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Acquired copper intoxication: symptoms, diagnosis, treatment
Last reviewed: 08.07.2025
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Acquired copper intoxication results from ingesting or absorbing excessive amounts of copper (e.g., consuming foods or drinks that have been stored in copper containers for a long time). A self-limited gastroenteritis with nausea, vomiting, and diarrhea may occur. More severe copper intoxication results from ingesting (usually with suicidal intent) a few grams of copper salt (copper sulfate) or from absorbing large amounts through the skin (e.g., compresses saturated with copper salt solution used to treat extensive burns). Hemolytic anemia and anuria may develop, eventually being fatal.
Indian infantile cirrhosis, non-Indian infantile cirrhosis, and idiopathic copper toxicity are probably identical diseases in which excess copper causes cirrhosis. All are caused by drinking milk that has been boiled or stored in corroded copper or brass vessels. Recent research suggests that idiopathic copper toxicity may only occur in infants with an unknown genetic defect. Diagnosis usually requires a liver biopsy that reveals Mallory hyaline bodies.
[ Treatment of acquired copper intoxication
In copper intoxication caused by ingestion of a few grams, urgent gastric lavage, followed by daily intramuscular injections of at least 300 mg of dimercaprol, is necessary to prevent death. The chelating agent penicillamine binds copper, facilitating its excretion. Doses of 1-4 g/day orally promote excretion of copper absorbed through burned skin. Hemodialysis is effective in early onset. Copper intoxication is occasionally fatal despite treatment.
In Indian childhood cirrhosis, treatment with penicillamine may be effective.