Contributions
Abstract: P1221
Type: Poster
Abstract Category: Therapy - disease modifying - 30 Tools for detecting therapeutic response
Background: Evidence in clinical practice is needed to understand effect of fingolimod on slowing down brain atrophy progression in clinically active multiple sclerosis (MS) patients.
Objective: To investigate the effect of fingolimod on development of brain atrophy in MS patients with clinically and radiologically active and inactive disease at baseline.
Design and methods: Multiple Sclerosis and clinical outcome and MRI in the US (MS-MRIUS) is a multicenter (33 sites), retrospective study that included 590 RRMS patients in the US, 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, or presence of gadolinium enhancing lesion(s) at baseline MRI scan, whereas patients with inactive disease at baseline (345, 58.5%) did not fulfill these criteria. Annualized percent brain volume change (PBVC) and percent lateral ventricle volume change (PLVVC) over the follow-up were compared in both groups.
Results: Patients with active disease at baseline had lower age (40 vs. 44 yrs, p< 0.0001) and lower disease duration (6 vs 9 yrs, p< 0.0001) compared to inactive patients when starting fingolimod. No other clinical or MRI differences were found between the two groups at baseline. Over the follow-up, patients with active disease at baseline had significantly higher annualized relapse rate (p=0.02), but no changes in walking (p=0.619) or EDSS progression (0.275) were detected. The rate of PBVC was -0.38% in active and -0.25% in inactive patients (p=0.076), whereas the rate of PLLVC was 1.76% in active and 0.28% in inactive patients (p=0.046).
Conclusions: The study provides real-world evidence that fingolimod slows down the rate of brain atrophy in patients with both active and inactive disease at baseline to that below of pathological cut-off for PBVC (< -0.4%) and for PLVVC (< 3.5%).
Disclosure: Acknowledgments: The authors would like to thank all of the MS-MRIUS principal investigators and their study coordinator for providing data for this study.
Disclosure of conflict of interest:
Source of funding
Analyses were supported by Novartis Pharma AG, Basel, Switzerland.
Acknowledgments
MS-MRIUS Principal Investigators and study coordinators for providing data.
Conflict of interest
Authors: R. Zivadinov1,2, J. Medin3 , N. Khan4, J. R. Korn5, N. Bergsland1, M.G. Dwyer1, T Chitnis6, R. Naismith7, E Alvarez8, P. Kinkel9, S. Cohan10, S. F. Hunter11, D. Silva3, B. Weinstock-Guttman12 on behalf of MS-MRIUS investigators
Robert Zivadinov received personal compensation from EMD Serono, Genzyme-Sanofi and Novartis, Claret-Medical, Celgene for speaking and consultant fees. He received financial support for research activities from Genzyme-Sanofi, Novartis, Claret Medical, Intekrin-Coherus and IMS Health.
Jennie Medin is an employee of Novartis Pharmaceuticals AG, Switzerland
Nasreen Khan is a paid consultant for QuintilesIMS, Switzerland
Jonathan Korn is an employee of QuintilesIMS, United States
Niels Bergsland has nothing to disclose.
Michael G. Dwyer has received consultant fees from Claret Medical and EMD Serono and research grant support from Novartis.
Tanuja Chitnis has served as a consultant for Bayer and Sanofi-Genzyme. She serves on clinical trial advisory boards for Novartis, Sanofi-Genzyme and Roche-Genentech, and has received research support from Biogen, Novartis, Serono and Verily.
Robert Naismith has received consultant fees from Alkermes, Acorda, Bayer, Biogen, EMD Serono, Genentech, Genzyme, Novartis, and Teva.
Enrique Alvarez has received consultant fees from Biogen, Teva, Genzyme, Genentech, and Novartis and research grant support from Biogen, Novartis, Acorda, and the Rocky Mountain MS Center.
Peter Kinkel has served as consultant for Novartis.
Stanley Cohan has received personal compensation for activities with Biogen, Mallinckrodt, Novartis and Sanofi-Genzyme, Acorda, Genentech. Dr. Cohan has received research support from Biogen, Genentech, Mallinckrodt, Novartis, Opexa, Roche and Sanofi-Genzyme.
Samuel F. Hunter received honoraria as speaker for Acorda, Bayer, Genzyme, Mallinckrodt, Novartis, and Teva. Research support has been received from Alkermes, Biogen Idec, Genzyme, Actelion, Novartis.
Diego Silva is an employee of Novartis Pharmaceuticals AG, Switzerland
Bianca Weinstock- Guttman received honoraria as a speaker and as a consultant for Biogen Idec, Teva Pharmaceuticals, EMD Serono, Genzyme&Sanofi, Novartis and Acorda. Dr Weinstock-Guttman received research funds from Biogen Idec, Teva Pharmaceuticals, EMD Serono, Genzyme&Sanofi, Novartis, Acorda.
Abstract: P1221
Type: Poster
Abstract Category: Therapy - disease modifying - 30 Tools for detecting therapeutic response
Background: Evidence in clinical practice is needed to understand effect of fingolimod on slowing down brain atrophy progression in clinically active multiple sclerosis (MS) patients.
Objective: To investigate the effect of fingolimod on development of brain atrophy in MS patients with clinically and radiologically active and inactive disease at baseline.
Design and methods: Multiple Sclerosis and clinical outcome and MRI in the US (MS-MRIUS) is a multicenter (33 sites), retrospective study that included 590 RRMS patients in the US, 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, or presence of gadolinium enhancing lesion(s) at baseline MRI scan, whereas patients with inactive disease at baseline (345, 58.5%) did not fulfill these criteria. Annualized percent brain volume change (PBVC) and percent lateral ventricle volume change (PLVVC) over the follow-up were compared in both groups.
Results: Patients with active disease at baseline had lower age (40 vs. 44 yrs, p< 0.0001) and lower disease duration (6 vs 9 yrs, p< 0.0001) compared to inactive patients when starting fingolimod. No other clinical or MRI differences were found between the two groups at baseline. Over the follow-up, patients with active disease at baseline had significantly higher annualized relapse rate (p=0.02), but no changes in walking (p=0.619) or EDSS progression (0.275) were detected. The rate of PBVC was -0.38% in active and -0.25% in inactive patients (p=0.076), whereas the rate of PLLVC was 1.76% in active and 0.28% in inactive patients (p=0.046).
Conclusions: The study provides real-world evidence that fingolimod slows down the rate of brain atrophy in patients with both active and inactive disease at baseline to that below of pathological cut-off for PBVC (< -0.4%) and for PLVVC (< 3.5%).
Disclosure: Acknowledgments: The authors would like to thank all of the MS-MRIUS principal investigators and their study coordinator for providing data for this study.
Disclosure of conflict of interest:
Source of funding
Analyses were supported by Novartis Pharma AG, Basel, Switzerland.
Acknowledgments
MS-MRIUS Principal Investigators and study coordinators for providing data.
Conflict of interest
Authors: R. Zivadinov1,2, J. Medin3 , N. Khan4, J. R. Korn5, N. Bergsland1, M.G. Dwyer1, T Chitnis6, R. Naismith7, E Alvarez8, P. Kinkel9, S. Cohan10, S. F. Hunter11, D. Silva3, B. Weinstock-Guttman12 on behalf of MS-MRIUS investigators
Robert Zivadinov received personal compensation from EMD Serono, Genzyme-Sanofi and Novartis, Claret-Medical, Celgene for speaking and consultant fees. He received financial support for research activities from Genzyme-Sanofi, Novartis, Claret Medical, Intekrin-Coherus and IMS Health.
Jennie Medin is an employee of Novartis Pharmaceuticals AG, Switzerland
Nasreen Khan is a paid consultant for QuintilesIMS, Switzerland
Jonathan Korn is an employee of QuintilesIMS, United States
Niels Bergsland has nothing to disclose.
Michael G. Dwyer has received consultant fees from Claret Medical and EMD Serono and research grant support from Novartis.
Tanuja Chitnis has served as a consultant for Bayer and Sanofi-Genzyme. She serves on clinical trial advisory boards for Novartis, Sanofi-Genzyme and Roche-Genentech, and has received research support from Biogen, Novartis, Serono and Verily.
Robert Naismith has received consultant fees from Alkermes, Acorda, Bayer, Biogen, EMD Serono, Genentech, Genzyme, Novartis, and Teva.
Enrique Alvarez has received consultant fees from Biogen, Teva, Genzyme, Genentech, and Novartis and research grant support from Biogen, Novartis, Acorda, and the Rocky Mountain MS Center.
Peter Kinkel has served as consultant for Novartis.
Stanley Cohan has received personal compensation for activities with Biogen, Mallinckrodt, Novartis and Sanofi-Genzyme, Acorda, Genentech. Dr. Cohan has received research support from Biogen, Genentech, Mallinckrodt, Novartis, Opexa, Roche and Sanofi-Genzyme.
Samuel F. Hunter received honoraria as speaker for Acorda, Bayer, Genzyme, Mallinckrodt, Novartis, and Teva. Research support has been received from Alkermes, Biogen Idec, Genzyme, Actelion, Novartis.
Diego Silva is an employee of Novartis Pharmaceuticals AG, Switzerland
Bianca Weinstock- Guttman received honoraria as a speaker and as a consultant for Biogen Idec, Teva Pharmaceuticals, EMD Serono, Genzyme&Sanofi, Novartis and Acorda. Dr Weinstock-Guttman received research funds from Biogen Idec, Teva Pharmaceuticals, EMD Serono, Genzyme&Sanofi, Novartis, Acorda.