I also had a problem with the conclusions section of the abstract:
The lack of strong associations of CCSVI with HLA DRB1*1501 suggests that the role of the underlying associations of CCSVI in MS should be interpreted with caution. Further longitudinal studies should determine whether interactions between these factors can contribute to disease progression in MS
It's actual the word caution that bugs me, it reads as a negative. Let me explain what I'm thinking.
If HLA DRB1 1501 is a susceptability gene, which is known to be related to northern European ancestry, acts as an immune system response gene, and also shown to be related to MS vis a vis a three time higher susceptability risk of contracting MS with this gene...how does the lack of "strong associations with CCSVI and HLA DRB1 1501" lead to caution in associating CCSVI in MS?
The HLA DRB1 1501 allele does not cause MS, it does not mean one with this allele will get MS. Having this allele means that the likelihood is increased. Do you see where I'm going with this.....
What if MS is a vascular condition which might secondarily activate this immune response, and people with the allele have more likelihood of this activation becoming MS? Not everyone with MS has HLA DRB 1501---actually, only 53% tested in this study had it. Isn't that an avenue which should be explored? In fact, the body of the paper goes further into the environmental and external factors related to both CCSVI and this allele....and suggests further studies need to be undertaken.
Other than the report of Ferlini et al. , who conducted preliminary analysis of copy number variations associated with CCSVI in a group of 15 MS patients, no information is available on the role of genetic factors in CCSVI. These authors reported that CCSVI was associated of copy number variations in the HLA region for a small group of 15 MS patients . In other diseases with venous pathophysiologies, a role for gender, and environmental and genetic factors is suggested. Female gender, older age, and pregnancy are risk factors for chronic venous diseases  and women have greater frequency of variant hepatic veins . Women have also been reported to have a smaller internal jugular vein size than men (1.48 for men vs. 1.27 in women) . Venous malformations may have genetic contributions and a “double-hit” mechanism has been invoked to explain incomplete penetrance and variability , . The R849W substitution in the angiopoietin receptor Tie2 , an endothelial receptor tyrosine kinase, has been linked to familial venous malformations and results in variable thickness or lack of smooth-muscle cells in the veins of patient lesions. Interestingly Tie2 activates Stat1, which is also critical in interferon signaling. We did not observe, age, gender or disease duration differences in the occurrence of CCSVI (results not shown) in MS. However, a more detailed analysis of candidate gender-dimorphic factors, e.g., vein diameters and autoimmune factors, is warranted as these could strongly interact with changes in cerebral venous outflow.
Why does the abstract take such a negative stance, when the full paper is much more neutral? That's my question. The Buffalo doctors wrote the paper....who wrote the abstract? I don't think it was the same author.
Did the editor write the abstract? Editor: Christoph Kleinschnitz, Julius-Maximilians-Universität Würzburg, Germany
Here's the full paper, see if you think the abstract is a bit more negative, patient. Am interested in your take on this--
http://www.plosone.org/article/info:doi ... ne.0016802
Or, I could be completely over-reacting...(but I don't think so)