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Author Notes:

Address correspondence and reprint requests to: Dr. Juna Konomi, Department of Pediatrics, Division of Pediatric Gastroenterology, Hepatology, and Nutrition, Emory University, 1760 Haygood Drive, Suite W440B, Fax 404-727-8997, Phone 404-727-9876, junakonomi@emory.edu

MM – collected data, interpreted data results, wrote first draft of manuscript, SC – interpreted histology and results, reviewed manuscript, MS – study design, contributed to manuscript, LS – data analysis and interpretation, contributed to manuscript, JK – data analysis and interpretation, contributed to manuscript, CM – study design, contributed to manuscript, MV – study design, interpretation of results, contributed to manuscript.

Dr. Vos reports paid and unpaid consulting for pediatric NAFLD: Aegerion, Allegan, Intercept, Shire, Immuron and Target Pharmasolutions; and money or inkind research services: AMRA, Resonance Health and Target Pharmasolutions.

All other authors have no conflicts of interest to declare.


Research Funding:

The study was funded, in part, from grants from the National Institutes of NIH R03 DK096157 (MBV) and NIH K23 DK080953-05 (MBV).


  • Adolescent
  • Biomarkers
  • Case-Control Studies
  • Child
  • Child, Preschool
  • Copper
  • Female
  • Humans
  • Liver
  • Male
  • Non-alcoholic Fatty Liver Disease
  • Retrospective Studies
  • Severity of Illness Index
  • Trace Elements
  • Young Adult

Low Hepatic Tissue Copper in Pediatric Nonalcoholic Fatty Liver Disease.


Journal Title:

Journal of Pediatric Gastroenterology and Nutrition


Volume 65, Number 1


, Pages 89-92

Type of Work:

Article | Post-print: After Peer Review


OBJECTIVE: Animal models and studies in adults have demonstrated that copper restriction increases severity of liver injury in nonalcoholic fatty liver disease (NAFLD). This has not been studied in children. We aimed to determine if lower tissue copper is associated with increased NAFLD severity in children. METHODS: This was a retrospective study of pediatric patients who had a liver biopsy including a hepatic copper quantitation. The primary outcome compared hepatic copper concentration in NAFLD versus non-NAFLD. Secondary outcomes compared hepatic copper levels against steatosis, fibrosis, lobular inflammation, balloon degeneration, and NAFLD activity score (NAS). RESULTS: The study analysis included 150 pediatric subjects (102 with NAFLD and 48 non-NAFLD). After adjusting for age, body mass index z score, gamma glutamyl transferase, alanine aminotransferase, and total bilirubin, NAFLD subjects had lower levels of hepatic copper than non-NAFLD (P = 0.005). In addition, tissue copper concentration decreased as steatosis severity increased (P < 0.001). Copper levels were not associated with degree of fibrosis, lobular inflammation, portal inflammation, or balloon degeneration. CONCLUSIONS: In this cohort of pediatric subjects with NAFLD, we observed decreased tissue copper levels in subjects with NAFLD when compared with non-NAFLD subjects. In addition, tissue copper levels were lower in subjects with nonalcoholic steatohepatitis, a more severe form of the disease, when compared with steatosis alone. Further studies are needed to explore the relationship between copper levels and NAFLD progression.

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