Essential metal required for enzymatic reactions involving connective tissue, free radical scavenging electron transfer, pigment production, and neurotransmission.

Foods rich in copper include nuts, chocolate, dry legumes, whole grains, raisins, and meat, shellfish and poultry.

Average daily intake 1.5-5 mg.

Deficiency associated with hypochromic, microcytic anemia and neutropenia.

Deficiency associated with bone marrow megaloblastoid changes, ringed sideroblasts and erythroid hyperplasia can confuse the diagnosis with myelodysplastic syndrome.

Deficiency associated with impaired iron absorption and transfer from reticuloendothelial cells to plasma.

Copper is absorbed in the upper G.I. tract by copper transporter 1, expressed on the luminal surface of the duodenum.

Activity of cytochrome oxidase decreased in copper deficient mitochondria.

Deficiency impairs iron in mitochondria from inserting into protoporphyrin and iron accumulates in the mitochondria with formation of ringed sideroblasts.s

Cause infections of mainly skin and soft tissue or contiguous sites, such as bone and joints but rarely can cause endocarditis.

Most common neurological manifestation is ataxic myelopathy with or without neuropathy.

Neurologic toxicity includes myelopathy affecting the dorsal columns, similar to B12 deficiency, as well as peripheral neuropathy and hyporelexia with some presenting with spastic gait and sensory ataxia.

Copper deficiency really develop some patients without a history of malabsorption, is the average intake of 1-1.6 mg/dL typically exceeds the estimating requirement of 0.9 mg/dL.

Copper deficiency occurs in patients with a history of gastric bypass, other causes of malabsorption, zinc overload, and those who receive parenteral nutrition exclusively.

Gastric bariatric bypass procedures are underrecognized causes of copper deficiency.

These procedures bypass portions of the stomach and proximal small intestine, the major sites of copper absorption in the gut.

The incidence of copper deficiency after Roux-en-Y gastric bypass varies and is estimated to range from 4-19% in the first 2-5 years after the procedure.

Other conditions associated with copper deficiency include excessive zinc ingestion and celiac disease, and prolonged enteral and parenteral nutrition administration when copper is not supplemented.

Excess zinc ingestion impairs copper absorption due to an increase in metallothionein levels leading to increased fecal excretion of copper.

Zinc update contributes the copper deficiency by production of metallothionein into enterocytes which sequesters copper in enterosites.

Deficiency may be associated with peripheral neuropathy and CNS demyelination, myopathy, optic neuritis have been described as well.

Rarely aneurysms are caused by copper deficiency, which results in a decreased activity of the lysyl oxidase enzyme, affecting elastin, a key component in vessel walls.


Copper deficiency results in vessel wall thinning, and thus has been noted as a cause of death in copper-deficient humans.

Acquired copper deficiency has hematologic manifestations, which are reversible, and neurologic manifestations which are generally not.

Hematologic manifestations include: anemia, neutropenia, and rarely thrombocytopenia.

Bone marrow evaluation with copper deficiency reveals a high number of immature precursors, dysplasia and ringed sideroblasts

Neurologic findings of copper deficiency include myeloneuropathic changes with unsteady gait, distal muscle weakness, or sensory defects in the extremities.

Prolonged deficiency can develop neurologic and hematologic abnormalities.

Hematologic manifestations of deficiency include: anemia and neutropenia.

Copper is a cofactor in ferrooxidases involved in hematopoiesis, so many hematologic consequences of copper deficiency are linked to iron abnormalities.

Bone marrow examination can show ringed sideroblasts, hypoellularity, vacuolized erythroid and granulocytic precursors.

Deficiency associated with MRI changes on T2 weighted images involving the dorsal column of the cervical spinal cord.

Oral copper gluconate maintenance is 2 mg daily.

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