One focus of this years meeting was progressive MS. There were a number of talks on the
mechanism of damage in progressive MS, and some talks on treatment. There is currently no
treatment which has a marked benefit in progressive MS, and there is increasing interest in finding
new treatments for this type of MS along with better ways to measure changes in progressive MS.
A study done in the UK with three drugs already approved for other uses; fluoxetine, amiloride, and
riluzole; had negative results.
Another focus was risk management for current treatments. Two useful and reassuring
presentations reported on death rate and cancer risk with some of the highly effective MS
treatments that I currently use. There was no significant increase in the death rate with rituximab,
and there was no signal for an increase in any type of cancer, and in particular no increase in risk of
breast cancer with rituximab. The current label for ocrelizumab raises the question of increased risk
of breast cancer, but it seems unlikely that is a real cause and effect relation since it was not seen in
the much larger rituximab group. Rituximab and ocrelizumab are very similar, and I expect they
should have the same risks.
Unlike previous years, there were very few clinical trial results and very few completely new
approaches to treatment. The main exception is the study of the tyrosine kinase inhibitor
evobrutinib. This drug inhibits a protein found in B cells and macrophages that is important for
regulation of immune responses. In the phase II study, it had encouraging results on MRI activity
and possibly clinical relapses over 24 weeks. The phase III study is currently beginning, and this
will be an interesting drug to watch.
My major research interest is the role of Epstein-Barr virus in MS, and there were a few
presentations on this topic. Dr. Olsson reported that a protein called anoctamin-2 cross-reacts with
the EBV nuclear antigen, and that a significant fraction of MS patients have an antibody against
anoctamin. Increased antibodies against anoctamin predict risk of MS in the future. Dr. Klemens
reported that in a large cohort of new MS patients from Germany, all persons were infected with
EBV. This supports the idea that infection with EBV is required to get MS. One poster reported that
MS patients with more active disease were more likely to have a high level of antibodies against
EBV, and another reported that many of the cytotoxic T cells in MS brain are specific for EBV.