Hemotest: Copper (blood) (venous blood) - get tested at an affordable price in Moscow and other cities

Detailed description of the study

Copper (Cu2+) is a trace element that is vital for humans. It is part of proteins (mainly enzymes) and structural components of genes. The daily requirement for copper is about 2 mg. Products high in copper include: beef and cod liver; almonds, walnuts and other nuts; sesame and pumpkin seeds; legumes; greens, vegetables (beets, tomatoes) and fruits (pineapple, grapefruit, banana).

Copper metabolism occurs in the liver. The microelement enters there from the bloodstream after absorption in the small intestine. Normally, in liver cells, copper is incorporated into proteins and becomes part of enzymes. For example, the microelement is part of enzymes such as superoxide dismutase and cytochrome C oxidase. However, the amount of this microelement in them does not exceed 5% of the total amount in the body.

Up to 95% of copper in blood serum is bound to proteins, mainly ceruloplasmin. This protein is produced in the liver, just like copper. Ceruloplasmin plays an important role in the metabolism of another microelement - iron. The enzyme is a ferrooxidase, which promotes the conversion of ferrous iron (Fe2+) into ferric iron (Fe3+) and further binds the trace element to transferrin (serum iron transport protein).

Copper metabolism is disrupted in Wilson-Konovalov disease, or hepatolenticular dystrophy. This is a severe congenital disease caused by a deficiency of an enzyme involved in the removal of copper from liver and brain cells. The balance between the intake and excretion of microelements in the body is disrupted, and an excess of copper occurs. It begins to be deposited in many organs and tissues (mainly in the central nervous system, liver, brain, liver). Microelement deposits in the cornea of the eye look like a yellow-brown rim around it.

The disease can manifest itself both in preschool age and in old age. This depends on the severity of the copper metabolism disorder. The deposition of this trace element in the liver causes inflammation of the organ (hepatitis), which ultimately progresses to liver failure.

Often the disease is detected already at the stage of liver cirrhosis, when most of the organ cells are destroyed.

Damage to the nervous system can cause a variety of symptoms - impaired speech, gait, trembling of the limbs (tremor), seizures similar to epileptic ones. The ability to learn suffers, and children experience developmental delays. Mental disorders are noted.

Another disease associated with impaired copper metabolism is Menkes disease. It is rare and is also caused by a genetic mutation in the transporter of this trace element. Damage to organs and tissues in Menkes disease is already observed in utero; after the birth of the child, the disease progresses. There is a delay in growth and development, failure of many organs.

In addition, causes of decreased serum copper concentrations include malnutrition, decreased absorption of micronutrients from the digestive tract, ingestion of toxic substances containing copper, and overdose of zinc supplements (prevents normal absorption of copper from the gastrointestinal tract).

The destruction of liver cells leads to a temporary increase in copper levels in the blood. It is observed in various acute liver lesions, infectious and malignant diseases, and increased activity of the thyroid gland (hyperthyroidism). Serum copper concentrations are also elevated in patients taking contraceptives or estrogens and during pregnancy.

Assessing the level of copper in the blood allows us to identify diseases associated with impaired copper metabolism.

Daily intake of copper

The recommended daily intake of copper for adult men and women is 900 micrograms per day (or 0.9 milligrams per day).

Most adults living in developed countries obtain adequate amounts of copper from food, dietary supplements, and fortified drinking water. Copper deficiency is much more common in malnourished people who suffer from a general lack of calories and a lack of copper-rich foods.

Recommended copper intake levels for different groups of people are as follows:

Infants 0–12 months: 200 mcg/day
Children 1-3 years: 300 mcg/day
Adults and children over 4 years of age: 900 mcg/day
Pregnant and breastfeeding women: 1300 mcg/day

Causes of copper deficiency

Lack of copper in the body can be acquired or hereditary. When acquired, causes may include malnutrition and poor nutrition, malabsorption, or excessive intake of zinc.

Violation of rules for taking food additives

Copper absorption may be impaired by very high iron intake, usually from dietary supplements. Zinc is another nutrient that interacts closely with copper. Like iron, the human body needs copper and zinc in a healthy balance, as too much zinc can reduce copper levels.

So always – if you take iron supplements, then you need to take zinc and copper at the same time. Similarly with copper - if you use it as a supplement - you need to take zinc and iron at the same time. All these three minerals are spread over a period of at least 3 hours. You cannot drink at the same time, as they will compete with each other for digestibility.

Malabsorption

Copper deficiency is also sometimes present in people suffering from serious digestive disorders that impair nutrient absorption, such as Crohn's disease.

Banal hypoacidity will also affect copper absorption. Therefore, it is important to know your level of acidity in the stomach in order to correct this situation if something happens.

Protein deficiency

Other causes may include severe protein deficiency in childhood, persistent infantile diarrhea (usually associated with a milk-restricted diet), gastric surgery, and vitamin B12 deficiency.

Taking COCs

Long-term use of oral contraceptives has been shown to disrupt the balance of copper in the body, resulting in excessively high or low copper levels.

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Early gray hair is one of the symptoms of copper deficiency in the body

Signs and symptoms

Blood symptoms

The characteristic hematologic (blood) consequences of copper deficiency are: anemia (which may be microcytic, normocytic, or macrocytic) and neutropenia.[6] Thrombocytopenia (low blood platelets) is uncommon.[3][7]

Peripheral blood and bone marrow aspirate findings of copper deficiency may mimic myelodysplastic syndrome.[8] Bone marrow aspirate in both conditions may show dysplasia of blood cell precursors and the presence of ring sideroblasts (erythroblasts containing several iron granules around a nucleus). Unlike most cases of myelodysplastic syndrome, bone marrow aspirate from copper deficiency usually shows cytoplasmic vacuoles in red and white cell precursors, and karyotyping in copper deficiency does not reveal the cytogenetic features characteristic of myelodysplastic syndrome.[6][7]

Anemia and neutropenia usually resolve within six weeks of copper replacement.[8]

Neurological symptoms

Copper deficiency can cause a wide range of neurological problems, including: myelopathy, peripheral neuropathy, and optic neuropathy.[2][7]

Myelopathy

Myelopathy due to copper deficiency in humans was discovered and first described by Schleper and Stürenburg in 2001.[9] They described a patient with a history of gastrectomy and partial colon resection who had severe tetraparesis and painful paresthesias and who was found to have T2 hyperintensity in the dorsomedial cervical spinal cord. Upon further analysis, the patient was found to have decreased levels of serum ceruloplasmin, serum copper, and cerebrospinal fluid copper. The patient was treated with parenteral copper and the patient's paresthesia resolved. Since this discovery, there has been more and more awareness of copper deficiency myelopathy and its treatment, and this disease has been reviewed by Kumar. gait difficulties) caused by sensory ataxia (irregular muscle coordination) due to spinal column dysfunction[7] or spinal cord degeneration (myelopathy).[2][10] Patients with ataxic gait have problems with balance and exhibit an unsteady, wide gait. They often feel tremors in the torso, causing jerking and lunging to the sides.[11]

Brain MRI often shows increased signaling in the dorsal columns of the spinal cord in patients with copper deficiency myelopathy.[2][7][12] T2 signaling is often an indicator of some kind of neurodegeneration. MRI of the spinal cord shows some changes affecting the thoracic, cervical, and sometimes both.[2][7] Copper deficiency myelopathy is often compared to subacute combined degeneration (SCD).[10] Subacute combined degeneration is also spinal cord degeneration, but instead vitamin B12 deficiency is the cause of spinal degeneration.[2] SCD also has the same high intensity of T2 signaling in the posterior column as a patient with copper deficiency on MRI.[12]

Peripheral neuropathy

Another common symptom of copper deficiency is peripheral neuropathy, which is a numbness or tingling that can begin in the extremities and sometimes progress radially inward toward the torso.[7][13] In a published case report, a 69-year-old patient had progressively worsening neurological symptoms.[14] These symptoms included decreased upper extremity reflexes with abnormal lower extremity reflexes, decreased sensitivity to light touch and pin pricks above the waist, and loss of and marked decrease in sensation of vibration in the sternum. proprioception, or the sense of one's own orientation.[14] Many people suffering from the neurological consequences of copper deficiency complain of symptoms very similar or identical to the patient's.[2][13] Numbness and tingling are dangerous for older adults because they increase their risk of falling and injury. Peripheral neuropathy, if not properly diagnosed, can become very disabling, leaving some patients dependent on wheelchairs or canes for mobility. In rare cases, copper deficiency can cause severe disabling symptoms. Deficiencies will have to be present for a long time before such disabling conditions become apparent.

Optic neuropathy

Some patients with copper deficiency show signs of vision loss and color loss.[13] Vision is usually lost when looking at the periphery of the eye.[13] Bilateral vision loss is usually very gradual.[13][15] An optical coherence tomography (OCT) showed some loss of the nerve fiber layer in most patients, suggesting that vision loss and color vision loss were secondary to optical neuropathy or neurodegeneration.[13]

Recommendations

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How does a lack of copper manifest itself in the body - the main symptoms

What are the symptoms of copper deficiency caused by zinc? Changes in bones can distinguish copper deficiency from excess zinc intake. Acquired copper deficiency as a result of zinc overload is not common, but research suggests that it can be detected by bone marrow examination followed by additional testing.

Symptoms of copper deficiency in the body include:

anemia
bone abnormalities
osteoporosis
copper neuropathy
low number of white blood cells known as neutrophils (neutropenia)
increased susceptibility to infections
growth disorder
premature graying of hair
pale skin
neurological symptoms

Diagnosis of copper deficiency

A blood test can determine whether you have acquired copper deficiency. The test evaluates copper and ceruloplasmin levels. Ceruloplasmin is a protein made in your liver that stores and transports most of the copper throughout your body.