Interferons and Glatiramer Acetate for Relapsing MS

EP: 1.Revised Recommendations for Diagnosing Relapsing MS

EP: 2.Tailoring Therapy for Patients With Relapsing MS

EP: 3.Overcoming Treatment Challenges in Relapsing MS

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EP: 4.Interferons and Glatiramer Acetate for Relapsing MS

EP: 5.Cladribine Treatment for Relapsing MS

EP: 6.Risk of Relapse/Progression in MS

EP: 7.Clinical Experience Treating Relapsing MS With Cladribine

EP: 8.S1P1 Receptor Modulators for Relapsing MS

EP: 9.Selecting an S1P Modulator for Relapsing MS

EP: 10.Anti-CD20 Therapies for Relapsing MS

EP: 11.Anti-CD20 Utilization in Relapsing MS

EP: 12.Fumarates for Relapsing MS

EP: 13.Sequencing Therapies in RRMS

EP: 14.Lifestyle Interventions to Manage MS

EP: 15.Looking Ahead at Managing MS

EP: 16.Managing MS in the Community: Advice and Resources

Transcript:

Amy Perrin Ross, APN, MSN, CNRN, MSCN:How about the role and the mechanism of action of interferons and glatiramers? This is often either where we start, if we’re looking at escalation, or it’s a place where many of our patients have remained. I’ll turn this to Christen.

Christen Kutz, PhD, PA-C: Thanks, Amy. I have to give the disclosure up front that the exact mechanism of action of these medications is not fully understood. But this is what we know about the interferons. There’s interferon beta-1a, interferon beta-1b. What we know is that it does reduce the proinflammatory cytokines; we believe that it suppresses T-cell activation and can prevent the migration of activated immune cells across the blood-brain barrier. There have even been some thoughts that there are antiviral properties to the interferons. With glatiramer acetate, the mechanism of action’s a little bit clearer. We do know that it helps shift T-cell populations from the proinflammatory Th1 [T helper cell type 1] cells to regulatory Th2 [T helper cell type 2] cells. As far as what the role of these drugs are in clinical practice, I would say in my personal experience, I’m not starting too many new patients on interferons or glatiramer acetate. But as many of you mentioned, I do have many patients who have been on these therapies for years and years, and they’re doing well. Some of their reasonings for either maintaining the medicine, or those rare new starts, are these are patients who maybe are risk adverse, they’re concerned about some of the potential safety concerns with the newer DMTs [disease modifying therapies]. They may want a medication that’s been around for a while. The safety monitoring also comes into play, too, because some of these higher efficacy therapies, they may have extensive safety monitoring requirements. Also, specific to glatiramer acetate, I would say it’s commonly used in our females with child-bearing potential who may want to get pregnant in the near future, or maybe have aggressive disease enough where they need to stay on a disease-modifying therapy during pregnancy. Those are probably my best examples of clinical experience with these 2 classes of drugs right now. I don’t know if others have similar experiences.

Amy Perrin Ross, APN, MSN, CNRN, MSCN: I see a lot of nodding heads here, and yes, indeed. I do have similar experiences. Although, in the whole spirit of shared decision-making, it’s not unbelievable that I might start a patient on an interferon or a glatiramer, depending upon circumstances. Glatiramer in particular, if I’ve got a woman wants to become pregnant imminently, this is very often a good and safe option. But again, we look at what is their disease activity and how do we go from there.

Thank you all so much. I would like to thank this wonderful panel, Christen Kutz, Stephanie Agrella, Bryan Walker, and Patricia Melville, for this wonderful discussion. I’d like to thank you as an audience for watching NeurologyLive® Peer Exchange. If you enjoyed the content, I would suggest that you subscribe to the NeurologyLive® newsletters to receive information about upcoming Peer Exchanges and other content available to you. Thank you all so much.

Transcript edited for clarity.