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Hemochromatosis CausesHemochromatosis Causes
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Excess iron is stored in body tissues, especially the liver, heart and pancreas.
Genetic or hereditary hemochromatosis is mainly associated with a defect in a gene called HFE, which helps regulate the amount of iron absorbed from food. There are two known important mutations in HFE, named C282Y and H63D. C282Y is the most important. When C282Y is inherited from both parents, iron is overabsorbed from the diet and hemochromatosis can result. H63D usually causes little increase in iron absorption, but a person with H63D from one parent and C282Y from the other may rarely develop hemochromatosis.
The genetic defect of hemochromatosis is present at birth, but symptoms rarely appear before adulthood. A person who inherits the defective gene from both parents may develop hemochromatosis. A person who inherits the defective gene from only one parent is a carrier for the disease but usually does not develop it. However, carriers might have a slight increase in iron absorption.
Scientists hope that further study of HFE will reveal how the body normally metabolizes iron. They also want to learn how iron injures cells and whether it contributes to organ damage in other diseases, such as alcoholic liver disease, hepatitis C, porphyria cutanea tarda, heart disease, reproductive disorders, cancer, autoimmune hepatitis, diabetes, and joint disease.
Juvenile hemochromatosis and neonatal hemochromatosis are two forms of the disease that are not caused by an HFE defect. Their cause is unknown. The juvenile form leads to severe iron overload and liver and heart disease in adolescents and young adults between the ages of 15 and 30, and the neonatal form causes the same problems in newborn infants.
Other pages about Hemochromatosis:
See also WikiLiver (Search for WikiLiver) for details about the effect on liver function...
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