Copper, Serum or Plasma

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Turnaround Time: 2 - 4 days
CPT Code:


Test Type: 1 mL Serum or plasma
Stability Time:



Room temperature

14 days


14 days


14 days

Freeze/thaw cycles

Stable x3

Reference Range:

Environmental exposure: 72-166 µg/dL. Levels may be somewhat higher in pregnant women and children and in patients receiving estrogen therapy.


It is used, along with serum ceruloplasmin and urine copper, to test for Wilson's disease and (more often) in monitoring the nutritional adequacy of parenteral or enteral nutrition, especially when copper deficiency may be suspected because of ongoing gastrointestinal losses of the element (see table). The test is done in suspected copper toxicity in premature infants when they are acutely ill and may not be able to assimilate the copper in their prescribed nutrition; in acute copper intoxications; or in “Indian childhood cirrhosis,” an illness not limited to Indian children.1 Serum copper is low in Menkes syndrome. Copper in the CSF is reported to mirror the neurotoxicity of copper in Wilson's disease.2 Liver copper is used to confirm Wilson's disease and Menkes syndrome and may be measured in liver disease of uncertain etiology. It can confirm ICC in the right setting. Liver copper rises with time in biliary cirrhosis, but does not confirm the diagnosis.

Serum ceruloplasmin is an acute-phase reactant type protein, and since it binds a large portion of serum copper, both serum copper and ceruloplasmin increase under the influence of inflammatory conditions and estrogen. Serum copper is, therefore, elevated in pregnancy, in patients on estrogens and estrogen-containing contraceptive drugs, in rheumatoid arthritis, and a number of other pathologic entities. It may be low with low serum proteins as in nephrosis, malabsorption, and malnutrition without necessarily reflecting inadequate liver copper stores. It is reduced under the influence of ACTH or glucocorticoids, or valproate3 therapy. Although serum copper levels are usually ordered to work up possible cases of Wilson's disease, Menkes syndrome, and ICC, serum copper alone is of only limited value. Elevations in liver tissue copper are found in Wilson's disease but may occur also in other types of liver disease, especially in primary biliary cirrhosis.4

This test was developed and its performance characteristics determined by LabCorp. It has not been cleared or approved by the Food and Drug Administration.

The demand for sensitive noninvasive tests for Wilson's disease, especially for children in families where the disease is known to occur, has stimulated search for newer indices of copper metabolism. Urine copper after penicillamine load has recently been proposed.5

1. Weiss M, Müller-Höcker J, Wiebecke B, et al. First description of "Indian childhood cirrhosis” in a non-Indian infant in Europe. Acta Paediatr Scand. 1989 Jan; 78(1):152-156. PubMed 2919520

2. Weisner B, Hartard C, Dieu C. CSF copper concentration: A new parameter for diagnosis and monitoring therapy of Wilson's disease with cerebral manifestation. J Neurol Sci. 1987; 79(1-2):229-237. PubMed 3612170

3. Kaji M, Ito M, Okuno T, et al. Serum copper and zinc levels in epileptic children with valproate treatment. Epilepsia. 1992; 33(3):555-557. PubMed 1592036

4. Nadal D, Baerlocher K. Menkes' disease: Long-term treatment with copper and D-penicillamine. Eur J Pediatr. 1988; 147(6):621-625. PubMed 3181204

5. Martins da Costa C, Baldwin D, Portmann B, et al. Value of urinary copper excretion after penicillamine challenge in the diagnosis of Wilson's disease. Hepatology. 1992 Apr; 15(4):609-615. PubMed 1551638

A unified hypothesis of copper transport and uptake. Nutr Rev. 1988 Sep; 46(9):332-333. PubMed 3067152

Clayton BE. Clinical chemistry of trace elements. Adv Clin Chem. 1980; 21:147-176. PubMed 6771970

Danks DM. Copper deficiency in humans. Annu Rev Nutr. 1988; 8:235-257. PubMed 3060166

Danks DM. Disorders of copper transport. In Scriver CR, Beaudet AL, Sly WS, et al, eds.The Metabolic Basis of Inherited Disease. 6th ed. New York, NY: McGraw-Hill Information Services Co; 1989:1411-1431.

Davidoff GN, Votaw ML, Coon WW, et al. Elevations in serum copper, erythrocytic copper, and ceruloplasmin concentrations in smokers. Am J Clin Pathol. 1978 Nov; 70(5):790-792. PubMed 717285

Pereira GR, Zucker AH. Nutritional deficiencies in the neonate. Clin Perinatol. 1986; 13(1):175-189. PubMed 3514049

Prasad AS. Trace elements: Biochemical and clinical effects of zinc and copper. Am J Hematol. 1979; 6(1):77-87. PubMed 453197

Scheinberg IH. Wilson's disease and the physiological chemistry of copper. Inorg Chem Biol Med. 1980; 21:373-380.

Wachnik A. The physiological role of copper and the problems of copper nutritional deficiency. Nahrung. 1988; 32(8):755-765. PubMed 3068548

Youssef AAR, Wood B, Baron DN. Serum copper: A marker of disease activity in rheumatoid arthritis. J Clin Pathol. 1983; 36(1):14-17.

Yuzbasiyan-Gurkan V, Johnson V, Brewer GJ. Diagnosis and characterization of presymptomatic patients with Wilson's disease and the use of molecular genetics to aid in the diagnosis. J Lab Clin Med. 1991; 118(5):458-465. PubMed 1940586

Collection Details:

Collection Instructions:

Royal blue-top (EDTA) tube or royal blue-top without EDTA.

Serum must be separated from cells within 45 minutes of collection and transferred to a certified metal-free plastic transport tube (PeopleSoft N° 111166). Plasma may be separated immediately and transferred to a certified metal-free transport tube (PeopleSoft N° 111166) for shipment to the laboratory.

Maintain specimen at room temperature.