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ECTRIMS 2012

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The 2012 European MS meeting was held October 10-12 in Lyon, France.  Compared with previous meetings, there were not as many reports from large clinical trials.  Still, there were several reports of interest. 

There were several promising preliminary reports about possible effects on progression.  Our current treatments are much better at stopping relapses than at preventing accumulation or progression of disability.  There were suggestive reports that simvastatin (a cholesterol lowering drug), cannabinoids, and natalizumab may slow progression.  These findings need to be confirmed before these treatments are recommended for general use.  There were several presentations on human endogenous retroviruses (HERV).  These are viruses which have become part of human DNA.  Some are inactive, but others still make virus proteins.  Some of these virus proteins can stimulate immune function, and might lead to chronic inflammation.  It is still not clear that HERV play any role in MS, but it is an interesting story worth following.   The one new agent was an antibody which neutralizes IL-17A.  This cytokine is felt to play a major role in causing MS.  This was a small phase I study which tested different doses.  The antibody decreased activity on MRI scans.  There was some new information about existing treatments.  The results of the second phase III trial of teriflunomide were similar to the first phase III trial.  The relapse rate decreased from 22% with the lower dose and 36% with the higher dose.  This agent is now approved in the US for relapsing MS.   A phase II study of ponesimod had expected results.  This agent is similar to fingolimod (Gilenya) but more selective.  And glatiramer (Copaxone) at 40 mg 3 times a week reduced relapses by 34%.  This drug is currently used at 20 mg once a day, so this would reduce the number of shots people on Copaxone have to take if it is approved. 

CCSVI:   There were a number of presentations, including one from our group, on CCSVI.   Several studies looked at whether CCSVI even exists.  A very large study reported by Dr. Comi found a low incidence of CCSVI by ultrasound in 1165 MS patients.  Their reported rate of CCSVI of about 3% in MS patients is similar to the rate we found in our study.  The prevalence of CCSVI was similar in controls and patients in both studies.  This is very strong evidence that CCSVI is uncommon and not likely to be related to MS.  In addition, Dr. Ghezzi reported an observational study from Italy on patients who had a procedure done to open their supposedly blocked veins. These treatments were not done as part of a clinical study, and were not done on the advice of their neurologist.  Of the 462 cases, 15 had a serious adverse event, mostly blood clots in the veins.  There was no evidence of any benefit for MS.  I think the evidence that CCSVI does not cause MS is undeniable at this point. 

J. William Lindsey, MD
University of Texas Multiple Sclerosis Research Group
Houston, Texas

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