The major new results presented at this meeting were on daclizumab in relapsing MS. The results
of this study were first presented last fall, and more complete results were presented at this meeting. This treatment
blocks the receptor for interleukin-2, a major signal in the immune system. In contrast to other monoclonal antibodies,
which are given by intravenous infusion, it is given as a subcutaneous injection every 4 weeks. In this trial, daclizumab
was compared to Avonex, one of the standard MS treatments. The annualized relapse rate was decreased 45% in the daclizumab
group, and all of the secondary outcomes favored daclizumab. Side effects included increased infections, rash, and liver
problems. The remainder of the presentations in the main clinical trials session were followup and extension results
on already approved treatments. There were no surprising or remarkable findings to report.
were 2 presentations on treatments for progressive MS. One was a poster on fingolimod (Gilenya) in primary progressive
MS. They had two different outcome measures, and followed patients for 3 years. Most patients progressed on at
least one of the outcome measures during the trial. There was no benefit from the fingolimod treatment. The second
presentation was on high dose biotin for progressive MS. This company announced a positive result in a press release,
and their data were being presented in a session on Friday, which I was not able to attend. According to the abstract
and press release, they enrolled 154 people with primary or secondary progressive MS and moderate disability. The primary
outcome was the number of people showing improvement in the EDSS score or the timed 25 foot walk. In the treated group,
13% improved and 4% worsened. In the placebo group, 0% improved and 13% worsened. These are very interesting results,
and I am looking forward to finding out more details.
There were 2 reports on studies of
treatments that are supposed to increase remyelination. This is different than most of the approved disease-modifying
treatments, which slow down the activity of disease and inhibit the immune system in some way. These treatments do not
affect the autoimmune attack, but are aiming to increase repair and recovery after the attack. If proven effective,
they will be used in conjunction with one of the current agents. Biogen reported the results of a trial of an antibody
to LINGO-1 in optic neuritis. This antibody increases remyelination after injury in several animal models of MS.
They had some encouraging results with improved nerve conduction in the optic nerve in the treated group. This treatment
is also being studied in MS. The second remyelinating treatment reported was rhIgM22. This is a natural autoantibody
that promotes remyelination in animal models. This was a phase I study, which had no assessment for effectiveness.
They did not identify any serious side effects. A treatment strategy related to remyelination is neuroprotection. A neuroprotective treatment
would have no effect on inflammation or autoimmunity, but would support the nerve cells in some way and help them to survive
demyelination and autoimmune attack. A study in 86 patients with optic neuritis found evidence that phenytoin reduced
damage to the retina, with 30% less damage to the nerve fiber layer. Again, this was presented on Friday after the main
meeting, so the details I have are from press releases. Phenytoin is a drug used to treat seizures for over 50 years,
so the side effects are well known. These results are interesting.
There were many scientific topics of interest
to me, a few of which may be of general interest. Several groups are looking at different aspects of the immune response
in cerebrospinal fluid. One reported that the T cells in CSF are likely selected and dividing, based on sequencing of
their T cell receptors. This supports the idea that there is an ongoing autoimmune response in the brain. A second
reported that the T cells in the CSF are increased in a particular type of T cell that helps B cells (Tfh cells). A
third poster I found interesting correlated antibodies to Epstein-Barr virus with damage to grey matter seen on MRI.