Why measure Copper, Serum or Plasma?
Blood serum is the portion of an individual’s blood that is not a red or white blood cell and not a blood clotting agent. Therefore, blood serum contains all of the minerals, proteins, electrolytes, and hormones that are found in blood. One of the minerals found in blood serum is copper, and the copper blood serum test is used to assess how much copper is in the serum. If free copper levels are too high, doctors may suspect Wilson’s disease or overuse of dietary supplements containing copper – the latter being the most common cause of abnormally high copper blood levels. If free copper serum test levels are too low (relatively uncommon), one may be suffering from malnourishment or may have Menkes syndrome, a hereditary condition that normally develops in infancy and is very often fatal.
Copper functions:
The human body needs approximately 50 to 80 milligrams of copper to function properly. Copper is taken from ingested food and absorbed into the blood stream. Once in the blood stream, copper attaches to a protein called ceruloplasmin, which transports the copper all over the body. Copper in the blood that does not attach to ceruloplasmin is called free copper. Having too much free copper in the blood can be very dangerous. The free copper will start to move out of the bloodstream and into tissue of the brain, eyes, and kidneys. As the copper starts to build up, it destroys the cells around it, which decreases the functioning of these organs.
What is Wilson's disease (WND)?
Wilson’s disease is hereditary and, as of yet, there is no cure. Fortunately, however, the symptoms can be managed. If symptoms are left untreated, the disease can be fatal.
A copper plasma/serum test is most often used to test for or rule out the presence of Wilson’s disease. The condition disrupts the body’s process for eliminating copper from the body; and so as copper continues to be consumed, copper levels in the blood continue to rise. Much of the body’s copper is found in the liver, which is supposed to filter excess copper into waste so that it can pass out of the body. Wilson’s disease stops copper filtering through the liver appropriately, and one is left with free copper blood levels as much as six times greater than an individual without the disorder. The copper plasma test assesses how much free copper is in an individual’s blood.
Wilson's disease (WND) is an autosomal recessive disorder of copper metabolism caused by mutations in the ATP7B gene. The worldwide prevalence of Wilson's disease is estimated at about 30 in 1 million. In WND, copper stored in the hepatocytes cannot be properly eliminated or complexed to ceruloplasmin, leading to excessive copper accumulation in the liver and other organs, particularly the brain. This condition manifests with various symptoms, including neurological, psychiatric, ophthalmological, and hepatic manifestations.
To diagnose and monitor Wilson's disease, several laboratory tests related to copper metabolism are used. Traditionally, the assessment of copper metabolism in WND involved tests such as serum ceruloplasmin concentration, radioactive copper test, total serum copper concentration, urinary copper excretion, and liver copper content. However, the results of these tests may not always be straightforward and can be challenging to interpret.
Copper levels as a diagnostic tool:
Copper levels in different biological samples can provide valuable diagnostic information. For instance, low serum copper levels are observed in Menkes syndrome. Copper in the cerebrospinal fluid (CSF) is reported to mirror the neurotoxicity of copper in Wilson's disease. Liver copper measurement is used to confirm Wilson's disease and Menkes syndrome and may be applied in cases of liver disease with uncertain etiology.
In certain situations, copper testing is employed to assess copper toxicity in premature infants when they are acutely ill and unable to assimilate copper in their prescribed nutrition. Copper testing is also used in cases of acute copper intoxication and "Indian childhood cirrhosis," a condition not limited to Indian children.
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Hypercupremia is found in primary biliary cholangitis (formerly primary biliary cirrhosis), primary sclerosing cholangitis, hemochromatosis, malignant diseases (including leukemia), thyrotoxicosis, and various infections. Serum copper concentrations are also elevated in patients taking contraceptives or estrogens and during pregnancy.
Since the GI tract effectively excludes excess copper, it is the GI tract that is most affected by copper ingestion. Increased serum concentration does not, by itself, indicate copper toxicity.
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Low serum copper, most often due to excess iron or zinc ingestion and infrequently due to dietary copper deficit, results in severe derangement in growth and impaired erythropoiesis. Low serum copper is also observed in hepatolenticular degeneration (Wilson disease) due to a decrease in the synthesis of ceruloplasmin and allelic variances in cellular metal ion transporters. In Wilson disease, the albumin-bound copper may actually be increased, but ceruloplasmin-bound copper is low, resulting in low serum copper. However, during the acute phase of Wilson disease (fulminant hepatic failure), ceruloplasmin and copper levels may be normal; in this circumstance, hepatic inflammation causes increased release of ceruloplasmin. It is useful to relate the degree of liver inflammation to the ceruloplasmin and copper-see discussion on hypercupremia below. Significant hepatic inflammation with normal ceruloplasmin and copper suggest acute Wilson disease.
Other disorders associated with decreased serum copper concentrations include malnutrition, hypoproteinemia, malabsorption, nephrotic syndrome, Menkes disease, copper toxicity, and megadosing of zinc-containing vitamins (zinc interferes with normal copper absorption from the gastrointestinal [GI] tract).
Excess use of denture cream containing zinc can also cause hypocupremia.
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