9296. Copper

Copper is an essential trace element required for many processes in the body. A blood copper test is used to diagnose copper deficiency or excess. The test can help determine the causes of anemia and neurological disorders, assess liver diseases (for example, Wilson–Konovalov disease), and monitor nutritional status.

Copper exists in the human body in two oxidation states, Cu²⁺ and Cu⁺. The ability to readily switch between these states underlies its redox properties. Copper binds strongly to proteins, peptides, and other organic compounds. The liver is the key organ involved in copper metabolism, where copper is incorporated into copper-containing enzymes and other proteins. More than 90% of copper is transported from the liver to peripheral tissues bound to ceruloplasmin.

Copper is a catalytic component of numerous enzymes and a structural component of many proteins. Most copper-containing proteins are oxidases. Superoxide dismutase protects cells and plasma from free radicals, cytochrome c oxidase plays an important role in intracellular energy production, and lysyl oxidase is required for stabilization of the extracellular matrix, including the formation of cross-links in collagen and elastin. Copper-containing enzymes are also involved in iron metabolism, the conversion of dopamine to norepinephrine, melatonin synthesis, and gene transcription.

Good dietary sources of copper include red meat and seafood, nuts, whole grains, bran, and cocoa-containing products. Lower amounts are found in dairy products, particularly cow's milk, and white meat.

Congenital disorders of copper metabolism can cause severe conditions, including Menkes syndrome and Wilson–Konovalov disease. Symptoms of copper deficiency may include neutropenia, anemia that does not respond adequately to iron supplementation, osteoporosis and other bone and joint disorders, reduced skin pigmentation, neurological symptoms, and impaired cardiac function.

Impaired copper absorption may occur in diffuse diseases of the small intestine and with the use of preparations containing high concentrations of zinc or cadmium ions. Copper deficiency may also occur in infants, particularly premature infants, receiving copper-deficient formula; in patients receiving long-term parenteral nutrition without adequate trace-element supplementation; and in patients taking zinc-containing medications such as penicillamine.

Elevated copper levels may be observed in primary biliary cholangitis, primary sclerosing cholangitis, hemochromatosis, malignant diseases, thyrotoxicosis, infections, and in patients taking oral contraceptives or estrogens, as well as during pregnancy. Symptoms of copper salt poisoning, including exposure to fungicides or ingestion of copper-containing solutions, may include nausea, vomiting, headache, diarrhea, and abdominal pain. Severe copper poisoning can cause liver injury, jaundice, and hemolytic shock.

• When a disorder of copper metabolism is suspected, particularly for the diagnosis of Wilson–Konovalov disease (excessive copper accumulation) or Menkes disease (copper deficiency).
• In the presence of symptoms of copper deficiency, such as anemia, neutropenia, osteoporosis, and neurological disorders.
• When copper excess is suspected, which may occur due to poisoning or certain liver diseases.
• To monitor the effectiveness of treatment for disorders of copper metabolism.
• As prescribed by a physician for patients with diseases of the blood, liver, nervous system, and other conditions associated with impaired copper metabolism.

• Venous blood

In order to exclude factors that may affect the test results, we recommend to follow the preparation rules: