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Fingolimod's Impact on MRI Brain Volume Measures in Multiple Sclerosis: Results from MS-MRIUS
Robert Zivadinov1,2, Jennie Medin3, Nasreen Khan4
1Buffalo Neuroimaging Analysis Center, Buffalo, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, The State University of New York, Buffalo, NY.
Background And Purpose:
Evidence is needed to understand the effect of fingolimod on slowing down brain atrophy progression in multiple sclerosis (MS) patients in clinical practice. We investigated the effect of fingolimod on brain atrophy in MS patients with active disease (clinically and/or magnetic resonance imaging [MRI]) versus no evidence of active disease (NEAD).
Methods:
MS and clinical outcome and MRI in the United States (MS-MRIUS) is a multicenter, retrospective study that included 590 relapsing-remitting MS patients, who initiated fingolimod, and were followed for a median of 16 months. Patients with active disease at baseline (245, 41.5%) were defined as those who had one or more relapses in the year previous starting fingolimod, and/or displayed gadolinium enhancing lesions(s) at baseline MRI scan, whereas patients with NEAD at baseline (345, 58.5%) did not fulfill these criteria. Annualized percentage brain volume change (PBVC) and percentage lateral ventricle volume change (PLVVC) over the follow-up were analyzed in both groups.
Results:
Over the follow-up, the rate of PBVC was -.38% in active disease and -.25% in NEAD patients (P = .076), whereas PLLVC was 1.76% in active disease and .28% in NEAD patients (P = .046). No changes in timed 25-foot walk (P = .619) and Expanded Disability Status Scale (P = .275) scores or MRI lesion accumulation (P > 0.08) were detected, although the active disease group had a higher proportion of relapses during the follow-up period (P = .02).
Conclusions:
The study provides real-world evidence that rate of brain atrophy in MS patients with underlying active disease and NEAD in fingolimod treated patients is below the established pathological cutoff for loss of whole brain volume (>-.4%) or expansion of lateral ventricles (> 3.5%).
Insights
Fingolimod treatment slowed brain atrophy in multiple sclerosis (MS) patients, including those with active disease. This real-world evidence shows fingolimod is effective in managing brain volume loss in MS patients.
Area of Science:
- Neurology
- Neuroimmunology
- Radiology
Background:
- Brain atrophy is a key indicator of multiple sclerosis (MS) progression.
- Understanding fingolimod's effect on brain atrophy in clinical practice is crucial.
- Distinguishing between active disease and no evidence of active disease (NEAD) is important for treatment assessment.
Purpose of the Study:
- To evaluate the impact of fingolimod on slowing brain atrophy progression in MS patients.
- To compare the effects of fingolimod on brain atrophy in MS patients with active disease versus NEAD.
- To provide real-world evidence on fingolimod's efficacy in managing brain volume changes.
Main Methods:
- A retrospective multicenter study (MS-MRIUS) of 590 relapsing-remitting MS patients initiating fingolimod.
- Patients were categorized into 'active disease' (relapses or gadolinium-enhancing lesions) and NEAD groups at baseline.
- Annualized brain volume change (PBVC) and lateral ventricle volume change (PLVVC) were analyzed over a median 16-month follow-up.
Main Results:
- The rate of brain volume loss (PBVC) was -.38% in active disease and -.25% in NEAD patients (P = .076).
- Lateral ventricle volume expansion (PLVVC) was 1.76% in active disease and .28% in NEAD patients (P = .046).
- No significant changes were observed in walking tests, disability scores, or MRI lesion accumulation, though active disease patients had more relapses.
Conclusions:
- Fingolimod treatment demonstrated rates of brain atrophy below pathological cutoffs in both active disease and NEAD MS patients.
- Real-world data suggest fingolimod effectively mitigates brain volume loss and lateral ventricle expansion.
- The findings support fingolimod's role in managing brain atrophy progression in diverse MS patient populations.