Cupremia: Definition, Tests, Results, Associated Pathologies and Signs of Copper Deficiency

It refers to the presence of copper in the bloodstream.

Copper is widely distributed in nature and is considered an essential trace element, acting in various physiological and biochemical functions, and is the component of many metalloproteins and metalloenzymes.

For the general population, most of this micronutrient is usually obtained from the daily diet through foods such as liver and other organ meats, shellfish, nuts, beans, and other whole grains, vegetables, meat, and beverages, even water. The daily intake of copper in adults ranges from 0.9 to 2.2 mg.

On the other hand, the presence of copper in the blood may be due to occupational exposure that occurs in workers in factories, mines, and in those who perform welding, metal smelting, and related activities.

Copper is an intensely active redox metal, predominantly in the form of a cupric ion (Cu II) but can also appear as a cuprous ion (Cu I) within cells.

This redox capacity makes it useful in various stages of power generation. But it is also what allows it to catalyze when in its “free” state, the age of reactive oxygen species that are harmful to the body.

About 85% to 95% of copper is covalently bound to serum ceruloplasmin, so its quantification is preferably performed in serum in most laboratory studies.


Total copper serum test

The serum total copper test measures the total amount of copper present in the blood. Copper in the blood is usually carried by a protein called ceruloplasmin.

Adults have between 50 and 80 mg of copper in the body, mainly in the muscles and the liver. Copper helps the formation of melanin, bones, and connective tissue.

It also supports other metabolic processes in the body. The elimination of copper is carried out with stool and urine.

Generally, a regular diet provides enough copper; copper deficiency is very unlikely, but some diseases can alter normal copper levels.

Too much copper can be toxic; you can get too much copper from dietary supplements or drinking contaminated water. You can also get too much copper from being around fungicides with copper sulfate or if you have a condition that makes it impossible for your body to remove copper.

Pathologies associated with copper levels in the body

Several pathologies are related to copper levels in the body.

Copper deficiency is rare in humans as this nutrient is easily consumed and has a shallow daily dose required.

However, when there is a deficiency, the function of different organs and various defense systems of the body is compromised, and problems with connective tissue, muscle weakness, anemia, low white blood cell count, and neurological problems can occur.

It can occur in malnourished children, especially premature babies who do not receive nutritional supplements.

Childhood is a critical period for brain development, and abnormal levels cause severe neurological effects, some abnormalities, and bone fractures.

Copper deficiency can also result from a rare genetic disorder called Menkes disease, an inherited condition in which incorrect genetic coding in the production of ATP7A protein causes a defect in intracellular copper transport, causing less absorption of metals. And distribution investment.

Copper-deficient patients can also develop hematopoietic deficits, resulting in microcytic hypochromic anemia associated with leukopenia and neutropenia.

As already mentioned, copper acts as a cofactor for ceruloplasmin. This iron-oxidizing enzyme allows its mobilization and transport of liver reserves to the bone marrow for use in erythropoiesis.

Therefore, copper deficiency produces an excess of iron in the liver and an iron deficiency in the bone marrow, making effective erythropoiesis impossible.

Hematological changes caused by copper deficiency can also be observed in patients who, due to some chronic disease, have become dependent on enteral or parenteral nutrition, using them long-term, without concomitant copper supplementation.

More recently, the role of copper deficiency in the pathogenesis of high blood pressure and cardiovascular diseases has been demonstrated. It is known that the plasma concentration of this metal significantly modifies the activity of blood transport systems.

Although it is an essential trace element for the body, when it is in excess, it can cause toxic effects. Conditions associated with copper deficiency include Wilson’s disease, which prevents the liver from safely storing copper and transporting it out of the body in the stool.

The extra copper present in the liver passes into the bloodstream and accumulates in the kidneys, brain, and eyes. This additional copper can kill liver cells and cause nerve damage.

Wilson’s disease is caused by autosomal recessive inheritance on chromosome 13 that can occur even after age 50.

The mechanism of this disease is the accumulation of copper in the hepatocytes, which causes well-established irreversible changes in the brain and liver.

Another characteristic of this disease is the deposition of copper in the cornea, forming the Kayser-Fleischer rings.

Wilson’s disease is fatal if it is not treated. The extra copper that occurs in Wilson’s disease can obstruct the absorption of other trace elements such as zinc and iron.

There is now some concern about the limits of copper homeostasis, as self-administration of microminerals and vitamin supplements has become common practice worldwide.

Along these lines, there are reports that some people may develop lifelong toxicity due to its relationship with chronic degenerative diseases, even presenting concentrations within the reference values ​​for copper in the blood.

Several studies report the role of copper in neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease, which generally affect the elderly, and show that high copper intake may be associated with accelerated cognitive decline, especially if there is also a diet rich in saturated fat and trans fat.

Furthermore, most neurodegenerative diseases originate from reactions with free radicals or reactive species.

The elevation of copper also causes toxicity related to the lipid peroxidation of the membranes when it is in the monovalent form (Cu I).

The metal can transfer an electron, generating reactive oxygen species, such as hydroxyl radicals, hydrogen peroxide, and superoxide ions, which are closely related to oxidative stress, causing cell damage, protein oxidation, and DNA damage.

Uses of the total copper serum test

Signs and symptoms that occur with a copper deficiency can include:

Symptoms of toxicity include:

Copper toxicity can cause:

  • Kidney and heart failure.
  • Liver problems
  • Brain diseases.
  • Anillos de Kayser-Fleischer.
  • Death.

Tests to verify a diagnosis.

Your doctor will likely recommend additional tests to check for possible copper deficiency, copper toxicity, or Wilson’s disease with these tests:

  • Ceruloplasmin blood.
  • 24-hour urine test for copper.
  • Liver copper, or measurement of copper in a liver biopsy.
  • Vitamin B12 level.

The level of copper in the blood can be linked to many different conditions. These include liver problems or inflammation.

Total Copper Serum Test Results

The Total Copper Serum Test results can be modified by age, gender, health history, and the method used for the test, among other things.

The normal range for the serum total copper blood test is 70 to 140 micrograms per deciliter (mcg / dL).

In people with Wilson’s disease who also have acute liver failure, copper in the blood may be higher than usual.

Some conditions could elevate the total copper serum test result:

  • Toxicity through consumption of water or dietary supplements.
  • Anemia
  • Biliary cirrhosis
  • Hemochromatosis.
  • Hyperthyroidism
  • Hypothyroidism
  • Infection.
  • Leukemia.
  • Lymphoma
  • Rheumatoid arthritis.
  • Medications such as corticosteroids and corticotropins.
  • The pregnancy.
  • Birth control pills.
  • Infections.
  • Inflammations and stress.