Volume 2, Issue 27, 07/13/2010
Why are patients with genetic defects to the hepcidin antimicrobial peptide (HAMP) gene at an increased risk for developing iron toxicity or hemochromatosis with iron supplements?
The previous three newsletter publications dedicated to the topic of pharmacogenetics provided a review of the common genetic defects or polymorphisms associated with an increased risk for the development of hemochromatosis and the mechanisms of iron toxicity specifically in patients with Hereditary Hemochromatosis and Hemochromatosis Type 2A. As one might expect, there are a number of genetic influences that can predispose certain patients to an increased risk of iron overload/toxicity. The last two issues in this series will address the mechanisms behind Hemochromatosis Type 2B and then Types 3 and 4. This newsletter publication will focus on the mechanism involved in patients with Hemochromatosis Type 2B, which is the other form of Juvenile Hemochromatosis that predisposes patients to increased or excessive iron absorption. As with the other publications on this topic, we have included the previously published mechanism for oral iron absorption in the gastrointestinal tract (if needed).
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