Copper | Cu (blood)

General Information

Copper is an essential component of enzyme systems that participate in the formation of hemoglobin, carbohydrate metabolism, catecholamine biosynthesis, and the formation of cross-links in hair collagen, elastin, and keratin.

Copper deficiency causes anemia, neutropenia, and growth disorders in children.

Copper is mainly ingested with food. After absorption, it binds to albumin and ceruloplasmin and is deposited mainly in the liver and, to a lesser extent, in the kidneys. Copper is excreted mainly via the biliary system. Its excretion in the urine is insignificant.

Disturbances in copper homeostasis are associated with a number of diseases, such as Wilson's disease, Menkes syndrome, copper intoxication, and others.

When is the survey conducted?

• Suspicion of Wilson's disease (it is recommended to also determine ceruloplasmin).
• Suspicion of acute or chronic poisoning

Patient preparation – It is preferable to conduct the study without fasting.

Reference boundaries

Women on hormone therapy

15,7-31,5

Women without hormone therapy

10,7-26,6

BABY

< 1 month: 7,6 – 11,3

From 1 month to 6 years: 9,4- 20,5

>6 -17 years: 10,4 – 21,4

Women: >17 years old: 12,0 – 24,0

Men: > 17 years old: 11,0 – 22,0

Interpretation of results

The main part of plasma copper is bound to ceruloplasmin. Ceruloplasmin is an acute phase protein, therefore, in the acute phase of inflammation, plasma copper concentration increases along with ceruloplasmin: during rheumatoid arthritis, pregnancy, estrogen therapy.

Decreased serum copper concentration characterizes pathologies with hypoproteinemia (protein deficiency), such as nephrosis, malnutrition, malabsorption. Decreased copper levels also characterize the process of treatment with adrenocorticotropic hormone, glucocorticoids, and valproate.