This Is MS Multiple Sclerosis Community: Knowledge & Support

The origin of increased leg iron stores is extravasation of red blood cells (erythrocytes) in conditions of significant venous stasis. 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.4-9 In 1988, Ackermann found a twenty-fold higher average concentration of iron in lower limbs affected by venous ulcers as compared to the upper arm of the same subjects.8 The phenomenon of leg haemosiderin deposits seems to be significant for the entire body, since this protein has been demonstrated in the urine of patients affected by CVD.9

again, a study undertaken by neurologists, not venous specialists. They are looking at the wrong measure of CHRONIC venous disease. Ferritin is a good marker for a one time vascular insult of the brain, like a stroke--but NOT for ongoing venous disease.

Dr. Zamboni addresses ferritin and its role in chronic venous disease in his paper: The Big Idea: Iron-dependent inflammation in venous disease and proposed parallels in MS-

Great. So how does a paper like this get published? What exactly is this so-called peer review process? Because it's starting to seem more like a kangaroo court.

Great. So how does a paper like this get published? What exactly is this so-called peer review process? Because it's starting to seem more like a kangaroo court.

Rokkit, scientific journals are for people to publish their findings, theories, ideas, so long as there are no basic flaws. Science simply evolves, hopefully leaving behind things that do not work, and refining what works. No peer review can validate a theory in one go.

Absolutely right...but the problem with many of these papers that have been published very quickly is that they are not studying the correct vascular mechanism and coming to erroneous conclusions--ie: the Doepp German doppler tests (which actually proved CCSVI in MS), which Dr. Zamboni is addressing in a soon to be published response. And then this study, which is looking at a marker for a venous infarction, rather than a chronic venous disorder. The problem is that these negative studies are picked up by other journals and the press as conclusive proof there is no CCSVI, when they are not looking at the right indicators. These studies are not being completed by venous specialists and they are not peer-reviewed by venous specialist. So, these are very basic flaws in methodology.
cheer

Absolutely right...but the problem with many of these papers that have been published very quickly is that they are not studying the correct vascular mechanism and coming to erroneous conclusions

Markers for different glial cell responses in multiple sclerosis: clinical and pathological correlations

Disease progression in multiple sclerosis occurs within the interface of glial activation and gliosis. This study aimed to investigate the relationship between biomarkers of different glial cell responses: (i) to disease dynamics and the clinical subtypes of multiple sclerosis; (ii) to disability; and (iii) to cross‐validate these findings in a post‐mortem study. To address the first goal, 51 patients with multiple sclerosis [20 relapsing remitting (RR), 21 secondary progressive (SP) and 10 primary progressive (PP)] and 51 neurological control patients were included. Disability was assessed using the ambulation index (AI), the Expanded Disability Status Scale score (EDSS) and the 9‐hole PEG test (9HPT). Patients underwent lumbar puncture within 7 days of clinical assessment. Post‐mortem brain tissue (12 multiple sclerosis and eight control patients) was classified histologically and adjacent sites were homogenized for protein analysis. S100B, ferritin and glial‐fibrillary acidic protein (GFAP) were quantified in CSF and brain‐tissue homogenate by ELISA (enzyme‐linked immunosorbent assay) techniques developed in‐house. There was a significant trend for increasing S100B levels from PP to SP to RR multiple sclerosis (P < 0.05). S100B was significantly higher in RR multiple sclerosis than in control patients (P < 0.01), whilst ferritin levels were significantly higher in SP multiple sclerosis than in control patients (P < 0.01). The S100B : ferritin ratio discriminated patients with RR multiple sclerosis from SP, PP or control patients (P < 0.05, P < 0.01 and P < 0.01, respectively). Multiple sclerosis patients with poor ambulation (AI ≥7) or severe disability (EDSS >6.5) had significantly higher CSF GFAP levels than less disabled multiple sclerosis or control patients (P < 0.01 and P < 0.001, respectively). There was a correlation between GFAP levels and ambulation in SP multiple sclerosis (r = 0.57, P < 0.01), and between S100B level and the 9HPT in PP multiple sclerosis patients (r = –0.85, P < 0.01). The post‐mortem study showed significantly higher S100B levels in the acute than in the subacute plaques (P < 0.01), whilst ferritin levels were elevated in all multiple sclerosis lesion stages. Both GFAP and S100B levels were significantly higher in the cortex of multiple sclerosis than in control brain homogenate (P < 0.001 and P < 0.05, respectively). We found that S100B is a good marker for the relapsing phase of the disease (confirmed by post‐mortem observation) as opposed to ferritin, which is elevated throughout the entire course. GFAP correlated with disability scales and may therefore be a marker for irreversible damage. The results of this study have broad implications for finding new and sensitive outcome measures for treatment trials that aim to delay the development of disability. They may also be considered in future classifications of multiple sclerosis patients.

Ferritin, transferrin and iron concentrations in the cerebrospinal fluid of multiple sclerosis patients.

MS patients with active or stable relapsing-remitting disease had ferritin levels that were comparable to those found in normal individuals. There were no significant differences in transferrin or iron levels in the CSF between MS and normal individuals. Both ferritin and transferrin levels were elevated in patients that had high CSF IgG values but not in patients with a high IgG index. Since ferritin binds iron, the increase of CSF ferritin levels in chronic progressive MS patients could be a defense mechanism to protect against iron induced oxidative injury. Ferritin levels could be a laboratory measure that helps to distinguish between chronic progressive and relapsing-remitting MS.

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Therefore my question/point "is it really wise to ask the guy selling the Rolex how to tell a real from a fake?" and who is REALLY to blame for follow up researchers not wanting to consult with the salesman?

There is no avoiding the fact that this is a highly unusual situation and no one can blame researchers attempting to replicate for trying to make due on their own.

Therefore my question/point "is it really wise to ask the guy selling the Rolex how to tell a real from a fake?" and who is REALLY to blame for follow up researchers not wanting to consult with the salesman?