Normal CSF ferritin levels suggest against ccsvi cause of ms

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.
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1eye
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Post by 1eye »

Lyon sez:

"But I guess that's the point of this whole thing....questioning whether Zamboni is causing all this misinformation by NOT making the necessary information needed to replicate his findings easier to come by. Every other researcher historically has put that information in their initial study articles specifically to make replication attempts easier. Zamboni charges for lessons."

To which I replyz:

I'm sure there are some good fund-raisers in these parts if you are short on cash...

I think Dr. Zamboni has made huge amounts of information available. Not misinformation. Dr. McDonald has seen that this is not enough, partly by doing actual venoplasty. So he has gone to Ferrara and later sent other people in his lab there, to learn how to properly do the screening. This kind of training would be very necessary in a MASH-type triage situation such as might occur shortly in MS. But it's becoming clear that MRI imaging is really going to tell us a lot about MS, and those who can afford it are going to learn a lot more. JMO

Also, the day is coming (soon I hope) when all the animosity (stressful even being here, sorry to say) and attempts to disprove will die down and most MS patients will be assumed to have CCSVI. I am not in a position to profit from that, and I think many of the people working in this area are shortening their own lives with stress (partly because of the animosity :evil:), out of a desire to help and the sheer size of the need for it. JMO

He is not a practicing surgeon and I doubt he personally gives any lessons in venography.
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Lyon
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Post by Lyon »

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Last edited by Lyon on Sun Nov 20, 2011 4:50 pm, edited 1 time in total.
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Zeureka
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Post by Zeureka »

There is certainly a "patto Zambo" as Salvi himself called it in a recent presentation where stents placed outside the Italian territory were represented as devils - and only certain docs get access to that pact. And a certain attempt to monopolise/protect the invention with unfortunately partly self-destructing side effects - that also make us patients suffer....

But I think this is very sadly political and has nothing to do with the science behind it in itself. Unfortunately politics are difficult to exclude (and to seperate them from science completely impossible) and often destroy or obstacle the science that may help patients. But politics in Italy related to the healthcare system in place are in particular not easy and also Zamboni has gone through a struggle to get his research approved and generally get on with CCSVI where we are standing now!
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cheerleader
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Post by cheerleader »

So, back to ferritin levels in CSF--as stated earlier, ferritin is an appropriate bio-marker for an acute hemorrhage in the brain. We find ferritin in the CSF of those with stroke.

http://pubget.com/paper/20719531
The doctors in the study alluded to the fact that those with stroke or infarction had elevated ferritin. This is because ferritin is elevated right after the infarction, until the body is able to clear it. Or, if it is not able to clear it, the protein changes to hemosiderin.

Dr. Zamboni has never tested ferritin levels in CSF, nor has he ever written about this. As a vascular doctor, he has not tested CSF. He uses blood and urine.

What he has written about is an easy, cost-effective test for iron binding proteins. A urine test for hemosiderin.

From the Big Idea: Iron Dependent Inflammation in Venous Disease
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
Dr. Zamboni is not holding on to some secret protocol. He is a vascular doctor, and speaks to changes in the vasculature he sees in chronic venous disease. He tests blood and urine. It was a group of neurologists that determined they could prove or disprove CCSVI by testing for ferritin in CSF....while there is nothing in any medical literature to link ferritin to chronic venous disease, or to Zamboni's studies.
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Bethr
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Post by Bethr »

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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PCakes
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Post by PCakes »

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.
bethr..are you saying... possible scenario .. hypoxia = low hepcidin = anemia?? and in this case would iron supplements/injections commonly administered for anemia be cause for concern?
wow!
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