Copper is a component of many body proteins; almost all of the body’s copper is bound to copper proteins. Unbound (free) copper ions are toxic. Genetic mechanisms control the incorporation of copper into apoproteins and the processes that prevent toxic accumulation of copper in the body. Copper absorbed in excess of metabolic requirements is excreted through bile.
(See also Overview of Mineral Deficiency and Toxicity Overview of Minerals Six macrominerals are required by people in gram amounts. Four cations: Sodium, potassium, calcium, and magnesium Two accompanying anions: Chloride and phosphorus Daily requirements range from... read more .)
Copper toxicity may be acquired or inherited (as Wilson disease Wilson Disease Wilson disease results in accumulation of copper in the liver and other organs. Hepatic or neurologic symptoms develop. Diagnosis is based on a low serum ceruloplasmin level, high urinary excretion... read more 
).
Acquired copper toxicity can result from ingesting or absorbing excess copper (eg, from ingesting an acidic food or beverage that has had prolonged contact with a copper container). Self-limited gastroenteritis with nausea, vomiting, and diarrhea may occur.
More severe toxicity results from ingestion (usually with suicidal intent) of gram quantities of a copper salt (eg, copper sulfate) or from absorption of large amounts through the skin (eg, if compresses saturated with a solution of a copper salt are applied to large areas of burned skin). Hemolytic anemia and anuria can result and may be fatal.
Indian childhood cirrhosis, non-Indian childhood cirrhosis, and idiopathic copper toxicity are probably identical disorders in which excess copper causes cirrhosis. All appear to be caused by ingesting milk that has been boiled or stored in corroded copper or brass vessels. Studies suggest that infants with idiopathic copper toxicity may have an as yet unidentified genetic defect.
Diagnosis of acquired copper toxicity usually requires liver biopsy, which may show Mallory hyalin bodies.
Treatment of Copper Toxicity
Chelation
Supportive measures
For copper toxicity due to ingesting grams of copper, prompt gastric lavage is done.
Copper toxicity that causes complications such as hemolytic anemia, anuria, or hepatotoxicity is also treated with chelation therapy Guidelines for Chelation Therapy 
with one of the following:
Oral penicillamine 250 mg every 6 hours to 750 mg every 12 hours (1000 to 1500 mg/day in 2 to 4 doses)
Dimercaprol 3 to 5 mg/kg IM every 4 hours for 2 days, then every 4 to 6 hours
If used early, hemodialysis may be effective.
Occasionally, copper toxicity is fatal despite treatment.
Drugs Mentioned In This Article
| Drug Name | Select Trade |
|---|---|
copper |
No brand name available |
penicillamine |
Cuprimine, Depen, D-PENAMINE |
dimercaprol |
BAL in Oil |
