Severe iron overload with a novel aminolevulinate synthase mutation and hepatitis C infection. A case report

Blood Cells Mol Dis. 2009 Jan-Feb;42(1):1-4. doi: 10.1016/j.bcmd.2008.08.001. Epub 2008 Sep 26.

Abstract

A 55 year old man with a history of chronic hepatitis C infection was found to have severe hemochromatosis: hepatic cirrhosis, cardiomyopathy, arrhythmia, hypogonadism, diabetes and bronzed skin color. After 50 phlebotomies, he underwent a combined heart and liver transplant. Genetic analyses identified a novel mutation in the iron responsive element of the ALAS2 gene. No mutations were found in other genes associated with adult or juvenile hemochromatosis including HFE, transferrin receptor-2 (TFR2), ferroportin (SLC40A1), hepcidin (HAMP) and hemojuvelin (HJV). We suggest that the ALAS2 mutation together with chronic hepatitis C infection may have caused the severe iron overload phenotype.

Publication types

  • Case Reports
  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • 5-Aminolevulinate Synthetase / genetics*
  • 5-Aminolevulinate Synthetase / metabolism
  • Heart Transplantation
  • Hemochromatosis / etiology
  • Hemochromatosis / genetics
  • Hemochromatosis / surgery
  • Hemochromatosis / therapy
  • Hepatitis C, Chronic / complications*
  • Hepatitis C, Chronic / virology
  • Humans
  • Iron / metabolism
  • Iron Overload / etiology*
  • Iron Overload / genetics*
  • Iron Overload / surgery
  • Iron Overload / therapy
  • Liver Transplantation
  • Male
  • Middle Aged
  • Mutation / genetics
  • Response Elements / genetics

Substances

  • Iron
  • 5-Aminolevulinate Synthetase
  • ALAS2 protein, human