Talk:Hemochromatosis

Article Checklist for "Hemochromatosis"

Workgroup category or categories	Biology Workgroup [Please add or review categories]
Article status	Developing article: beyond a stub, but incomplete
Underlinked article?	Not specified
Basic cleanup done?	No
Checklist last edited by	Nobody

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Imported text from Wikipedia. Now in process to revert it to CZ:Live status. Thomas Simmons 10:17, 19 March, 2007 (EPT)

We must pick one version for the title; presumably, the one in more common usage by native English-speaking scientists. --Larry Sanger 18:58, 18 March 2007 (CDT)

Right. How do we do that? Thomas Simmons 12:02, 19 March, 2007 (EPT)

Substantive changes include additional information and sources in the introduction, additional information in the Signs and Symptoms section and deletion of two subsections without sources from

• Pathophysiology

• Crypt cell hypothesis

The sensor pathway inside the enterocyte is disrupted due to the genetic errors. The enterocyte in the crypt must sense the amount of circulating iron. Depending on this information, the cell can regulate the quantity of receptors and channel proteins for iron. If there is little iron, the cell will express many of these proteins. If there is a lot, the cell will turn off the expression of this transporters.

In haemochromatosis, the cell is constantly fooled into thinking there is iron depletion. As a consequence, it overexpresses the necessary channel proteins, this leading to a massive, and unnecessary iron absorption.

These proteins are named DMT-1 (divalent metal transporter), for the luminal side of the cell, and ferroportin, the only known cellular iron exporter, for the basal side of the cell.

• Hepcidin-ferroportin axis

Recently, a new unifying theory for the pathogenesis of hereditary hemochromatosis has been proposed that focuses on the hepcidin-ferroportin regulatory axis. Inappropriately low levels of hepcidin, the iron regulatory hormone, can account for the clinical phenotype of hereditary hemochromatosis. In this view, low levels of circulating hepcidin result in higher levels of ferroportin expression in intestinal epithelial cells and reticuloendothelial macrophages. As a result, this causes increased levels of serum iron, first biochemically detected as increasing transferrin saturation. HFE, hemojuvelin, BMP's and TFR2 are implicated in regulating hepcidin expression. Higher serum iron levels lead to progressive iron loading in tissues.

These may be included later but need rewriting and sources.

I may be going out on a limb here but if these are three or more substantive changes then hopefull this will qualify as CZ:Live. Will continue to work on this. Thomas Simmons 12:02, 19 March, 2007 (EPT)

deleted from original WP article

This section needs to be reworked and agreement with current information established. However, some of it actually refers to secondary hemochromatosis and is to that extent, inaccurate. Thomas Simmons 13:49, 19 March, 2007 (EPT)

Differential diagnosis There exist other causes of excess iron accumulation, which have to be considered before Haemochromatosis is diagnosed.

• African iron overload, formerly known as Bantu siderosis, was first observed among people of African descent in Southern Africa. Originally, this was blamed on ungalvanised barrels used to store home-made beer, which led to increased oxidation and increased iron levels in the beer. Further investigation has shown that only some people drinking this sort of beer get an iron overload syndrome, and that a similar syndrome occurred in people of African descent who have had no contact with this kind of beer (e.g., African Americans). This led investigators to the discovery of a gene polymorphism in the gene for ferroportin which predisposes some people of African descent to iron overload.
• Transfusion hemosiderosis is the accumulation of iron, mainly in the liver, in patients who receive frequent blood transfusions (such as those with thalassemia).
• Dyserythropoeisis is a disorder in the production of red blood cells. This leads to increased iron recycling from the bone marrow and accumulation in the liver.