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ECTRIMS 2016
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From September 14 to 17,2016 I attended the ECTRIMS meeting in London.  I forgot to take a nice picture to put on the website so that the page doesn't look so boring.  

Clinical trials

Compared to previous years, there were relatively few large clinical trials of new treatments reported.  The only large phase III trial was siponimod, an agent similar to fingolimod (Gilenya) which may have more selectivity and less side effects.  They studied patients with secondary progressive MS (SPMS), and the primary outcome measure was change in disability.  They demonstrated a 20% decrease in progression, and a robust effect on relapses and multiple MRI measures.  Subgroup analyses suggested that the treatment was more effective in younger patients with more inflammatory disease.  This study is encouraging because it is one of the few positive results in SPMS. 

Another encouraging study was lipoic acid in SPMS.  This treatment is meant to be neuroprotective, and showed a benefit on the 25 foot timed walk and brain atrophy as measured by MRI.  Another potentially neuroprotective treatment, fluoxetine, had some positive effects but less definite results. 

There were also two studies on the effect of Vitamin D.  For the last several years, we have been measuring vitamin D in clinic, and putting patients on replacement treatment for low vitamin D levels, based on studies showing that MS patients with low vitamin D had more relapses and MRI activity.  But we didn’t know if replacing vitamin D would help in MS.  Two small trials were reported that added vitamin D to rebif, and both showed a benefit on MRI.  This isn’t definitive data, but it does support the continued use of vitamin D replacement. 

Another noteworthy report was a long term study of CIS patients which found that treatment before the second clinical relapse delays time to early disability.  This supports the benefit of early treatment, which has been a clinical emphasis for the last several years.  

Scientific results

The scientific sessions included the usual large number of interesting results covering a huge variety of topics, many of them unfamiliar to me.  There were several presentations on my particular interest, the role of Epstein-Barr virus in MS.  One especially strong study investigated cells from brain lesions of people with MS.  These were autopsy specimens, but the tissue was collected rapidly enough that they could obtain and study live cells from active MS lesions, which is unique.  They found that most cells were the CD8 type, and that many were specific for Epstein-Barr virus.  Other presentations found the presence of EBV in MS brain tissue by various methods.  In contrast, a different group measuring antibodies in blood suggested that human herpesvirus 6A was more strongly related to MS than other viruses. 

Another interesting session was on mitochondrial function in MS.  Mitochondria are the power generators of the cell, and increasing evidence links dysfunction of mitochondria to degenration of myelin or neurons.  The problem with the mitochondria could be either from low oxygen in the tissues or absence of one of the proteins. 

A major recurrent topic was the role of the gut and the bacteria in the gut on MS.  Surprisingly the bacteria that normally live in your intestines have strong effects on how your immune system responds, and several presentations dealt with bacteria.  Some species of bacteria seem to protect against MS and others increase risk of MS.  Efforts are underway to figure out which are the beneficial bacteria and find out whether increasing numbers of those bacteria will improve disease.  

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

copyright 2007-2017 John William Lindsey