. Vitamin K chapter.
Medical Disclaimer: The tools and content provided here are for educational and reference purposes only. They are not intended to substitute for professional medical advice, diagnosis, or treatment. Clinical decisions should always be based on the comprehensive assessment of a qualified healthcare professional.