© 2003 by BMJ Publishing Group & British Society of Gastroenterology
COMMENTARY
Liver disease
Lessons from liver transplantation: flip, flop, and why?
Department of Medicine, London Health Sciences Centre, 339 Windermere Rd, London, Ontario, Canada N6A 5A5; padams@uwo.ca
A case of hereditary haemochromatosis developing in a non-hereditary haemochromatosis recipient following transplantation of a C282Y heterozygous donor liver
Keywords: haemochromatosis; iron overload; liver transplantation; HFE; C282Y mutation; missense mutation
| The first 150 words of the full text of this article appear below. |
The widespread application of liver transplantation has been the single most important therapy to extend long term survival in patients with a variety of acute and chronic liver diseases. A fringe benefit of liver transplantation has been identification, confirmation, and cure of the metabolic basis of diseases.1 Haemophilia patients transplanted for chronic hepatitis C are cured of their clotting disorder, and patients transplanted for Wilson disease show no signs of copper accumulation following transplantation. Although many transplant recipients have mild to moderate iron overload at the time of transplantation, liver transplantation has been uncommon in homozygotes for the C282Y mutation of the HFE gene for haemochromatosis, and the metabolic effects on iron metabolism have not been clearly established.2 Studies in which C282Y homozygous donors have been transplanted into normal recipients have usually demonstrated a return to normal liver iron concentrations over time, and transplantation of a C282Y homozygous
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Gut 2003 52: 433-435.[Abstract] [Full Text] [PDF]
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