Excess copper chelating therapy for Wilson disease induces anemia and liver dysfunction

Intern Med. 2011;50(14):1461-4. doi: 10.2169/internalmedicine.50.5209. Epub 2011 Jul 15.

Abstract

A 37-year-old man was diagnosed with Wilson disease at the age of 14. His first manifestations were neurological. He was treated with trientine for more than 10 years and suffered from anemia and liver dysfunction. Wilson disease is a genetic disorder characterized by accumulation of copper in the body. Excess copper is toxic, but copper is an essential trace element. Copper-binding ceruloplasmin is important for iron metabolism. Excess copper chelating treatment-induced anemia and iron deposition in the liver was suspected. Proper monitoring of copper status is important for the management of Wilson disease.

Publication types

  • Case Reports

MeSH terms

  • Adult
  • Anemia / blood
  • Anemia / chemically induced*
  • Ceruloplasmin / metabolism
  • Chelating Agents / administration & dosage
  • Chelating Agents / adverse effects*
  • Chelation Therapy / adverse effects*
  • Copper* / metabolism
  • Hemochromatosis / etiology
  • Hemochromatosis / metabolism
  • Hepatolenticular Degeneration / complications
  • Hepatolenticular Degeneration / drug therapy*
  • Hepatolenticular Degeneration / metabolism
  • Humans
  • Iron / metabolism
  • Liver Diseases / etiology*
  • Liver Diseases / metabolism
  • Male
  • Trientine / administration & dosage
  • Trientine / adverse effects

Substances

  • Chelating Agents
  • Copper
  • Iron
  • Ceruloplasmin
  • Trientine