COMMENTARY

Two Updates in Multiple Sclerosis

Stephen Krieger, MD

Disclosures

April 26, 2019

This transcript has been edited for clarity.

Hello. I'm Dr Stephen Krieger from Mount Sinai in New York, reporting for Medscape on the latest in multiple sclerosis (MS) research and development.

New Diagnostic Testing

In 2018, the most recent revisions to the McDonald criteria for diagnosing MS were published.[1] The McDonald criteria still maintain that no better explanation for a patient's symptoms should be found while arriving at a diagnosis of MS. At the same time, there's been an increased understanding of the role of a new antibody, the myelin-oligodendrocyte glycoprotein (MOG), as a cause of inflammatory demyelinating disease.

For many years, we've incorporated the neuromyelitis optica (NMO) antibody—the anti-aquaporin-4 antibody—into our diagnostic workup for MS, and have recognized that NMO spectrum disorder is truly a separate diagnosis. But anti-MOG is now gaining in prominence, as we've come to realize that many of our patients with optic neuritis have it as a consequence of anti-MOG antibody syndrome. Bilateral optic neuritis is particularly suggestive of the anti-MOG antibody syndrome.

Ordering now commercially available anti-MOG antibody testing in nearly all patients presenting with inflammatory demyelinating disease, particularly optic neuritis, appears to be warranted. It's helped us to understand that in many cases, patients who we thought of as having clinical syndromes like chronic relapsing inflammatory optic neuropathy, probably have anti-MOG disease. Similarly, anyone who had an NMO spectrum disorder–type phenomenology, but did not have the antibody, we considered seronegative NMO. I think that's also where the anti-MOG antibody syndrome seems to fit. Therefore, I recommend adding the serum blood anti-MOG assay to your diagnostic workup of MS, in addition to optic neuritis and NMO.

Treatment Strategies in MS

Oral medicines have been available for MS now for nearly a decade, beginning with the 2010 approval of fingolimod by the US Food and Drug Administration (FDA). This year, the FDA issued new guidance on the use of fingolimod,[2] noting that when this treatment is stopped, it may result in some patients experiencing a rebound-type phenomenon of excessive inflammatory MS disease activity.

This is something that we've known scientifically for a number of years, but it's interesting to see it rise to the level of the FDA offering guidance around how this agent should be utilized. The lesson here is fairly clear: When we use and then stop agents such as natalizumab or fingolimod, in some cases there can be a resurgence of disease activity when the migration of activated lymphocytes is no longer being blocked.

Certainly, fingolimod is a highly effective medicine, which was approved in 2018 for pediatric MS. Yet the guidance from the FDA is clear that we should discuss with patients the potential risks for a rebound-type phenomenon associated with stopping this drug. I also think it's important that when we do take patients off of fingolimod, we observe them closely. I have more regularly scheduled follow-ups with those patients, and I plan an MRI scan in the post-fingolimod period to look for the recurrence of disease activity. It's important for our sequencing strategies to know that if we're taking a patient off of a medicine like fingolimod, we need to have a next-step treatment in mind, which we then must try to migrate that patient to relatively promptly.

It should be noted that adherence to medicines has always been an issue in MS, particularly as this is a chronic disease impacting young people. Given the risks associated with nonadherence to or outright stopping this type of medication, I think it is even more important for us to attend to not just our appropriate treatment strategy, but also to ensuring that our patients understand the underlying rationale. We must highlight for them the risks associated with nonadherence of these medicines.

In conclusion, keep in mind the latest information on diagnosing demyelinating disease with the use of anti-MOG assays in cases that are suggestive of NMO or NMO spectrum disorder, and be sure to appropriately use fingolimod and carefully monitor patients for any signs of recurrence and rebound disease activity when it is discontinued.

Reporting for Medscape from Mount Sinai in New York, I'm Stephen Krieger.

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