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 Definition Hereditary disorder affecting iron metabolism in which excessive amounts of iron accumulate in the body tissues, characterized by diabetes mellitus, liver dysfunction, and a bronze pigmentation of the skin. [d] [e]

Source and Title

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)

Well, decide which title you want it under, and send a mail to or contact one of your friendly local constables. --Larry Sanger 21:23, 20 March 2007 (CDT)

While I am thinking of it, we could use a redirect for the alternative UK spelling. I also need to set up a redirect for the common names for the malady, i.e.:

  • Iron overload disease
  • Primary hemochromatosis
  • Hereditary hemochromatosis (HH or HHC)
  • Classical hemochromatosis
  • Genetic iron poisoning
  • Genetic hemochromatosis
  • Secondary hemochromatosis
  • Acquired hemochromatosis

How do I do this? Thomas Simmons 22:18, 19 March, 2007 (EPT)

Substantive Changes fro WP Original

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 Thomas Simmons 22:18, 19 March, 2007 (EPT)

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

Deleted from original WP aticle

  • Pathophysiology
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 1), 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 transferrin receptor type 2 (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.(noted 19, March, 2007) Thomas Simmons 15:34, 23 March, 2007 (EPT)

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.[1]
  • 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.


See also

External links


till we can decide on the extent and kind of external links and check them out. Thomas Simmons 15:22, 23 March, 2007 (EPT)

Article moved

As per your request, this page has been moved from Hemochromatosis/Haemochromatosis. The re-direct is already made so things should be set. Any problems just contact me on my talk page. Have fun! --Matt Innis (Talk) 22:15, 22 March 2007 (CDT)

Be careful calling Hemochromatosis the "English" version, because I believe it is the British version... which is also England English! I may be wrong though. -Tom Kelly (Talk) 22:18, 22 March 2007 (CDT)

Oops, good point:-) though I have no idea which English is British! --Matt Innis (Talk) 22:35, 22 March 2007 (CDT)
I made a redirect from the British title to here. -Tom Kelly (Talk) 22:19, 22 March 2007 (CDT)
Good Job! You got it. --Matt Innis (Talk) 22:34, 22 March 2007 (CDT)
Had this same argument as an undergraduate during the Nixon administration. I was taking "English" Literature as opposed to "American" literature. Technically the British are the folks living in Brittany, France and the Welsh (Cymru). D. Webster, towering intellect though he was, does not get to rename the ancient tribes just because he wrote well. Anyway, old debate, more smoke than fire I think. I did refer to English English as "UK spelling" though. Avoiding all the fun. Thomas Simmons 15:41. 23 March, 2007 (EPT)


This is to discuss picture ideas for this article. -Tom Kelly (Talk) 00:16, 23 March 2007 (CDT)

Pictures would be good, I agree. Most of the pics placed n the Wikipedia article did not have a clear line of permission. I started to trun them down but never finished that aspect. Thomas Simmons 13:25, March 30, 2007 (EPT)


Histology: Prussian blue histology pictures. H+E histology pics. histology of kidney, heart, liver, Bone Marrow (?) lung (?)... please make criticism on each type of histological section option.

-Tom Kelly (Talk) 00:16, 23 March 2007 (CDT)

The histology would be very good. A graph of blood levels to demonstrate the iron level lab tests? I wonder where we could get some MRI pictures showing the changes in various organs. To round it out, external signs-- possibly a shot of someone who demonstrates the change in pigmentation. Another idea would be a map for demographics, showing the various concentrations of the occurrence of the disease Thomas Simmons 13:30, 30 March, 2007 (EPT)

Corrections / Suggestions / Etc

"The less common exogenous form (secondary or acquired form) is caused by metabolic iron overload whch may occur in cases of chronic anemia, chronic liver disease and excessive iron supplementation (rare).[1]"

I think hemosiderin (haemosiderin - needs redirect) vs. hemochromatosis should be clearly defined in the begining of the article. -Tom Kelly (Talk) 00:23, 23 March 2007 (CDT)
  1. Gordeuk V, Caleffi A, Corradini E, Ferrara F, Jones R, Castro O, Onyekwere O, Kittles R, Pignatti E, Montosi G, Garuti C, Gangaidzo I, Gomo Z, Moyo V, Rouault T, MacPhail P, Pietrangelo A (2003). "Iron overload in Africans and African-Americans and a common mutation in the SCL40A1 (ferroportin 1) gene". Blood Cells Mol Dis 31 (3): 299-304. PMID 14636642.