CHRONIC COPPER TOXICOSIS PRESENTING AS LIVER-FAILURE IN AN AUSTRALIANCHILD

A 20 month old Caucasian male child, after a five week illness, develo ped liver failure which was successfully treated by liver transplantat ion. The explanted liver had a histology identical to that seen in Ind ian childhood cirrhosis and its copper content was increased tenfold. Water used to prepare the child's milk feeds came from a bore via copp er conduits and at times contained 120 mu mol/l of copper, eight times the recommended maximum for human consumption. Because non-Indian cas es of Indian childhood cirrhosis associated with excess copper ingesti on are increasingly being recognised, and as early treatment can resto re normal liver morphology, we support the use of the previously sugge sted alternative term for this condition, ie; 'copper-associated liver disease in childhood'. Measurement of hepatic copper concentrations i n all children less than six years of age who develop hepatic failure of unknown cause will increase its recognition. On diagnosis sources o f increased dietary copper should be investigated to ensure that young er siblings are not similarly exposed.