nutritional disorders
Copper Toxicity
Introduction
Copperis a component of many body proteins; almost all of the body’scopperis bound tocopperproteins. Unbound (free)copperions are toxic. Genetic mechanisms control the incorporation ofcopperinto apoproteins and the processes that prevent toxic accumulation ofcopperin the body.Copperabsorbed in excess of metabolic requirements is excreted through bile. (See also Overview of Minerals .) toxicity may be acquired or inherited (as Wilson Disease ). Acquiredcoppertoxicity can result from ingesting or absorbing excesscopper(eg, from ingesting an acidic food or beverage that has had prolonged contact with acoppercontainer). Self-limited gastroenteritis with nausea, vomiting, and diarrhea may occur. More severe toxicity results from ingestion (usually with suicidal intent) of gram quantities of acoppersalt (eg,coppersulfate) or from absorption of large amounts through the skin (eg, if compresses saturated with a solution of acoppersalt 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 idiopathiccoppertoxicity are probably identical disorders in which excesscoppercauses cirrhosis. All appear to be caused by ingesting milk that has been boiled or stored in corrodedcopperor brass vessels. Studies suggest that infants with idiopathiccoppertoxicity may have an as yet unidentified genetic defect. Diagnosisof acquiredcoppertoxicity usually requires liver biopsy, which may show Mallory hyalin bodies. 