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Updated: Jun 18, 2026
10:46
A Method of Trigonometric Modelling of Seasonal Variation Demonstrated with Multiple Sclerosis Relapse Data
Published on: December 9, 2015
[Glatiramer acetate in interferon beta non respondent relapsing-remitting multiple sclerosis]
C Oreja-Guevara1, P E Bermejo, A Miralles
1Servicio de Neurologia, Unidad de Neuroinmunologia Clínica y Esclerosis Múltiple, Hospital Universitario La Paz, Madrid. unidadem.lapaz@gmail.com
Neurologia (Barcelona, Spain)
|November 19, 2009
Summary
Glatiramer acetate (GA) is a viable treatment option for relapsing-remitting multiple sclerosis (RRMS) patients who stopped interferon beta due to poor response or side effects. GA demonstrated reduced relapse rates in patients previously experiencing suboptimal outcomes with interferon beta.
Area of Science:
- Neurology
- Immunology
- Pharmacology
Context:
- Relapsing-remitting multiple sclerosis (RRMS) is a chronic autoimmune disease affecting the central nervous system.
- Interferon beta (IFN-beta) and glatiramer acetate (GA) are common first-line immunomodulatory treatments for RRMS.
- Patient outcomes can be limited by suboptimal response or adverse events associated with IFN-beta therapy.
Purpose:
- To evaluate the efficacy of glatiramer acetate (GA) in RRMS patients who discontinued interferon beta (IFN-beta) therapy.
- To compare relapse rates in patients switching from IFN-beta to GA due to suboptimal response versus adverse events.
Summary:
- This observational, retrospective study analyzed 58 RRMS patients who switched from IFN-beta to GA.
- Patients discontinuing IFN-beta for suboptimal response (n=20) showed a decrease in annual relapses from 1.38 to 0.52 with GA.
- Patients discontinuing IFN-beta for adverse events (n=38) showed a slight increase in annual relapses from 0.33 to 0.37 with GA.
Impact:
- Glatiramer acetate (GA) represents a beneficial alternative for RRMS patients experiencing inadequate response or intolerance to interferon beta (IFN-beta).
- The findings suggest distinct mechanisms of action between GA and IFN-beta, supporting personalized treatment strategies in multiple sclerosis management.
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