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In summary, increased iron deposition has been consistently reported to occur in MS, but its role in pathogenetic processes of this disease has not yet been completely clarified. Whether increased brain iron levels are also the cause or only the consequence of tissue destruction is still a matter of debate. Future longitudinal studies combining clinical disease status, quantitative MRI techniques sensitive for iron, and additional analyses of iron in CSF/serum and iron-related proteins (as well as iron regulator proteins), might help to unravel the implication of increased iron accumulation in MS. Quantitative MRI and histopathologic analyses of postmortem MS brains should complement these studies.

Iron has been implicated in multiple sclerosis for many years. It has been observed by MRI and has been seen in vessel wall for small venules. More recent work has shown that there can be iron build up around MS lesions and inside the lesions although not all lesions show an increase in iron content. Further, different parts of the brain associated with the medial venous drainage system also can show increases in iron content that appear to be affiliated with the draining veins. This iron is often not present MS lesions although in some cases it is and appears as either a uniform intensity or as a ring-like structure around the lesion. Iron in the pulvinar thalamus can increase and is seen in roughly 50% of MS cases especially for young people.

It is quite possible these increases in iron are related to the chronic venous insufficiency and may represent iron in one of three forms: oligodendrocyte ferritin after macrophage activity, iron from blood products or iron in the vessel wall or some combination of these. It is unknown what role iron plays at this time and the main effect may remain the demyelinating inflammatory aspects of MS with iron representing either an outcome of endothelial damage or as part of the inflammatory pathway.

Hi Vicki, My sister and I both inherited just one C282Y gene, so are heterozygotes, my brother is also. HH runs in our family, my mother and a cousin had it.
Both my sister and brother have higher iron levels than I ever had. You cannot donate blood once diagnosed with MS in NZ, so no luck there for my sister.
My brother has ferritin about 700 currently, and he can't donate blood either. He has hep.c. and has failed on interferon and his liver is near the end, still they won't phleb him, even though that is becoming the norm overseas, especially if interferon fails.

It's hard to watch this happen to my family. I'd so love to see my sister get some energy back and relief from the pains. It is certainly worth trying.
The comment about "the dark ages" came from a Wellington Hemotologist.
Unfortunately the only one available in our area, so a second opinion is going to be difficult.
Anyway, getting the iron out really worked a treat for me.
I still get the odd tingle in my fingers which is a leftover from
the lesion. Only thing left now is the bronzed skin up my arms that came up a few years ago and never left even in winter.
I start to get fatigued and sleep afternoons when I'm due for a phleb. Getting one tomorrow. I've been doing them 3-4 monthly since Jan 2010.

There are several types of genetic hemochromatosis. These include: Type I or Classic (HHC); Type II a, b or Juvenile (JHC); Type III or Transferrin Receptor Mutation; and Type IV or Ferroportin Mutation.
Here is the link: [url]http://www.irondisorders.org/hemochromatosis

Vicki[/url]

Clin Invest. doi:10.1172/JCI44490.
Published February 7, 2011
The American Society for Clinical Investigation.
Research Article
An unrestrained proinflammatory M1 macrophage population induced by iron impairs wound healing in humans and mice

Uncontrolled macrophage activation is now considered to be a critical event in the pathogenesis of chronic inflammatory diseases such as atherosclerosis, multiple sclerosis, and chronic venous leg ulcers. However, it is still unclear which environmental cues induce persistent activation of macrophages in vivo and how macrophage-derived effector molecules maintain chronic inflammation and affect resident fibroblasts essential for tissue homeostasis and repair. We used a complementary approach studying human subjects with chronic venous leg ulcers, a model disease for macrophage-driven chronic inflammation, while establishing a mouse model closely reflecting its pathogenesis. Here, we have shown that iron overloading of macrophages — as was found to occur in human chronic venous leg ulcers and the mouse model — induced a macrophage population in situ with an unrestrained proinflammatory M1 activation state. Via enhanced TNF-α and hydroxyl radical release, this macrophage population perpetuated inflammation and induced a p16INK4a-dependent senescence program in resident fibroblasts, eventually leading to impaired wound healing. This study provides insight into the role of what we believe to be a previously undescribed iron-induced macrophage population in vivo. Targeting this population may hold promise for the development of novel therapies for chronic inflammatory diseases such as chronic venous leg ulcers.

Hemochromatosis C282Y gene mutation increases the risk of venous ...by P Zamboni - 2005 - Cited by 30 - Related articles
CONCLUSIONS: The overlap of primary CVD and the C282Y mutation consistently increases the risk of developing venous leg ulceration

Summary This paper presents a hypothetical model of role for iron in the development of venous leg ulcers and
multiple sclerosis. Elevated concentrations of iron were found in the skin affected by venous hypertension and also in
the areas of brain with multiple sclerosis lesions. Individuals with hemochromatosis gene (HFE) mutations: C282Y and
H63D, which result in a less efficient transport of iron by macrophages, are characterized by an increased risk for
venous leg ulcer and multiple sclerosis. Multiple sclerosis is a T cell-mediated disease, and T cells probably participate
in the development of venous ulcers. This deleterious role of ferric ions could be related to the regulation of T cell
proliferation and apoptosis. Under normal conditions excessive accumulation of T cells cannot take place, because
nitric oxide and interferon-gamma drive these cells toward apoptosis. However, in tissues with a high concentration of
iron, T lymphocytes proliferate instead of undergoing apoptosis. This is possible due to the internalization of the INFcR2
chain of the interferon-gamma receptor, the downregulation of inducible nitric oxide synthase expression in
macrophages and the inactivation of the active site of caspases. Yet, it should be emphasized that this hypothesis does
not claim for the increased concentration of iron as a direct causal factor for the development of venous ulcerations or
multiple sclerosis, but rather, iron is a factor that modulates and exaggerates the autoimmune process. Iron chelators,
administered systemically or locally, should potentially exhibit therapeutic and prophylactic activity against venous leg
ulcers and multiple sclerosis.
c 2008 Elsevier Ltd. All rights reserved.

Full article here: [url]http://www.direct-ms.org/pdf/CCSVI/Simka%20Fe%20overload%20ulcers%20lesions%2008.pdf

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