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Hemochromatosis, inflammation and anemia

Patients with inflammatory diseases such as arthritis, chronic infections and some types of cancer, often become anemic a condition called anemia of chronic disease (ACD). While ACD rarely kills patients, it can make their lives miserable. A discovery at EMBL, in collaboration with researchers at Children's Hospital Boston and Harvard Medical School, now links the gene HFE to ACD. The HFE gene is mutated in patients suffering from the common iron overload disease hemochromatosis. This finding gives hope that one day an effective and specific therapy may be developed to treat ACD (featured in Nature Genetics, April 18, 2004).

When people are infected with microbes, the level of iron in their blood drops. This has an important function: iron is essential for the growth of infectious microbes, so one way for the body to fight back is to lower the amount of iron in circulation.

"Unfortunately, while this decrease in iron hinders the spread of parasites and is beneficial in the short term, it can cause anemia," notes EMBL Group Leader Matthias Hentze. "During a long term inflammatory condition, low levels of iron can starve the bone marrow of this metal which is essential for blood cells, leading to ACD."

Because the anemia is a consequence of a natural immune defense, it has been difficult to think of a therapy that wouldn't also disturb the immune system itself.

Now scientists may have found a way to combat the anemia of chronic diseases by blocking the action of only one gene HFE without having much effect on the rest of the immune response, and without any serious consequences for the organism.

HFE is the gene mutated in the common genetic disease hemochromatosis, a condition in which the body becomes overloaded with iron. Researchers believe that when there are increased iron levels in the body, HFE signals to another molecule, an iron hormone called hepcidin. The role of hepcidin is to decrease the level of iron
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Contact: Trista Dawson
dawson@embl.de
49-622-138-7452
European Molecular Biology Laboratory
18-Apr-2004


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