Serum and Hepatic Copper Concentrations in Egyptian Infants with Cholestasis

Biliary excretion is the major elimination route of copper, therefore increased hepatic copper concentrations could be caused by cholestasis. Hepatic copper accumulation is cytotoxic and results in fibrosis in hepatic tissues. Aim: The aim of this work is to determine the concentration of copper in serum and hepatic tissue in infants with cholestasis and its impact on liver function tests. Subjects and Methods: Forty-one cholestatic infants were selected from the Pediatric Hepatology Unit, Cairo University Children’s Hospital, between January 2005 and December 2006, after an informed consent. Their aged ranged between 1 and 22 months; 63.5% were males. The duration of illness ranged between 15 days and 20 months. All were selected with normal synthetic liver functions. Liver biopsy was done for all patients [25 (61%) had neonatal hepatitis, the rest had extrahepatic biliary atresia]. Twenty eight healthy children served as controls. Serum copper indices (free copper and ceruloplasmin) and hepatic copper content were assessed using atomic absorption apparatus. Results: Significantly elevated levels of serum copper and ceruloplasmin were found in cholestatic patients when compared to the controls. The mean hepatic copper concentration in the cholestatic infants was 627.8±238.5mg/g. There was a positive correlation between serum copper, tissue copper and serum ceruloplasmin (p 0.01). There was neither significant correlation between tissue copper and the duration of illness or liver function tests. Conclusion: Serum and hepatic copper concentrations and also serum ceruloplasmin were significantly higher in patients with cholestasis regardless of the etiology. Due to the sophisticated and costly technique of hepatic and serum copper evaluation, serum ceruloplasmin as a cheap easy test could replace both and used as an indicator for serum and hepatic copper due to the significant statistical positive correlation between them.