Andrew N. Wilner, MD


October 13, 2014

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This is Dr Andrew Wilner, reporting for Medscape from MSBoston 2014, the Americas Committee for Treatment and Research in Multiple Sclerosis (ACTRIMS)/European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS) meeting, in Boston, Massachusetts. Today I am here to give you a few of the highlights from this very exciting meeting.


Immunopathogenesis of multiple sclerosis.


This figure shows the immunopathogenesis of multiple sclerosis (MS), and it supports the main point of the plenary session[1] by Dr David Hafler, from the Yale University School of Medicine in New Haven, Connecticut. Dr Hafler said that there is no longer any doubt that MS is an immune-mediated disease that includes genetic and environmental components.

We know that there is a genetic risk because there is a 2% to 4% elevated risk in siblings of patients with MS and a 30% greater risk in identical twins.[2] But Dr Hafler presented data from genome-wide association studies, which have identified 150 genetic variants, and he speculated that there may be as many as 400 variants. The technology behind these studies was truly awesome. Dr Hafler said, however, "It is not bad genes or a bad environment; it is the bad interaction between genes and environment." In terms of environmental factors, it now seems clear that cigarette smoking, decreased vitamin D, elevated body mass index, Epstein-Barr virus, and possibly increased salt intake are all environmental triggers for the disease.

Peripheral vs Central Beginnings

One persistent question has been whether MS begins in the peripheral immune system or in the brain. Dr Hafler underscored the enormous progress in the understanding of this disease by explaining how MS begins in the periphery and moves on from there. Peripheral T cells enter the choroid plexus, then the cerebrospinal fluid; and then, in a second wave, Th17 T cells and Th1 cells enter the brain parenchyma with the resulting persistent inflammation. This is quite exciting and lays the groundwork for future research and the development of new medications.

A Game-Changing Study

Results of the GATE trial[3] are another game-changer. The GATE trial compared generic glatiramer acetate with Copaxone® and with placebo. The 700 patients in this randomized, double-blind trial had a greater than 90% completion rate. The endpoint was number of T1 gadolinium-enhancing lesions. The study found that both generic glatiramer acetate and Copaxone were significantly better than placebo. Not only that, they were almost identical in outcomes; safety and tolerability were also similar.

In addition, investigators found no significant difference in annualized relapse rate in any of the arms. The study was relatively short, however, lasting about 9 months; nonetheless, the results were very convincing.

The next question is: Will the US Food and Drug Administration approve generic glatiramer? This would be the first generic drug for MS. I have written about generic drugs in Epilepsy & Behavior,[4] and generic drugs have their pros and cons. But if this generic formulation of glatiramer is approved, it will initiate a new discussion and a new approach to the treatment of MS.

It has been quite exciting to be at ACTRIMS/ECTRIMS in Boston, Massachusetts. I hope you have enjoyed these brief highlights. This is Dr Andrew Wilner, reporting for Medscape.


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