Copper Unit Converter

Q: How do I convert serum copper from µg/dL to µmol/L?

Multiply by 0.15737, and divide µmol/L by 6.3546 to go back. The factor is ten divided by copper's standard atomic weight of 63.546, so it is exact rather than conventional. A copper of 105 µg/dL is 16.5 µmol/L. Micrograms per litre is the µg/dL figure multiplied by ten and milligrams per litre is it divided by a hundred.

Q: Why does a copper result need a caeruloplasmin with it?

Because roughly 90 to 95% of serum copper is incorporated into caeruloplasmin, so the total copper largely reports that protein rather than copper status. Caeruloplasmin is an acute-phase reactant and is raised by oestrogen and pregnancy, so the total copper rises in inflammation and on the combined pill; it falls in Wilson disease, in copper deficiency, in aceruloplasminaemia and in protein-losing or severe liver disease. Without the caeruloplasmin there is no way to tell which of those a given total copper represents.

Q: Can a normal serum copper exclude Wilson disease?

No. The EASL guideline records that in Wilson disease the total serum copper is usually decreased in proportion to the decreased caeruloplasmin, that inflammation in the liver or elsewhere may push the caeruloplasmin and hence the copper back into the normal range, and that in Wilson disease presenting as acute liver failure the copper may be markedly elevated from release out of necrotic hepatocytes. Low, normal and high all occur in the same disease. The diagnosis rests on the caeruloplasmin, 24-hour urinary copper, hepatic copper, Kayser-Fleischer rings and ATP7B genotyping.

Q: What is non-caeruloplasmin-bound or free copper, and does this page calculate it?

It is the copper not carried on caeruloplasmin — normally under 10% of the total, 30 to 50% in Wilson disease, and above 200 µg/L in untreated disease. This page tables the derivation and deliberately does not calculate it. It is obtained by subtracting an estimated caeruloplasmin-bound copper from the total, using one of two published coefficients that differ by about 5%, and a published evaluation found 17% of results were negative — impossible, since caeruloplasmin-bound copper cannot exceed total copper — concluding that the calculated figure should not be considered when investigating Wilson disease. A calculator would hide that behind a tidy answer.

Q: Why is the adult female reference interval for copper so much wider?

Because oestrogen increases caeruloplasmin synthesis, and caeruloplasmin carries most of the circulating copper. One reference laboratory gives 73 to 129 µg/dL for males 18 and over and 77 to 206 µg/dL for females, and the difference at the top is essentially that effect, amplified by pregnancy and by combined oral contraceptives. It means a single high-normal copper in a woman of reproductive age carries less information than the same number in a man, and that the drug and pregnancy history belongs with the result.

Q: How does zinc cause copper deficiency?

Zinc induces metallothionein in the intestinal enterocyte, and metallothionein binds copper more avidly than zinc, trapping it in the cell so it is lost rather than absorbed. Sustained zinc intake therefore produces genuine copper depletion, which presents as anaemia, neutropenia or a subacute myelopathy and is regularly mistaken for vitamin B12 deficiency. Anyone on long-term zinc, after bariatric surgery or on long-term parenteral nutrition should have a copper and caeruloplasmin checked, and a normal copper during an inflammatory episode does not exclude it.

Convert serum copper between µg/dL, µmol/L, µg/L and mg/L. Then read it for what it is: nine-tenths of the copper in the sample is bound to caeruloplasmin, so a total copper mostly reports caeruloplasmin, rises as an acute-phase reactant, and can be low, normal or high in Wilson disease.

Last updated 18 Sep 2026

Copper converter

µg/dL ⇄ µmol/L

Serum copper

µg/dL × 0.15737 = µmol/L, from copper’s atomic weight of 63.546. Divide µmol/L by 6.354 to go back. Interpret alongside a caeruloplasmin, not on its own.

Reference interval forOne reference laboratory’s age- and sex-specific intervals. Notice how much wider the adult female one is at the top — 206 against 129 µg/dL — which is not noise: oestrogen raises caeruloplasmin synthesis, and because caeruloplasmin carries most of the circulating copper the total copper follows it. Pregnancy and combined oral contraceptives do the same thing. Confirm against the interval printed on your own report.

16.5µmol/LExample

Serum copper 105 µg/dL in an adult man, with a caeruloplasmin also requested

The ladder, and the protein that is really being measured

µmol/L = µg/dL × 0.15737
µg/dL = µmol/L × 6.3546
because 1 µg/dL is 1 × 10⁻⁵ g/L, and 10⁻⁵ ÷ 63.546 g/mol = 1.5737 × 10⁻⁷ mol/L

0.15737: ten divided by copper’s standard atomic weight of 63.546. Copper is an element, so the molar mass is fixed and the conversion is exact
6.3546: the reciprocal, numerically the atomic weight divided by ten. Useful because SI-reporting laboratories give copper in µmol/L and most published intervals and case reports are in µg/dL
µg/L and mg/L: µg/dL × 10 gives µg/L and µg/dL ÷ 100 gives mg/L. A trace-element laboratory running copper by mass spectrometry alongside zinc and selenium often reports in µg/L, so 105 µg/dL appears as 1,050 µg/L
what the number mostly is: caeruloplasmin. Roughly 90 to 95% of serum copper is incorporated into caeruloplasmin, the rest loosely bound to albumin and small molecules, so the total copper moves with a plasma protein that is also an acute-phase reactant and an oestrogen-responsive one
what it is not: an index of copper status, and not the quantity that matters in Wilson disease. That is non-caeruloplasmin-bound copper, a derived figure — see the table below, and note the objection printed with it

Worked example

Serum copper 105 µg/dL in an adult man, with a caeruloplasmin also requested
105 × 0.15737 = 16.5 µmol/L
105 × 10 = 1,050 µg/L, and 105 ÷ 100 = 1.050 mg/L
Inside the quoted interval of 73 to 129 µg/dL for males 18 years and over
That result is compatible with normal copper status, with Wilson disease, and with copper deficiency masked by inflammation — which is why the caeruloplasmin was requested with it
Had the same number come from an adult woman on a combined oral contraceptive it would carry even less information, because the oestrogen effect on caeruloplasmin is what widens that interval to 206 µg/dL
For the protein itself see the caeruloplasmin converter; for the pairing with zinc see the zinc to copper ratio calculator

What the total copper is actually reporting

This is the whole reason a copper result needs a caeruloplasmin beside it. Because more than nine-tenths of the analyte is bound to one protein, the total copper is close to a second-hand caeruloplasmin measurement, and it inherits caeruloplasmin’s behaviour: it rises with inflammation, with pregnancy and on oestrogen, and falls when caeruloplasmin falls for any reason. A total copper interpreted on its own confuses three quite different situations — normal status, copper deficiency, and copper overload with low caeruloplasmin — and the direction of the error is not predictable from the number.
Fraction	Share of serum copper	What moves it
Caeruloplasmin-bound	One laboratory’s own note: "In normal serum, more than 95% of the copper is incorporated into the enzyme, ceruloplasmin". Duncan et al. put non-caeruloplasmin copper at "< 10% of the total copper" in health, so 90 to 95% is the defensible range	Caeruloplasmin synthesis — up in any inflammatory state, in pregnancy and on oestrogens; down in Wilson disease, in copper deficiency, in aceruloplasminaemia and in severe liver disease or protein loss
Albumin- and small-molecule-bound	"the remaining copper is loosely bound to albumin" and to amino acids	The exchangeable pool. This is the fraction with pathological significance in copper overload, and it is not what the total assay reports
Reported as	The sum of both	Predominantly the first row, which is why the total tracks an acute-phase protein

Non-caeruloplasmin-bound copper: the derivation, and why this page does not compute it

The brief for this page asked for the derivation to be shown and for no second calculator to be built for it, and the literature turns that from a scoping decision into the right one. Non-caeruloplasmin-bound copper is the physiologically meaningful fraction in Wilson disease, but it is obtained by subtracting one imprecise measurement from another, and the published evaluation of that subtraction found nearly a fifth of results were negative — arithmetically impossible — and results spanning both the Wilson and the healthy ranges between laboratories. An input box would have concealed all of that behind a two-decimal answer. Two coefficients are in print, 3.15 µg/mg and 47 µmol/L per g/L, differing by about five per cent through different assumptions about caeruloplasmin’s mass, and a calculator would have had to pick one silently. Where the question is Wilson disease, the diagnosis rests on the Leipzig criteria — caeruloplasmin, 24-hour urinary copper, hepatic copper, Kayser-Fleischer rings, ATP7B genotype — and not on this subtraction.
Published as	Coefficient	What it implies
EASL Wilson’s disease guideline	"3.15 × ceruloplasmin in mg/L equals the amount of ceruloplasmin-bound copper in μg/L", subtracted from the total	3.15 µg Cu per mg caeruloplasmin is 49.6 µmol/L of copper per g/L of caeruloplasmin, implying about 121 kDa at six copper atoms per molecule
Duncan et al., Ann Clin Biochem	"NCBC(μmol/L)=total serum Cu(μmol/L)-(47×serum caeruloplasmin(g/L))"	47 µmol/L per g/L, implying about 128 kDa at six copper atoms. The two published coefficients are therefore about 5% apart
Normal and disease values	"normally, percentage NCBC is < 10% of the total copper with values of 30–50% in Wilson’s disease"; EASL puts untreated Wilson disease above 200 µg/L	The quantity is real and is the one that matters in copper overload
The objection	"16 of the 96 (17%) results were negative, an invalid finding which has been observed previously"	Caeruloplasmin-bound copper cannot exceed total copper. A negative answer means the two assays’ imprecision exceeds the difference being taken
The authors’ conclusion	"the calculated NCBC should not be considered when investigating Wilson’s disease", because "the combined imprecision of the caeruloplasmin and copper methods results in very large variations in NCBC between laboratories"	This is why the derivation is tabled here and not built as a calculator

Total copper in Wilson disease: low, normal or high

Four rows, three directions, one disease. This is the sharpest available demonstration that a total serum copper is not a copper-status measurement: in a condition defined by copper accumulation the total is usually LOW, can be normal, and in the most dangerous presentation is high. The reason is the first table — the total is dominated by caeruloplasmin, and caeruloplasmin is both the protein that fails to be loaded in Wilson disease and an acute-phase reactant that can be pushed back into range by unrelated inflammation. Do not use a total serum copper to exclude Wilson disease. Where it is suspected, a caeruloplasmin, a 24-hour urinary copper, slit-lamp examination and ATP7B genotyping are the tests that carry the diagnosis.
Situation	What the total copper does	Source wording
Typical untreated Wilson disease	Low, tracking the low caeruloplasmin	"Although a disease of copper overload, the total serum copper … in Wilson’s disease is usually decreased in proportion to the decreased ceruloplasmin"
Wilson disease with concurrent inflammation	Normal, because caeruloplasmin has risen	"inflammation in the liver or elsewhere may cause the ceruloplasmin concentration to rise to normal levels"
Wilson disease presenting as acute liver failure	Markedly high	copper "may even be markedly elevated due to the sudden release of the metal from liver tissue stores"
What is raised throughout	Non-caeruloplasmin-bound copper	above 200 µg/L in untreated disease, 30 to 50% of total against under 10% in health

Nine-tenths of this number is a protein measurement

The conversion needs one line and is exact. Copper is an element with a standard atomic weight of 63.546, a microgram per decilitre is 10⁻⁵ g/L, and the quotient is 1.5737 × 10⁻⁷ mol/L, so µg/dL × 0.15737 = µmol/L and µmol/L × 6.3546 = µg/dL. Micrograms per litre is the µg/dL figure times ten and milligrams per litre is it divided by a hundred, which is worth knowing because trace-element laboratories running copper next to zinc and selenium by mass spectrometry often report the whole panel in µg/L.

The interpretive problem is that the quantity being converted is not really a measure of copper status. Between ninety and ninety-five per cent of serum copper is incorporated into caeruloplasmin — one reference laboratory’s own note says more than ninety-five per cent, and the published work on non-caeruloplasmin copper puts the remainder at under ten per cent of the total in health — with the rest loosely bound to albumin and amino acids. A total serum copper is therefore close to a second-hand caeruloplasmin, and it inherits caeruloplasmin’s behaviour rather than copper’s. Caeruloplasmin is an acute-phase reactant, so any inflammatory state raises the total copper. It is oestrogen-responsive, which is why the adult female reference interval quoted on this page reaches 206 µg/dL against 129 for adult men, and why pregnancy and combined oral contraceptives raise it. And it falls in protein-losing states and in severe liver disease, dragging the total copper down with it.

Wilson disease is where this matters most and where the total copper behaves most misleadingly. In a disease of copper overload, the EASL guideline records that the total serum copper is usually decreased in proportion to the decreased caeruloplasmin. Add concurrent inflammation and the caeruloplasmin, and with it the total copper, can rise to normal levels. And in Wilson disease presenting as acute liver failure the total copper may be markedly elevated, from the sudden release of the metal out of necrotic hepatocytes. Low, normal and high, in the same diagnosis, for reasons that have nothing to do with how much copper the patient is carrying. A total serum copper cannot be used to exclude Wilson disease.

The quantity that does matter in overload is the copper not bound to caeruloplasmin — the exchangeable, potentially toxic fraction, normally under ten per cent of the total and thirty to fifty per cent in Wilson disease, with untreated patients above 200 µg/L. It is not measured directly in routine practice; it is derived, by subtracting an estimate of caeruloplasmin-bound copper from the total. The derivation is tabled above with both of the published coefficients, which disagree by about five per cent, and with the objection that accompanies it: in a published evaluation, seventeen per cent of calculated results were negative, which is arithmetically impossible and means the imprecision of the two assays exceeded the difference being taken, and the authors concluded that the calculated figure should not be considered when investigating Wilson disease. That is why this page shows the arithmetic and does not offer to do it. Where Wilson disease is the question, the diagnosis is assembled from the caeruloplasmin, the 24-hour urinary copper, hepatic copper, Kayser-Fleischer rings and ATP7B genotyping.

The commonest reason a copper is actually ordered, though, is the opposite question. Acquired copper deficiency is genuinely easy to miss and genuinely treatable: it arises from zinc supplementation, after bariatric surgery, on long-term parenteral nutrition and in malabsorption, and it presents as anaemia, neutropenia or a subacute myelopathy that is often attributed to vitamin B12 deficiency instead. Here the total copper is more useful, because it falls with the caeruloplasmin and both are low — but the same acute-phase behaviour can mask it, so a normal copper in an inflamed patient does not exclude depletion. If the patient takes zinc, measure both metals: the zinc to copper ratio calculator puts them side by side, the caeruloplasmin converter covers the carrier protein, and a CRP converter tells you whether either result can be read at face value. For the liver enzymes that usually accompany a copper request, see the ALT converter.

Frequently asked questions

How do I convert serum copper from µg/dL to µmol/L?

Multiply by 0.15737, and divide µmol/L by 6.3546 to go back. The factor is ten divided by copper’s standard atomic weight of 63.546, so it is exact rather than conventional. A copper of 105 µg/dL is 16.5 µmol/L. Micrograms per litre is the µg/dL figure multiplied by ten and milligrams per litre is it divided by a hundred.

Why does a copper result need a caeruloplasmin with it?

Because roughly 90 to 95% of serum copper is incorporated into caeruloplasmin, so the total copper largely reports that protein rather than copper status. Caeruloplasmin is an acute-phase reactant and is raised by oestrogen and pregnancy, so the total copper rises in inflammation and on the combined pill; it falls in Wilson disease, in copper deficiency, in aceruloplasminaemia and in protein-losing or severe liver disease. Without the caeruloplasmin there is no way to tell which of those a given total copper represents.

Can a normal serum copper exclude Wilson disease?

No. The EASL guideline records that in Wilson disease the total serum copper is usually decreased in proportion to the decreased caeruloplasmin, that inflammation in the liver or elsewhere may push the caeruloplasmin and hence the copper back into the normal range, and that in Wilson disease presenting as acute liver failure the copper may be markedly elevated from release out of necrotic hepatocytes. Low, normal and high all occur in the same disease. The diagnosis rests on the caeruloplasmin, 24-hour urinary copper, hepatic copper, Kayser-Fleischer rings and ATP7B genotyping.

What is non-caeruloplasmin-bound or free copper, and does this page calculate it?

It is the copper not carried on caeruloplasmin — normally under 10% of the total, 30 to 50% in Wilson disease, and above 200 µg/L in untreated disease. This page tables the derivation and deliberately does not calculate it. It is obtained by subtracting an estimated caeruloplasmin-bound copper from the total, using one of two published coefficients that differ by about 5%, and a published evaluation found 17% of results were negative — impossible, since caeruloplasmin-bound copper cannot exceed total copper — concluding that the calculated figure should not be considered when investigating Wilson disease. A calculator would hide that behind a tidy answer.

Why is the adult female reference interval for copper so much wider?

Because oestrogen increases caeruloplasmin synthesis, and caeruloplasmin carries most of the circulating copper. One reference laboratory gives 73 to 129 µg/dL for males 18 and over and 77 to 206 µg/dL for females, and the difference at the top is essentially that effect, amplified by pregnancy and by combined oral contraceptives. It means a single high-normal copper in a woman of reproductive age carries less information than the same number in a man, and that the drug and pregnancy history belongs with the result.

How does zinc cause copper deficiency?

Zinc induces metallothionein in the intestinal enterocyte, and metallothionein binds copper more avidly than zinc, trapping it in the cell so it is lost rather than absorbed. Sustained zinc intake therefore produces genuine copper depletion, which presents as anaemia, neutropenia or a subacute myelopathy and is regularly mistaken for vitamin B12 deficiency. Anyone on long-term zinc, after bariatric surgery or on long-term parenteral nutrition should have a copper and caeruloplasmin checked, and a normal copper during an inflammatory episode does not exclude it.

Related calculators

References

European Association for the Study of the Liver. EASL clinical practice guidelines: Wilson’s disease. J Hepatol. 2012;56(3):671–685. "3.15 × ceruloplasmin in mg/L equals the amount of ceruloplasmin-bound copper in μg/L"; untreated disease non-caeruloplasmin copper above "200 μg/L"; "Although a disease of copper overload, the total serum copper … in Wilson’s disease is usually decreased in proportion to the decreased ceruloplasmin"; in acute liver failure copper "may even be markedly elevated due to the sudden release of the metal from liver tissue stores"; caeruloplasmin is "an acute phase reactant" and "inflammation in the liver or elsewhere may cause the ceruloplasmin concentration to rise to normal levels".
Duncan A, Yacoubian C, Beetham R, Catchpole A, Bullock D. The role of calculated non-caeruloplasmin-bound copper in Wilson’s disease. Ann Clin Biochem. 2017;54(6):649–654. "NCBC(μmol/L)=total serum Cu(μmol/L)-(47×serum caeruloplasmin(g/L))"; "normally, percentage NCBC is < 10% of the total copper with values of 30–50% in Wilson’s disease"; "16 of the 96 (17%) results were negative, an invalid finding which has been observed previously"; "the calculated NCBC should not be considered when investigating Wilson’s disease".
Mayo Clinic Laboratories. Copper, Serum, test CUS1. Reference values "11-17 yrs. 75 – 145 mcg/dL", "≥18 yrs. (Males) 73-129 mcg/dL", "≥18 yrs. (Females) 77-206 mcg/dL", "13 mos. – 10 yrs. 80 – 180 mcg/dL"; royal-blue-top trace-element tube; "In normal serum, more than 95% of the copper is incorporated into the enzyme, ceruloplasmin; the remaining copper is loosely bound to albumin"; "Avoid hemolysis".
Willis MS, Monaghan SA, Miller ML, et al. Zinc-induced copper deficiency: a report of three cases initially recognized on bone marrow examination. Am J Clin Pathol. 2005;123(1):125–131.
Duncan A, Yacoubian C, Watson N, Morrison I. The risk of copper deficiency in patients prescribed zinc supplements. J Clin Pathol. 2015;68(9):723–725.

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.