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Acquired and hereditary deficit of copper
Medical expert of the article
Last reviewed: 23.04.2024
Approximately half of the consumed copper is suctioned. Copper, which has been absorbed above the metabolic needs, is excreted with bile. Copper is a component of many body proteins; almost all the copper in the body is bound to proteins. Unbound (free) copper ions are toxic. Genetic mechanisms control the incorporation of copper into apoproteins and processes that prevent toxic accumulation of copper in the body.
Acquired copper deficiency
If the genetic mechanisms that control the metabolism of copper function normally, then malnutrition in the food rarely causes clinically significant copper deficiency. The only reasons reported were kwashiorkor, a persistent diarrhea in infants (usually associated with only milk), severe malabsorption (as in the sprue), and excessive consumption of zinc. Deficiency of copper can cause neutropenia, a violation of calcification of bones and hypochromic, anemia that is not sensitive to iron supplements. The diagnosis is based on low levels in the serum of copper and ceruloplasmin. Treatment of the acquired copper deficiency is aimed at eliminating the cause of the deficit, and copper is prescribed in a dose of 1.5-3 mg / day inwards (usually in the form of copper sulfate).
[7], [8], [9], [10], [11], [12]
Hereditary deficiency of copper
Hereditary copper deficiency (Menkes syndrome) occurs in newborn boys who inherit a mutant gene linked to the X chromosome. The frequency is about 1 per 50,000 newborns. Copper is reduced in the liver, serum, proteins containing copper: cytochrome C-oxidase, ceruloplasmin, lysyloxidase. Symptoms - severe retardation of mental development; vomiting; diarrhea; enteropathy with protein loss; hypopigmentation; changes in bones; ruptured arteries; rare, hard, curly hair. The diagnosis is based on low levels of copper and ceruloplasmin, usually in infants younger than 2 weeks. A typical treatment is the introduction of copper parenterally (in the form of copper sulfate) at a dose of 20-30 mg / kg intravenously once. However, parenterally introduced copper does not enter the copper-containing enzymes. More effective may be the appointment of a copper-histidine complex in a dose of 100-600 mg subcutaneously once a day; in the treatment process, continuous monitoring is necessary.