Iron Related Changes in Clinically Isolated Syndrome (CIS)

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

Iron Related Changes in Clinically Isolated Syndrome (CIS)

Postby Shayk » Mon Dec 14, 2009 6:59 pm

Hi all

I'm having a hard time keeping up here so if this has already been posted...my apologies--it's recent research indicating there are iron related changes in people who've not yet been diagnosed with MS (CIS).

Deep gray matter T2 hypointensity is present in patients with clinically isolated syndromes suggestive of multiple sclerosis
Gray matter (GM) magnetic resonance imaging (MRI) T2 hypointensity, a putative marker of iron deposition, is a frequent finding in patients with clinically definite (CD) multiple sclerosis (MS).

The objective of this study was to assess: (a) how early deep GM T2 hypointensity occurs in MS, by studying patients with clinically isolated syndromes (CIS) suggestive of MS, and (b) whether they contribute to predict subsequent evolution to CDMS

In CIS patients, deep GM is not spared, suggesting that iron-related changes and neurodegeneration occurs early. The magnitude of such damage is only minor and not associated with an increased risk of evolution to CDMS.


And, there's also this research--which found changes in brain iron metabolism correlated with disease progression.

Transcranial brain sonography findings predict disease progression in multiple sclerosis
CONCLUSIONS: Neurodegenerative disease-like deep gray matter lesions can be frequently detected by transcranial sonography (TCS) in patients with multiple sclerosis (MS). Findings suggest that TCS shows changes of brain iron metabolism which correlate with future progress of MS


Take care all....it's such an exciting time. Thanks to all who are contributing so much to the advances we're witnessing. :D

Sharon
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Postby cheerleader » Mon Dec 14, 2009 7:37 pm

Thanks, Sharon-
Terrific research, as usual.
These are both new studies published this fall...and not from Dr. Haacke or NYU...our usual gray matter investigators. It is interesting to see this research spreading across the globe. Gray matter changes appear to happen early in the MS process, and continue as the disease progresses. These studies further corroborate Dr. Zamboni's findings.
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Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
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Postby mrhodes40 » Mon Dec 14, 2009 8:59 pm

suggesting iron related changes occur early


What I find interesting about that quote is the implied acceptance of the fact that iron related changes are simply a part of the picture we all know about.

HERE'S A PAPER FROM '02

Conclusions Gray matter T2 hypointensity in MS is associated with brain atrophy and is a stronger predictor of disability and clinical course than are conventional MRI findings. While longitudinal studies are warranted, these results suggest that pathologic iron deposition is a surrogate marker of the destructive disease process.


So to me the question is why all the mystery and head scratching about iron among people/neuros specifically newly hearing about CCSVI? This work relating iron as the big deal is OLD news...

If someone is trying to suggest that reflux and venous insufficiency is somehow only theoretically able to cause iron deposition and thus this is all a totally unknown mystery then they need to think about reading about venous ulcers
• The brown pigmentation of the skin associated with venous ulceration is caused by increased local iron deposition. Diagnostic x-ray spectrometry, a method based on x-ray fluorescence analysis, was used for the noninvasive determination of iron levels in the skin of patients with venous ulceration. The mean (±SEM) iron concentration in the skin around the venous ulcer was elevated, compared with control values of nonulcerated skin (250 ± 54 vs 128 ± 39 µg) and compared with normal skin from the forearm (250 ± 54 vs 14 ± 2.5 µg). These data suggest that dermal iron deposition may not be an incidental by-product of increased venous pressure, but may actively perpetuate tissue damage in venous ulcerations


that one from 1988 paper

If refluxing blood and venous insufficiency in the legs causes iron deposition they why wouldn't it in the head??
just MHO
I'm not offering medical advice, I am just a patient too! Talk to your doctor about what is best for you...
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Postby Shayk » Tue Dec 15, 2009 7:04 am

Marie
So to me the question is why all the mystery and head scratching about iron among people/neuros specifically newly hearing about CCSVI? This work relating iron as the big deal is OLD news

I hear you on that one. :lol:

And, while the work with regard to iron is old news, I think the fact that they found iron deposition in clinically isolated syndrome (i.e., prior to diagnosis) is news. The neurodegeneration is present from the gitgo and doesn't just start to develop after 10-15 years of inflammation. That might be news to some neuros.

Marie
If refluxing blood and venous insufficiency in the legs causes iron deposition they why wouldn't it in the head??

Great question....

Have a great day all

Sharon
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Postby jay123 » Tue Dec 15, 2009 7:23 am

With all this info on iron shouldn't the CCSVI 'protocol' include some sort of iron chelating process along with opening the veins to help remove it? And for those of us waiting for the procedure, should we perhaps be working on chelation while we wait?
Caution though - I did notice in my IP6 reading that it shouldn't be used in the weeks prior to and immediately after surgery as it does inhibit clotting (WebMD).
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