Contributions
Abstract: P1186
Type: Poster
Abstract Category: Therapy - disease modifying - 28 Long-term treatment monitoring
Background: Long-term disability progression and treatment outcomes in patients with multiple sclerosis (MS) may be predicted from Expanded Disability Status Scale (EDSS) score changes.
Objective: To describe disease characteristics and outcomes in MS patients receiving fingolimod categorised by disability trends over 96 months (M).
Methods: Patients were pooled from FREEDOMS/FREEDOMS II 24M core trials receiving fingolimod 0.5 mg or placebo (PBO), continuing/switching to fingolimod in the 48M extension phase, and those continuing fingolimod in the 96M LONGTERMS trial. Patients were categorised into 4 disability groups: improvement or worsening (decrease or increase in EDSS score from baseline [BL] by ≥1.0 point, confirmed for ≥6M or confirmed/sustained until 24/96M), minimal change (±0.5 or 0.0 point change in EDSS score from BL for BL scores ≤5.5 or >5.5, respectively) or fluctuating (changes in EDSS score differing from other patterns). Outcomes included relapses, MRI lesions (T2 lesion volume [T2LV] plus new/enlarging T2 lesions [neT2L]) and brain volume (BV). Analysis included the completer subgroup (individuals with values at BL and 96M).
Results: 505 fingolimod-treated patients completed 96M: 274 initially randomised to fingolimod, 231 to PBO. 28.3% patients had improving, 21.8% stable/minimal change, 19.6% fluctuating and 30.3% worsening EDSS scores. At BL, the improvement group had more men (37.1 vs 26.1%), younger age (36.3 vs 39.9 years), shorter disease duration (7.4 vs 9.7 years), higher EDSS (2.6 vs 2.3), lower T2LV (5120 vs 7716 mm3) and greater BV (1537 vs 1503 cm3) vs worsening group. There were no differences between groups in the number of relapses before enrolment or in previous treatment. At M96, number of patients with ≥1 confirmed relapse (32.9 vs 44.4%, p=0.0074) and annualised relapse rate (0.201 vs 0.358, p=0.0071) were lower in the improvement vs worsening group. Annualised rate of brain atrophy, neT2L numbers and T2LV change were numerically lower but not significant between groups.
Conclusions: After 8 years, disability had improved/remained stable in 50% of fingolimod-treated patients. Patients in the improved disability group were more likely to be men, had shorter disease duration, less T2LV and lower BV loss despite having higher EDSS at BL. This result underscores the value of early diagnosis and initiation of disease-modifying therapy in MS patients to maximise long-term disability reduction.
Disclosure:
Funding source: This study was funded by Novartis Pharma AG, Basel, Switzerland.
Anthony T. Reder has received honoraria or research support from Abbott Laboratories, Acorda Therapeutics, Astra/Merck, Athena Neurosciences, Bayer, BioMS Medical Corp, Biogen Idec, Blue Cross Blue Shield, Boehringer Ingelheim, Caremark, Cephalon, Connective Therapeutics, Elan, Eli Lilly, F. Hoffmann-La Roche, Genentech, Genzyme, GlaxoSmithKline, Immunex, Neurocrine Biosciences, Novartis, Parke-Davis, Pfizer, Pharmacia & Upjohn, Questcor, Quintiles, Serono, Takeda Pharmaceuticals and Teva Marion Partners.
Jeffrey Cohen reports personal compensation for consulting for Adamas, Merck, Mallinckrodt, Novartis and Receptos and as a Co-Editor of Multiple Sclerosis Journal - Experimental, Translational and Clinical
Bruce A.C. Cree has received personal compensation for consulting from Abbvie, Biogen Idec, EMD Serono and Novartis.
Diego Silva, Daniela Piani Meier, Davorka Tomic and Shannon Ritter are employees of Novartis.
Abstract: P1186
Type: Poster
Abstract Category: Therapy - disease modifying - 28 Long-term treatment monitoring
Background: Long-term disability progression and treatment outcomes in patients with multiple sclerosis (MS) may be predicted from Expanded Disability Status Scale (EDSS) score changes.
Objective: To describe disease characteristics and outcomes in MS patients receiving fingolimod categorised by disability trends over 96 months (M).
Methods: Patients were pooled from FREEDOMS/FREEDOMS II 24M core trials receiving fingolimod 0.5 mg or placebo (PBO), continuing/switching to fingolimod in the 48M extension phase, and those continuing fingolimod in the 96M LONGTERMS trial. Patients were categorised into 4 disability groups: improvement or worsening (decrease or increase in EDSS score from baseline [BL] by ≥1.0 point, confirmed for ≥6M or confirmed/sustained until 24/96M), minimal change (±0.5 or 0.0 point change in EDSS score from BL for BL scores ≤5.5 or >5.5, respectively) or fluctuating (changes in EDSS score differing from other patterns). Outcomes included relapses, MRI lesions (T2 lesion volume [T2LV] plus new/enlarging T2 lesions [neT2L]) and brain volume (BV). Analysis included the completer subgroup (individuals with values at BL and 96M).
Results: 505 fingolimod-treated patients completed 96M: 274 initially randomised to fingolimod, 231 to PBO. 28.3% patients had improving, 21.8% stable/minimal change, 19.6% fluctuating and 30.3% worsening EDSS scores. At BL, the improvement group had more men (37.1 vs 26.1%), younger age (36.3 vs 39.9 years), shorter disease duration (7.4 vs 9.7 years), higher EDSS (2.6 vs 2.3), lower T2LV (5120 vs 7716 mm3) and greater BV (1537 vs 1503 cm3) vs worsening group. There were no differences between groups in the number of relapses before enrolment or in previous treatment. At M96, number of patients with ≥1 confirmed relapse (32.9 vs 44.4%, p=0.0074) and annualised relapse rate (0.201 vs 0.358, p=0.0071) were lower in the improvement vs worsening group. Annualised rate of brain atrophy, neT2L numbers and T2LV change were numerically lower but not significant between groups.
Conclusions: After 8 years, disability had improved/remained stable in 50% of fingolimod-treated patients. Patients in the improved disability group were more likely to be men, had shorter disease duration, less T2LV and lower BV loss despite having higher EDSS at BL. This result underscores the value of early diagnosis and initiation of disease-modifying therapy in MS patients to maximise long-term disability reduction.
Disclosure:
Funding source: This study was funded by Novartis Pharma AG, Basel, Switzerland.
Anthony T. Reder has received honoraria or research support from Abbott Laboratories, Acorda Therapeutics, Astra/Merck, Athena Neurosciences, Bayer, BioMS Medical Corp, Biogen Idec, Blue Cross Blue Shield, Boehringer Ingelheim, Caremark, Cephalon, Connective Therapeutics, Elan, Eli Lilly, F. Hoffmann-La Roche, Genentech, Genzyme, GlaxoSmithKline, Immunex, Neurocrine Biosciences, Novartis, Parke-Davis, Pfizer, Pharmacia & Upjohn, Questcor, Quintiles, Serono, Takeda Pharmaceuticals and Teva Marion Partners.
Jeffrey Cohen reports personal compensation for consulting for Adamas, Merck, Mallinckrodt, Novartis and Receptos and as a Co-Editor of Multiple Sclerosis Journal - Experimental, Translational and Clinical
Bruce A.C. Cree has received personal compensation for consulting from Abbvie, Biogen Idec, EMD Serono and Novartis.
Diego Silva, Daniela Piani Meier, Davorka Tomic and Shannon Ritter are employees of Novartis.