All specimens from CCSVI veins showed: 1) thickening and sclerosis of the adventitia, 2) a significant difference of birefringence pattern, from a green birefringence to a red birefringence (P<0.001), between veins of CCSVI patients and those of controls, suggesting a switch from collagen type I to collagen type III expression; this modulation was confirmed by means of collagen type immunohistochemistry.
It appears that the changes affecting CCSVI veins in MS patients concern mainly the extracellular matrix, collagen in particular. The switch in collagen type from a prevalence of type I to a prevalence of type III may be implicated in the hemodynamic changes obseved in these patients.
STUDY OBJECTIVES: The connective tissue alterations in varicose vein wall are supposed to be one of the main causes of primary varicose vein (main sign of human lower limbs chronic venous insufficency).
METHODS: 5 varicose vein samples from 5 patients undergoing stripping surgery of long saphenous vein were compared with 5 control samples of healthy (non-dilated) long saphenous veins from necroptic material (with no history of varicosis). They were fixed in a Baker solution, processed by use of light microscopic method, cut to ultra-thin sections (4-5 microm) and stained with PicroSirius Red for collagen. Sections were scanned with light microscope (Leica, Germany) and camera Canon S50 (Germany) and analysed by morphometric programme Image J v.1.38g (National Institute of Health, USA).
RESULTS: In the group of healthy (non-dilated) veins the mean collagen I/III ratio value was 31.40 and in the group of varicose veins the mean collagen I/III ratio was 12.35; the difference is statistically significant: healthy veins contain significantly more of collagen subtype I and varicose veins contain significantly more of collagen subtype III in their walls.
CONCLUSION: The statistically significant difference in the collagen I/III ratio between the groups of healthy (non-dilated) and varicose (dilated) vein walls is worthy of further following.
Rokkit wrote:I'm also wondering if this is why the stenoses seem to progress. Some studies are correlating age and degree of disease progression with severity of stenoses. Could it be that the years of insult produced by reflux and altered hemodynamics resulting in slow, ongoing collagen shift is what accounts for the progression of CCSVI and MS?
Cece wrote:With the right search words, you can find them from all the CCSVI presenters at ISET. It's not actually his presentation, it's the slides and whatever was turned in ahead of time to ISET, but they finish up their work on the presentations more at the last minute, so some of what is in these ISET files did not make it into the actual presentations. It is an IT error, I believe, that these were posted by ISET and made available in google search results like this. It's why I haven't linked to it directly before. Fantastic material. Did you see the tricuspid valve malformation? And the sideways valve, both in the venogram image and then cut out as an actual tissue sample? Remarkable.
ikulo wrote:For those interested in the Dake ISET presentation: http://www.iset.org/files/content/event ... 075234.pdf
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