Erythrocytes are degraded by the interstitial macrophages, with the released iron incorporated into ferritin. Over time, with increasing overload of iron, the structure of ferritin changes to haemosiderin.
Iron overload in MS plaques has been demonstrated in vivo by MRI.28 In addition, we observed haemosiderin in the urine of patients with active inflammation of MS
Bethr wrote:These researchers seem to have tunnel vision.
The body is constantly balancing it's iron levels, because iron is toxic in excess. This involves many interactions.
When you get an increase in intracellular concentrations of iron, ferritin synthesis also increases. When the storage capacity is exceeded iron is released intracellularly in the form of hemosiderin and toxic nontransferrin-bound forms of iron.
So ferritin would stay within a range. The excess turning to hemosiderin etc.
The interesting research would be hepcidin levels, because hepcidin is needed to take the iron out of storage. Low hepcidin would mean iron is stuck in storage. Hypoxia causes low hepcidin levels, which could mean the iron in storage can can not be utilised and degrades to hemosiderin.
Hepsidin is also responsible for the anemia of chronic inflammation, as the iron is stuck in storage and is unavailable for use.
There is a lot of new research out on lowering and raising hepcidin levels to treat problems with iron metabolism, both anemia and iron overload disorders and all the associated diseases.
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