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Haemosiderin??
Posted: Wed Feb 10, 2010 11:02 am
by gauchito
Hi all
I am following this CCSVI incredible as excited as you are. I am MSer since 8 years ago and NOT A DOCTOR. What I learned by reading same materials as you did, is that Zamboni also proposes the test of Haemosiderin in urine as a potenti1al biomarker of an iron-driven neurodegenerative process taking place
Haemosiderin is a protein the body builds to capture inapropriate free iron in tissues.
It is a very common and simple urine test that complements very well all the imaging stuff. I took the test down here in Argentina along with 2 other MS mates. Guess what?: the 3 positive!!!
For some reason this issue has not come out in our forum although mentioned by Zamboni in his papers.
I think it might be an additional element to build a CCSVI case on an individual
Does anyone have additional/different info ?
Posted: Wed Feb 10, 2010 1:39 pm
by Bethr
Interesting Gauchito. We are looking at the effects of excess iron over on the "phlebotomy anyone" thread.
Hemosideran is of course part of the iron metabolism. And it has some connection to Porphyrins. So Zamboni is on to it in one connection. Good!
Maybe some in depth gene studies on people with MS, looking at hemochromatosis genes and Porphyria Genes would be incredibly interesting.
from Wiki
Hemosiderin
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Hemosiderin image of a kidney viewed under a microscope. The brown areas represent hemosiderin
Heme. Iron is at center.Hemosiderin or haemosiderin is an iron-storage complex. It is always found within cells (as opposed to circulating in blood) and appears to be a complex of ferritin, denatured ferritin and other material. The iron within deposits of hemosiderin is very poorly available to supply iron when needed.
Several disease processes result in deposition of larger amounts of hemosiderin in tissues; although these deposits often cause no symptoms, they can lead to organ damage.
Hemosiderin is most commonly found in macrophages and is especially abundant in situations following hemorrhage, suggesting that its formation may be related to phagocytosis of red blood cells and hemoglobin. Hemosiderin can accumulate in different organs in various diseases.
Iron is required by many of the chemical reactions (i.e. oxidation-reduction reactions) in the body but is toxic when not properly contained. Thus, many methods of iron storage have developed.
[edit] Pathophysiology
Hemosiderin often forms after bleeding (hemorrhage).[1] When blood leaves a ruptured blood vessel, the cell dies and the hemoglobin of the red blood cells is released into the extracellular space. White blood cells called macrophages engulf (phagocytose) the hemoglobin to degrade it, producing hemosiderin and porphyrin.
[edit] Diseases associated with hemosiderin deposition
Main article: Hemosiderosis
Hemosiderin may deposit in diseases associated with iron overload. These diseases are typically diseases in which chronic blood loss requires frequent blood transfusions, such as sickle cell anemia and thalassemia.
Posted: Wed Feb 10, 2010 1:58 pm
by gauchito
Thx Bethr
That might be the point. In principle one shouldn´t have hemosiderin disposed in urine.
If you have it, what is the meaning?
I am lookimg for conclusive evidence of hemodinamic alterations that can assist all the imaging approach that at the end of the day is man-dependant.
It would be great if we could formulate: if you have MS you have hemosiderin in urine, if you are healthy you don´t.
I think we need more info for that ambitious statement. Pls bear in mind I am not a Doctor professional.
More help from you all is neede here
Posted: Wed Feb 10, 2010 2:19 pm
by Bethr
I would like to be tested for haemosiderin. I am going to a specialist hemotologist in 12 days time. I'll ask him about it.
To see the tie up with genes, you need to read the "phlebotomy Anyone" thread. We are a group of woman whose MS symptoms of fatigue etc diminish with blood draws and menstruation. So we are trialling phlebotomy. My MS symptoms disappeared 24 hours after a full phleb in early January. It was miraculous.
We all have high iron/transferrin saturation levels and one gene for hemochromatosis, the iron overload disease. But these tests are often missed by our doctors, as we do not fit the classic DX for hemochromatosis or iron overload.
Cheers...........
Posted: Wed Feb 10, 2010 2:31 pm
by Bethr
This is a great lead for me. Thanks!
I have a lot of hyperpigmentation on my arms (pic over at phlebotomy Anyone thread)
Experimental hemosiderosis: relationship between skin pigmentation and hemosiderin.
Tsuji T
Acta Derm Venereol 1980; 60:109-14.
Abstract
Iron (totalling 7.5 mg per mouse in three doses) was injected into hairless mice to determine the relationship between skin pigmentation and hemosiderin deposition. The skin color reached its maximum 24 to 48 hours after the last injection and then gradually faded over the subsequent 8 months. In the skin, hemosiderin granules were present extracellularly between collagen bundles as well as within dermal macrophages, Langerhans cells and indeterminate dendritic cells of the epidermis. A larger amount of iron was deposited in the facial than in the dorsal skin, resulting in darker pigmentation of the former. This study suggests that brownish discoloration of skin in hemochromatosis might be attributable in some degree to accumulation of hemosiderin and that pronounced hyperpigmentation of the face in hemochromatosis might be due to increased activation of melanocytes by a high content of hemosiderin.
MeSH
Animals; Hemochromatosis; Hemosiderin; Hemosiderosis; Iron; Melanins; Mice; Mice, Nude; Skin; Skin Pigmentation
CAS Registry Number (Substance Name)
0 (Melanins), 7439-89-6 (Iron), 9011-92-1 (Hemosiderin)
MEDLINE record details
Publication Type:
Journal Article
ISSN:
0001-5555
Country:
SWEDEN
Language:
eng
Date of Entry:
19800728
Unique Identifier:
6155014
Journal Subset:
IM
http://www.ophsource.org/periodicals/op ... LN.6155014
Posted: Wed Feb 10, 2010 2:41 pm
by cheerleader
I wrote about this from Italy. Here are my notes from the pre-conference meeting in Bologna - you can find all of the notes on the first page of the research sticky.
In 2002, Dr. Zamboni noted that positive urine hemosiderin- a disease marker used to assess the severity of chronic venous disease- was administered to MS patients while they were in the midst of relapse. All of the MS patients tested positive. After he published a paper on this, he received an e-mail from Dr. FA Schelling- which referred him to Dr. Torben Fog’s paper- “Topography of Plaques in MS” The note from Dr. Schelling stated that perhaps Dr. Zamboni would now find what he was looking for...that the lesions of MS spread counter current from normal venous flow, and that there was where he should begin to study.
cheer
Posted: Wed Feb 10, 2010 3:25 pm
by shye
Bethr-
having porphyrins is not the same as having porphyria--porphyria is a disorder of porphyrins..porphyrins are in blood cells, some combine with iron to form heme...
Posted: Wed Feb 10, 2010 3:30 pm
by LR1234
So could someone please summarise for me what tests one should ask for to test all this iron stuff?!
I have had Serum Ferrin tested
Serum Iron
I have asked for Transferrin saturation levels but was told that it is not a standard test so need to go back and ask again.
Is a Haemosiderin test available yet ? I am sure my GP will be bemused by another random test I am requesting!:)
L
Posted: Wed Feb 10, 2010 6:37 pm
by gauchito
L, the test is perfectly available Rationale is whether urine hemosiderin is a biomarker of a venous problem (in CNS in our case). According to Zamboni it is. In principle hemosiderin should not be in urine if Fe metabolism is working correctly.
I wonder why this is not included in large studies as Buffalo´s. Perhaps it was. Or perhaps there are other medical reasons I ignore. The fact is that this element emerges from Zamboni´s work very strongly. I am kind of surprised why it is so absent or hidden in the talks.
For sure more clarification and help are needed on this
Posted: Thu Feb 11, 2010 8:59 am
by ama
gauchito wrote:L, the test is perfectly available Rationale is whether urine hemosiderin is a biomarker of a venous problem (in CNS in our case). According to Zamboni it is. In principle hemosiderin should not be in urine if Fe metabolism is working correctly.
I wonder why this is not included in large studies as Buffalo´s. Perhaps it was. Or perhaps there are other medical reasons I ignore. The fact is that this element emerges from Zamboni´s work very strongly. I am kind of surprised why it is so absent or hidden in the talks.
For sure more clarification and help are needed on this
Hi gauchito,
You are totally right. In the first article from Zamboni,
"The big Idea: Iron-dependent inflammation in venous disease and proposed parallels in multiple sclerosis", 2006
in "The Journal of the Royal Society of Medicine" Vol. 99, pp. 589-593
he is refering to MMP-9 and TIMP as measures of inflamation in MS. Since then it is mentioned nowhere. Their is no explanation for this lost.
Posted: Thu Feb 11, 2010 9:08 am
by Cece
This is interesting. I will ask my doctor about getting this tested.
It would seem that this was an early clue for Zamboni about the ms/venous link and that he moved on to the more dramatic imaging and surgical treatment studies.
Checking haemosiderin is noninvasive and this is yet another possible research offshoot: check the heamosiderin levels of 100 controls and 100 MSers in active relapse and 100 more MSers not in active relapse. If results indicated that MSers had haemosiderin in their urine, it would be evidence of chronic venous issues. If they had more of it during active relapse, it would be evidence that the venous issues are implicated (causally or correlatively) with active relapse. This would be a good piece of the puzzle to have.
Posted: Thu Feb 11, 2010 10:21 am
by gauchito
Hi Cece/Ama
Your comments are great and go straight to the point. Imagine if urine hemosiderin is an univocal biomarker of venous insufficiency. What type?
Any type of insufficiency. It might be liver venous insufficiency, or renal, or legs or stomach or......cerebro-spinal.
Subsequently. finding out what type is easier for symptoms´onset on a given individual is almost conclusive. Here we might have the explanation why some "healthy controls" tested positive. It would be easier to face imaging diagnostic step with pre- confirmation that we are carriers of a type of venous insufficiency which in our case is of the sort cerebro-spinal. See the point.
Pls remember I am not a Doctor and this is just an hypothesis to work out.