Contributions
Abstract: P737
Type: Poster
Abstract Category: Therapy - disease modifying - 28 Long-term treatment monitoring
Aim: Assess no evidence of disease activity (NEDA) using two alternative criteria for brain atrophy: percent brain volume change (PBVC) or percent lateral ventricular volume change (PLVVC); and evaluate the impact of baseline disease activity on NEDA, in patients with relapsing-remitting multiple sclerosis (RRMS) receiving fingolimod in US clinical practice.
Background: Challenges of assessing PBVC in clinical practice limit the use of these data for research purposes. PLVVC may be a strong proxy for PBVC and is more feasible in routine practice than PBVC.
Methods: Clinical and magnetic resonance imaging (MRI) data were retrospectively collected from 590 patients with RRMS who initiated fingolimod 0.5mg at 33 MS centres in the USA (index date: date of fingolimod initiation). Patients were required to have an index (6 months before or 1 month after fingolimod initiation) and post-index (9-24 months after fingolimod initiation) MRI scan. NEDA-4 [PBVC] was defined as the proportion of patients with no new/enlarged T2 lesions or gadolinium-enhancing (Gd+) lesions, no confirmed relapses, no disability progression (according to Expanded Disability Status Scale scores) and no pathological PBVC (≤0.4% annualized PBVC). An alternative definition, NEDA-4 [PLVVC], substituted PBVC for PLVVC (< 3.5% annualized PLVVC). Patients with active disease had ≥1 relapse in the year before index date or ≥1 Gd+ lesion in the index period.
Results: In total, 325 (55.1%) and 570 (96.6%) patients had data to assess NEDA-4 [PBVC] and NEDA-4 [PLVVC], respectively. During follow-up (median: 16 months), 37.2% and 38.4% of patients achieved NEDA-4 [PBVC] and NEDA-4 [PLVVC] status, respectively. When stratified by presence of Gd+ lesions in the index period, a greater proportion without Gd+ lesions versus those with ≥1 Gd+ lesion achieved NEDA-4 [PBVC] (40.1% vs 25.8%; p=0.038) and NEDA-4 [PLVVC] (42.3% vs 22.9%; p=0.0001) at follow-up. Similar observations were made when patients were stratified into those without active disease versus those with active disease at baseline for NEDA-4 [PBVC] (41.2% vs 31.0%; p=0.063) and NEDA-4 [PLVVC] (43.0% vs 32.1%; p=0.008).
Conclusion: Similar proportions achieved NEDA-4 status whether brain atrophy was measured using PLVVC or PBVC, but the number of patients eligible for assessment was nearly doubled when PLVVC was used. This supports the potential of NEDA-4 [PLVVC] in clinical practice; further studies should be performed to confirm this.
Disclosure: Study sponsored by Novartis Pharma AG.
R Zivadinov has received personal compensation from EMD Serono, Genzyme-Sanofi, Novartis and Teva Pharmaceuticals for speaking and consultant fees. He received financial support for research activities from Claret Medical, Genzyme-Sanofi, IMS Health, Intekrin-Coherus, Novartis and Teva Pharmaceuticals.
J Medin and D Silva are paid employees of Novartis Pharma AG.
MG Dwyer has received consultant fees from Claret Medical and research grant support from Novartis.
N Khan is a paid consultant for QuintilesIMS, Switzerland.
JR Korn is a paid employee of QuintilesIMS, USA.
J Price is a paid employee of QuintilesIMS, Switzerland.
N Bergsland has nothing to disclose.
E Lathi has received honoraria as a speaker and a consultant for Acorda, Biogen, Genzyme, Novartis, Teva, and Genentech.
J Silversteen has nothing to disclose.
J Calkwood has performed advisory, consultancy, and speaker activities for Acorda, Biogen, EMD Serono, Genzyme, Novartis, Roche and Teva; and received grant/research support from Biogen, Genzyme, Novartis, Roche, and Celgene.
KR Edwards has received consulting fees from and has been a speaker for Biogen and Genzyme. He has also received research support from Biogen, Genentech, Genzyme/Sanofi and Hoffmann-La Roche.
B Weinstock-Guttman has received honoraria as a speaker and as a consultant for Acorda, Biogen Idec, EMD Serono, Genzyme&Sanofi, Novartis and Teva Pharmaceuticals. She received research funds from Acorda, Biogen Idec, EMD Serono, Genzyme&Sanofi, Novartis and Teva Pharmaceuticals.
QuintilesIMS received funding from Novartis Pharma AG.
Editorial support was provided by Oxford PharmaGenesis, Oxford, UK, and funded by Novartis Pharma AG, Basel, Switzerland.
Abstract: P737
Type: Poster
Abstract Category: Therapy - disease modifying - 28 Long-term treatment monitoring
Aim: Assess no evidence of disease activity (NEDA) using two alternative criteria for brain atrophy: percent brain volume change (PBVC) or percent lateral ventricular volume change (PLVVC); and evaluate the impact of baseline disease activity on NEDA, in patients with relapsing-remitting multiple sclerosis (RRMS) receiving fingolimod in US clinical practice.
Background: Challenges of assessing PBVC in clinical practice limit the use of these data for research purposes. PLVVC may be a strong proxy for PBVC and is more feasible in routine practice than PBVC.
Methods: Clinical and magnetic resonance imaging (MRI) data were retrospectively collected from 590 patients with RRMS who initiated fingolimod 0.5mg at 33 MS centres in the USA (index date: date of fingolimod initiation). Patients were required to have an index (6 months before or 1 month after fingolimod initiation) and post-index (9-24 months after fingolimod initiation) MRI scan. NEDA-4 [PBVC] was defined as the proportion of patients with no new/enlarged T2 lesions or gadolinium-enhancing (Gd+) lesions, no confirmed relapses, no disability progression (according to Expanded Disability Status Scale scores) and no pathological PBVC (≤0.4% annualized PBVC). An alternative definition, NEDA-4 [PLVVC], substituted PBVC for PLVVC (< 3.5% annualized PLVVC). Patients with active disease had ≥1 relapse in the year before index date or ≥1 Gd+ lesion in the index period.
Results: In total, 325 (55.1%) and 570 (96.6%) patients had data to assess NEDA-4 [PBVC] and NEDA-4 [PLVVC], respectively. During follow-up (median: 16 months), 37.2% and 38.4% of patients achieved NEDA-4 [PBVC] and NEDA-4 [PLVVC] status, respectively. When stratified by presence of Gd+ lesions in the index period, a greater proportion without Gd+ lesions versus those with ≥1 Gd+ lesion achieved NEDA-4 [PBVC] (40.1% vs 25.8%; p=0.038) and NEDA-4 [PLVVC] (42.3% vs 22.9%; p=0.0001) at follow-up. Similar observations were made when patients were stratified into those without active disease versus those with active disease at baseline for NEDA-4 [PBVC] (41.2% vs 31.0%; p=0.063) and NEDA-4 [PLVVC] (43.0% vs 32.1%; p=0.008).
Conclusion: Similar proportions achieved NEDA-4 status whether brain atrophy was measured using PLVVC or PBVC, but the number of patients eligible for assessment was nearly doubled when PLVVC was used. This supports the potential of NEDA-4 [PLVVC] in clinical practice; further studies should be performed to confirm this.
Disclosure: Study sponsored by Novartis Pharma AG.
R Zivadinov has received personal compensation from EMD Serono, Genzyme-Sanofi, Novartis and Teva Pharmaceuticals for speaking and consultant fees. He received financial support for research activities from Claret Medical, Genzyme-Sanofi, IMS Health, Intekrin-Coherus, Novartis and Teva Pharmaceuticals.
J Medin and D Silva are paid employees of Novartis Pharma AG.
MG Dwyer has received consultant fees from Claret Medical and research grant support from Novartis.
N Khan is a paid consultant for QuintilesIMS, Switzerland.
JR Korn is a paid employee of QuintilesIMS, USA.
J Price is a paid employee of QuintilesIMS, Switzerland.
N Bergsland has nothing to disclose.
E Lathi has received honoraria as a speaker and a consultant for Acorda, Biogen, Genzyme, Novartis, Teva, and Genentech.
J Silversteen has nothing to disclose.
J Calkwood has performed advisory, consultancy, and speaker activities for Acorda, Biogen, EMD Serono, Genzyme, Novartis, Roche and Teva; and received grant/research support from Biogen, Genzyme, Novartis, Roche, and Celgene.
KR Edwards has received consulting fees from and has been a speaker for Biogen and Genzyme. He has also received research support from Biogen, Genentech, Genzyme/Sanofi and Hoffmann-La Roche.
B Weinstock-Guttman has received honoraria as a speaker and as a consultant for Acorda, Biogen Idec, EMD Serono, Genzyme&Sanofi, Novartis and Teva Pharmaceuticals. She received research funds from Acorda, Biogen Idec, EMD Serono, Genzyme&Sanofi, Novartis and Teva Pharmaceuticals.
QuintilesIMS received funding from Novartis Pharma AG.
Editorial support was provided by Oxford PharmaGenesis, Oxford, UK, and funded by Novartis Pharma AG, Basel, Switzerland.