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Copper deficiency, or hypocupremia, is defined as insufficient copper to meet the body's needs, or as a serum copper level below the normal range. [1] Symptoms may include fatigue , decreased red blood cells , early greying of the hair, and neurological problems presenting as numbness , tingling, muscle weakness, and ataxia . [ 2 ]
Acquired copper deficiency has recently been implicated in adult-onset progressive myeloneuropathy [71] and in the development of severe blood disorders including myelodysplastic syndrome. [18] [72] [73] Fortunately, copper deficiency can be confirmed by very low serum metal and ceruloplasmin concentrations in the blood.
Familial benign copper deficiency, also known as Familial benign hypocupremia is a rare genetic disorder which is characterized by hypocupremia that causes symptoms such as epilepsy, hypotonia, seborrheic skin, thriving failure and mild anemia. [2] Radiological findings include tibia and femur spurring. [3]
Medical treatments are available for Wilson's disease. Some increase the removal of copper from the body, while others prevent the absorption of copper from the diet. Generally, penicillamine is the first treatment used. This binds to copper (by chelation) and leads to excretion of copper in the urine. Hence, monitoring of the amount of copper ...
Menkes disease (MNK), also known as Menkes syndrome, [1] [2] is an X-linked recessive disorder caused by mutations in genes coding for the copper-transport protein ATP7A, [3] leading to copper deficiency. [4] [5] Characteristic findings include kinky hair, growth failure, and nervous system deterioration. Like all X-linked recessive conditions ...
In the case of copper the adult UL is set at 10 mg/day. [4] Copper gluconate is sold as a dietary supplement to provide copper. The typical dose is 2.0 mg copper per day. This is one-fifth what the IOM considers a safe upper limit. Long-term intake at amounts higher than the UL may cause liver damage. [4]
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Aceruloplasminemia is a rare autosomal recessive disorder [2] in which the liver can not synthesize the protein ceruloplasmin properly, which is needed to transport copper around the blood. Copper deficiency in the brain results in neurological problems that generally appear in adulthood and worsen over time. [3]