Treatment effectiveness of alemtuzumab compared with natalizumab, fingolimod, and interferon beta in relapsing-remitting multiple sclerosis: a cohort study
Alemtuzumab, an anti-CD52 antibody, is proven to be more efficacious than interferon beta-1a in the treatment of relapsing-remitting multiple sclerosis, but its efficacy relative to more potent immunotherapies is unknown. We compared the effectiveness of alemtuzumab with natalizumab, fingolimod, and...
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| Veröffentlicht in: | Lancet neurology Jg. 16; H. 4; S. 271 - 281 |
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| Format: | Journal Article |
| Sprache: | Englisch |
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Elsevier Ltd
01.04.2017
Elsevier Limited |
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| ISSN: | 1474-4422, 1474-4465, 1474-4465 |
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| Abstract | Alemtuzumab, an anti-CD52 antibody, is proven to be more efficacious than interferon beta-1a in the treatment of relapsing-remitting multiple sclerosis, but its efficacy relative to more potent immunotherapies is unknown. We compared the effectiveness of alemtuzumab with natalizumab, fingolimod, and interferon beta in patients with relapsing-remitting multiple sclerosis treated for up to 5 years.
In this international cohort study, we used data from propensity-matched patients with relapsing-remitting multiple sclerosis from the MSBase and six other cohorts. Longitudinal clinical data were obtained from 71 MSBase centres in 21 countries and from six non-MSBase centres in the UK and Germany between Nov 1, 2015, and June 30, 2016. Key inclusion criteria were a diagnosis of definite relapsing-remitting multiple sclerosis, exposure to one of the study therapies (alemtuzumab, interferon beta, fingolimod, or natalizumab), age 65 years or younger, Expanded Disability Status Scale (EDSS) score 6·5 or lower, and no more than 10 years since the first multiple sclerosis symptom. The primary endpoint was annualised relapse rate. The secondary endpoints were cumulative hazards of relapses, disability accumulation, and disability improvement events. We compared relapse rates with negative binomial models, and estimated cumulative hazards with conditional proportional hazards models.
Patients were treated between Aug 1, 1994, and June 30, 2016. The cohorts consisted of 189 patients given alemtuzumab, 2155 patients given interferon beta, 828 patients given fingolimod, and 1160 patients given natalizumab. Alemtuzumab was associated with a lower annualised relapse rate than interferon beta (0·19 [95% CI 0·14–0·23] vs 0·53 [0·46–0·61], p<0·0001) and fingolimod (0·15 [0·10–0·20] vs 0·34 [0·26–0·41], p<0·0001), and was associated with a similar annualised relapse rate as natalizumab (0·20 [0·14–0·26] vs 0·19 [0·15–0·23], p=0·78). For the disability outcomes, alemtuzumab was associated with similar probabilities of disability accumulation as interferon beta (hazard ratio [HR] 0·66 [95% CI 0·36–1·22], p=0·37), fingolimod (1·27 [0·60–2·70], p=0·67), and natalizumab (0·81 [0·47–1·39], p=0·60). Alemtuzumab was associated with similar probabilities of disability improvement as interferon beta (0·98 [0·65–1·49], p=0·93) and fingolimod (0·50 [0·25–1·01], p=0·18), and a lower probability of disability improvement than natalizumab (0·35 [0·20–0·59], p=0·0006).
Alemtuzumab and natalizumab seem to have similar effects on annualised relapse rates in relapsing-remitting multiple sclerosis. Alemtuzumab seems superior to fingolimod and interferon beta in mitigating relapse activity. Natalizumab seems superior to alemtuzumab in enabling recovery from disability. Both natalizumab and alemtuzumab seem highly effective and viable immunotherapies for multiple sclerosis. Treatment decisions between alemtuzumab and natalizumab should be primarily governed by their safety profiles.
National Health and Medical Research Council, and the University of Melbourne. |
|---|---|
| AbstractList | Alemtuzumab, an anti-CD52 antibody, is proven to be more efficacious than interferon beta-1a in the treatment of relapsing-remitting multiple sclerosis, but its efficacy relative to more potent immunotherapies is unknown. We compared the effectiveness of alemtuzumab with natalizumab, fingolimod, and interferon beta in patients with relapsing-remitting multiple sclerosis treated for up to 5 years.
In this international cohort study, we used data from propensity-matched patients with relapsing-remitting multiple sclerosis from the MSBase and six other cohorts. Longitudinal clinical data were obtained from 71 MSBase centres in 21 countries and from six non-MSBase centres in the UK and Germany between Nov 1, 2015, and June 30, 2016. Key inclusion criteria were a diagnosis of definite relapsing-remitting multiple sclerosis, exposure to one of the study therapies (alemtuzumab, interferon beta, fingolimod, or natalizumab), age 65 years or younger, Expanded Disability Status Scale (EDSS) score 6·5 or lower, and no more than 10 years since the first multiple sclerosis symptom. The primary endpoint was annualised relapse rate. The secondary endpoints were cumulative hazards of relapses, disability accumulation, and disability improvement events. We compared relapse rates with negative binomial models, and estimated cumulative hazards with conditional proportional hazards models.
Patients were treated between Aug 1, 1994, and June 30, 2016. The cohorts consisted of 189 patients given alemtuzumab, 2155 patients given interferon beta, 828 patients given fingolimod, and 1160 patients given natalizumab. Alemtuzumab was associated with a lower annualised relapse rate than interferon beta (0·19 [95% CI 0·14–0·23] vs 0·53 [0·46–0·61], p<0·0001) and fingolimod (0·15 [0·10–0·20] vs 0·34 [0·26–0·41], p<0·0001), and was associated with a similar annualised relapse rate as natalizumab (0·20 [0·14–0·26] vs 0·19 [0·15–0·23], p=0·78). For the disability outcomes, alemtuzumab was associated with similar probabilities of disability accumulation as interferon beta (hazard ratio [HR] 0·66 [95% CI 0·36–1·22], p=0·37), fingolimod (1·27 [0·60–2·70], p=0·67), and natalizumab (0·81 [0·47–1·39], p=0·60). Alemtuzumab was associated with similar probabilities of disability improvement as interferon beta (0·98 [0·65–1·49], p=0·93) and fingolimod (0·50 [0·25–1·01], p=0·18), and a lower probability of disability improvement than natalizumab (0·35 [0·20–0·59], p=0·0006).
Alemtuzumab and natalizumab seem to have similar effects on annualised relapse rates in relapsing-remitting multiple sclerosis. Alemtuzumab seems superior to fingolimod and interferon beta in mitigating relapse activity. Natalizumab seems superior to alemtuzumab in enabling recovery from disability. Both natalizumab and alemtuzumab seem highly effective and viable immunotherapies for multiple sclerosis. Treatment decisions between alemtuzumab and natalizumab should be primarily governed by their safety profiles.
National Health and Medical Research Council, and the University of Melbourne. Summary Background Alemtuzumab, an anti-CD52 antibody, is proven to be more efficacious than interferon beta-1a in the treatment of relapsing-remitting multiple sclerosis, but its efficacy relative to more potent immunotherapies is unknown. We compared the effectiveness of alemtuzumab with natalizumab, fingolimod, and interferon beta in patients with relapsing-remitting multiple sclerosis treated for up to 5 years. Methods In this international cohort study, we used data from propensity-matched patients with relapsing-remitting multiple sclerosis from the MSBase and six other cohorts. Longitudinal clinical data were obtained from 71 MSBase centres in 21 countries and from six non-MSBase centres in the UK and Germany between Nov 1, 2015, and June 30, 2016. Key inclusion criteria were a diagnosis of definite relapsing-remitting multiple sclerosis, exposure to one of the study therapies (alemtuzumab, interferon beta, fingolimod, or natalizumab), age 65 years or younger, Expanded Disability Status Scale (EDSS) score 6·5 or lower, and no more than 10 years since the first multiple sclerosis symptom. The primary endpoint was annualised relapse rate. The secondary endpoints were cumulative hazards of relapses, disability accumulation, and disability improvement events. We compared relapse rates with negative binomial models, and estimated cumulative hazards with conditional proportional hazards models. Findings Patients were treated between Aug 1, 1994, and June 30, 2016. The cohorts consisted of 189 patients given alemtuzumab, 2155 patients given interferon beta, 828 patients given fingolimod, and 1160 patients given natalizumab. Alemtuzumab was associated with a lower annualised relapse rate than interferon beta (0·19 [95% CI 0·14–0·23] vs 0·53 [0·46–0·61], p<0·0001) and fingolimod (0·15 [0·10–0·20] vs 0·34 [0·26–0·41], p<0·0001), and was associated with a similar annualised relapse rate as natalizumab (0·20 [0·14–0·26] vs 0·19 [0·15–0·23], p=0·78). For the disability outcomes, alemtuzumab was associated with similar probabilities of disability accumulation as interferon beta (hazard ratio [HR] 0·66 [95% CI 0·36–1·22], p=0·37), fingolimod (1·27 [0·60–2·70], p=0·67), and natalizumab (0·81 [0·47–1·39], p=0·60). Alemtuzumab was associated with similar probabilities of disability improvement as interferon beta (0·98 [0·65–1·49], p=0·93) and fingolimod (0·50 [0·25–1·01], p=0·18), and a lower probability of disability improvement than natalizumab (0·35 [0·20–0·59], p=0·0006). Interpretation Alemtuzumab and natalizumab seem to have similar effects on annualised relapse rates in relapsing-remitting multiple sclerosis. Alemtuzumab seems superior to fingolimod and interferon beta in mitigating relapse activity. Natalizumab seems superior to alemtuzumab in enabling recovery from disability. Both natalizumab and alemtuzumab seem highly effective and viable immunotherapies for multiple sclerosis. Treatment decisions between alemtuzumab and natalizumab should be primarily governed by their safety profiles. Funding National Health and Medical Research Council, and the University of Melbourne. Alemtuzumab, an anti-CD52 antibody, is proven to be more efficacious than interferon beta-1a in the treatment of relapsing-remitting multiple sclerosis, but its efficacy relative to more potent immunotherapies is unknown. We compared the effectiveness of alemtuzumab with natalizumab, fingolimod, and interferon beta in patients with relapsing-remitting multiple sclerosis treated for up to 5 years.BACKGROUNDAlemtuzumab, an anti-CD52 antibody, is proven to be more efficacious than interferon beta-1a in the treatment of relapsing-remitting multiple sclerosis, but its efficacy relative to more potent immunotherapies is unknown. We compared the effectiveness of alemtuzumab with natalizumab, fingolimod, and interferon beta in patients with relapsing-remitting multiple sclerosis treated for up to 5 years.In this international cohort study, we used data from propensity-matched patients with relapsing-remitting multiple sclerosis from the MSBase and six other cohorts. Longitudinal clinical data were obtained from 71 MSBase centres in 21 countries and from six non-MSBase centres in the UK and Germany between Nov 1, 2015, and June 30, 2016. Key inclusion criteria were a diagnosis of definite relapsing-remitting multiple sclerosis, exposure to one of the study therapies (alemtuzumab, interferon beta, fingolimod, or natalizumab), age 65 years or younger, Expanded Disability Status Scale (EDSS) score 6·5 or lower, and no more than 10 years since the first multiple sclerosis symptom. The primary endpoint was annualised relapse rate. The secondary endpoints were cumulative hazards of relapses, disability accumulation, and disability improvement events. We compared relapse rates with negative binomial models, and estimated cumulative hazards with conditional proportional hazards models.METHODSIn this international cohort study, we used data from propensity-matched patients with relapsing-remitting multiple sclerosis from the MSBase and six other cohorts. Longitudinal clinical data were obtained from 71 MSBase centres in 21 countries and from six non-MSBase centres in the UK and Germany between Nov 1, 2015, and June 30, 2016. Key inclusion criteria were a diagnosis of definite relapsing-remitting multiple sclerosis, exposure to one of the study therapies (alemtuzumab, interferon beta, fingolimod, or natalizumab), age 65 years or younger, Expanded Disability Status Scale (EDSS) score 6·5 or lower, and no more than 10 years since the first multiple sclerosis symptom. The primary endpoint was annualised relapse rate. The secondary endpoints were cumulative hazards of relapses, disability accumulation, and disability improvement events. We compared relapse rates with negative binomial models, and estimated cumulative hazards with conditional proportional hazards models.Patients were treated between Aug 1, 1994, and June 30, 2016. The cohorts consisted of 189 patients given alemtuzumab, 2155 patients given interferon beta, 828 patients given fingolimod, and 1160 patients given natalizumab. Alemtuzumab was associated with a lower annualised relapse rate than interferon beta (0·19 [95% CI 0·14-0·23] vs 0·53 [0·46-0·61], p<0·0001) and fingolimod (0·15 [0·10-0·20] vs 0·34 [0·26-0·41], p<0·0001), and was associated with a similar annualised relapse rate as natalizumab (0·20 [0·14-0·26] vs 0·19 [0·15-0·23], p=0·78). For the disability outcomes, alemtuzumab was associated with similar probabilities of disability accumulation as interferon beta (hazard ratio [HR] 0·66 [95% CI 0·36-1·22], p=0·37), fingolimod (1·27 [0·60-2·70], p=0·67), and natalizumab (0·81 [0·47-1·39], p=0·60). Alemtuzumab was associated with similar probabilities of disability improvement as interferon beta (0·98 [0·65-1·49], p=0·93) and fingolimod (0·50 [0·25-1·01], p=0·18), and a lower probability of disability improvement than natalizumab (0·35 [0·20-0·59], p=0·0006).FINDINGSPatients were treated between Aug 1, 1994, and June 30, 2016. The cohorts consisted of 189 patients given alemtuzumab, 2155 patients given interferon beta, 828 patients given fingolimod, and 1160 patients given natalizumab. Alemtuzumab was associated with a lower annualised relapse rate than interferon beta (0·19 [95% CI 0·14-0·23] vs 0·53 [0·46-0·61], p<0·0001) and fingolimod (0·15 [0·10-0·20] vs 0·34 [0·26-0·41], p<0·0001), and was associated with a similar annualised relapse rate as natalizumab (0·20 [0·14-0·26] vs 0·19 [0·15-0·23], p=0·78). For the disability outcomes, alemtuzumab was associated with similar probabilities of disability accumulation as interferon beta (hazard ratio [HR] 0·66 [95% CI 0·36-1·22], p=0·37), fingolimod (1·27 [0·60-2·70], p=0·67), and natalizumab (0·81 [0·47-1·39], p=0·60). Alemtuzumab was associated with similar probabilities of disability improvement as interferon beta (0·98 [0·65-1·49], p=0·93) and fingolimod (0·50 [0·25-1·01], p=0·18), and a lower probability of disability improvement than natalizumab (0·35 [0·20-0·59], p=0·0006).Alemtuzumab and natalizumab seem to have similar effects on annualised relapse rates in relapsing-remitting multiple sclerosis. Alemtuzumab seems superior to fingolimod and interferon beta in mitigating relapse activity. Natalizumab seems superior to alemtuzumab in enabling recovery from disability. Both natalizumab and alemtuzumab seem highly effective and viable immunotherapies for multiple sclerosis. Treatment decisions between alemtuzumab and natalizumab should be primarily governed by their safety profiles.INTERPRETATIONAlemtuzumab and natalizumab seem to have similar effects on annualised relapse rates in relapsing-remitting multiple sclerosis. Alemtuzumab seems superior to fingolimod and interferon beta in mitigating relapse activity. Natalizumab seems superior to alemtuzumab in enabling recovery from disability. Both natalizumab and alemtuzumab seem highly effective and viable immunotherapies for multiple sclerosis. Treatment decisions between alemtuzumab and natalizumab should be primarily governed by their safety profiles.National Health and Medical Research Council, and the University of Melbourne.FUNDINGNational Health and Medical Research Council, and the University of Melbourne. Background Alemtuzumab, an anti-CD52 antibody, is proven to be more efficacious than interferon beta-1a in the treatment of relapsing-remitting multiple sclerosis, but its efficacy relative to more potent immunotherapies is unknown. We compared the effectiveness of alemtuzumab with natalizumab, fingolimod, and interferon beta in patients with relapsing-remitting multiple sclerosis treated for up to 5 years. Methods In this international cohort study, we used data from propensity-matched patients with relapsing-remitting multiple sclerosis from the MSBase and six other cohorts. Longitudinal clinical data were obtained from 71 MSBase centres in 21 countries and from six non-MSBase centres in the UK and Germany between Nov 1, 2015, and June 30, 2016. Key inclusion criteria were a diagnosis of definite relapsing-remitting multiple sclerosis, exposure to one of the study therapies (alemtuzumab, interferon beta, fingolimod, or natalizumab), age 65 years or younger, Expanded Disability Status Scale (EDSS) score 6.5 or lower, and no more than 10 years since the first multiple sclerosis symptom. The primary endpoint was annualised relapse rate. The secondary endpoints were cumulative hazards of relapses, disability accumulation, and disability improvement events. We compared relapse rates with negative binomial models, and estimated cumulative hazards with conditional proportional hazards models. Findings Patients were treated between Aug 1, 1994, and June 30, 2016. The cohorts consisted of 189 patients given alemtuzumab, 2155 patients given interferon beta, 828 patients given fingolimod, and 1160 patients given natalizumab. Alemtuzumab was associated with a lower annualised relapse rate than interferon beta (0.19 [95% CI 0.14-0.23] vs 0.53 [0.46-0.61], p<0.0001) and fingolimod (0.15 [0.10-0.20] vs 0.34 [0.26-0.41], p<0.0001), and was associated with a similar annualised relapse rate as natalizumab (0.20 [0.14-0.26] vs 0.19 [0.15-0.23], p=0.78). For the disability outcomes, alemtuzumab was associated with similar probabilities of disability accumulation as interferon beta (hazard ratio [HR] 0.66 [95% CI 0.36-1.22], p=0.37), fingolimod (1.27 [0.60-2.70], p=0.67), and natalizumab (0.81 [0.47-1.39], p=0.60). Alemtuzumab was associated with similar probabilities of disability improvement as interferon beta (0.98 [0.65-1.49], p=0.93) and fingolimod (0.50 [0.25-1.01], p=0.18), and a lower probability of disability improvement than natalizumab (0.35 [0.20-0.59], p=0.0006). Interpretation Alemtuzumab and natalizumab seem to have similar effects on annualised relapse rates in relapsing-remitting multiple sclerosis. Alemtuzumab seems superior to fingolimod and interferon beta in mitigating relapse activity. Natalizumab seems superior to alemtuzumab in enabling recovery from disability. Both natalizumab and alemtuzumab seem highly effective and viable immunotherapies for multiple sclerosis. Treatment decisions between alemtuzumab and natalizumab should be primarily governed by their safety profiles. Funding National Health and Medical Research Council, and the University of Melbourne. Alemtuzumab, an anti-CD52 antibody, is proven to be more efficacious than interferon beta-1a in the treatment of relapsing-remitting multiple sclerosis, but its efficacy relative to more potent immunotherapies is unknown. We compared the effectiveness of alemtuzumab with natalizumab, fingolimod, and interferon beta in patients with relapsing-remitting multiple sclerosis treated for up to 5 years. Methods In this international cohort study, we used data from propensity-matched patients with relapsing-remitting multiple sclerosis from the MSBase and six other cohorts. Longitudinal clinical data were obtained from 71 MSBase centres in 21 countries and from six non-MSBase centres in the UK and Germany between Nov 1, 2015, and June 30, 2016. Key inclusion criteria were a diagnosis of definite relapsing-remitting multiple sclerosis, exposure to one of the study therapies (alemtuzumab, interferon beta, fingolimod, or natalizumab), age 65 years or younger, Expanded Disability Status Scale (EDSS) score 6·5 or lower, and no more than 10 years since the first multiple sclerosis symptom. The primary endpoint was annualised relapse rate. The secondary endpoints were cumulative hazards of relapses, disability accumulation, and disability improvement events. We compared relapse rates with negative binomial models, and estimated cumulative hazards with conditional proportional hazards models. Findings Patients were treated between Aug 1, 1994, and June 30, 2016. The cohorts consisted of 189 patients given alemtuzumab, 2155 patients given interferon beta, 828 patients given fingolimod, and 1160 patients given natalizumab. Alemtuzumab was associated with a lower annualised relapse rate than interferon beta (0·19 [95% CI 0·14-0·23]vs0·53 [0·46-0·61], p<0·0001) and fingolimod (0·15 [0·10-0·20]vs0·34 [0·26-0·41], p<0·0001), and was associated with a similar annualised relapse rate as natalizumab (0·20 [0·14-0·26]vs0·19 [0·15-0·23], p=0·78). For the disability outcomes, alemtuzumab was associated with similar probabilities of disability accumulation as interferon beta (hazard ratio [HR] 0·66 [95% CI 0·36-1·22], p=0·37), fingolimod (1·27 [0·60-2·70], p=0·67), and natalizumab (0·81 [0·47-1·39], p=0·60). Alemtuzumab was associated with similar probabilities of disability improvement as interferon beta (0·98 [0·65-1·49], p=0·93) and fingolimod (0·50 [0·25-1·01], p=0·18), and a lower probability of disability improvement than natalizumab (0·35 [0·20-0·59], p=0·0006). Interpretation Alemtuzumab and natalizumab seem to have similar effects on annualised relapse rates in relapsing-remitting multiple sclerosis. Alemtuzumab seems superior to fingolimod and interferon beta in mitigating relapse activity. Natalizumab seems superior to alemtuzumab in enabling recovery from disability. Both natalizumab and alemtuzumab seem highly effective and viable immunotherapies for multiple sclerosis. Treatment decisions between alemtuzumab and natalizumab should be primarily governed by their safety profiles. Funding National Health and Medical Research Council, and the University of Melbourne. |
| Author | Spelman, Tim Pucci, Eugenio Verheul, Freek Wilkins, Alastair Scolding, Neil Ramo, Cristina Coles, Alasdair Bergamaschi, Roberto Butzkueven, Helmut Prat, Alexandre Rozsa, Csilla McCombe, Pamela Lugaresi, Alessandra Brown, J William L Alroughani, Raed Terzi, Murat Hutchinson, Michael Slee, Mark Barnett, Michael Trojano, Maria Vucic, Steve Olascoaga, Javier Willis, Mark Horakova, Dana Sanchez-Menoyo, Jose Luis Pearson, Owen Robertson, Neil Cristiano, Edgardo Rice, Claire M Izquierdo, Guillermo Van Pesch, Vincent Ampapa, Radek Lechner-Scott, Jeannette Granella, Franco Havrdova, Eva Grand'Maison, François Boz, Cavit Hupperts, Raymond Spitaleri, Daniele Girard, Marc Duquette, Pierre Simo, Magdolna Hodgkinson, Suzanne Csepany, Tunde Jokubaitis, Vilija McGuigan, Christopher Grammond, Pierre Kalincik, Tomas Ziemssen, Tjalf Sola, Patrizia |
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of Neurology, Southmead Hospital, Westbury-on-Trym, Bristol, UK – sequence: 6 givenname: Claire M surname: Rice fullname: Rice, Claire M organization: Department of Neurology, Southmead Hospital, Westbury-on-Trym, Bristol, UK – sequence: 7 givenname: Alastair surname: Wilkins fullname: Wilkins, Alastair organization: Department of Neurology, Southmead Hospital, Westbury-on-Trym, Bristol, UK – sequence: 8 givenname: Owen surname: Pearson fullname: Pearson, Owen organization: Abertawe Bro Morgannwg University Local Health Board, Swansea, UK – sequence: 9 givenname: Tjalf surname: Ziemssen fullname: Ziemssen, Tjalf organization: Center of Clinical Neuroscience, Department of Neurology, MS Center Dresden, Dresden, Germany – sequence: 10 givenname: Michael surname: Hutchinson fullname: Hutchinson, Michael organization: School of Medicine and Medical Sciences, University College Dublin, St Vincent's University Hospital, Dublin, Ireland – sequence: 11 givenname: Christopher surname: McGuigan fullname: McGuigan, Christopher organization: School of Medicine and Medical Sciences, University College Dublin, St Vincent's University Hospital, Dublin, Ireland – sequence: 12 givenname: Vilija surname: Jokubaitis fullname: Jokubaitis, Vilija organization: Department of Medicine, University of Melbourne, Melbourne, VIC, Australia – sequence: 13 givenname: Tim surname: Spelman fullname: Spelman, Tim organization: Department of Medicine, University of Melbourne, Melbourne, VIC, Australia – sequence: 14 givenname: Dana surname: Horakova fullname: Horakova, Dana organization: Department of Neurology and Center of Clinical Neuroscience, General University Hospital and Charles University, Prague, Czech Republic – sequence: 15 givenname: Eva surname: Havrdova fullname: Havrdova, Eva organization: Department of Neurology and Center of Clinical Neuroscience, General University Hospital and Charles University, Prague, Czech Republic – sequence: 16 givenname: Maria surname: Trojano fullname: Trojano, Maria organization: Department of Basic Medical Sciences, Neuroscience and Sense Organs, University of Bari, Bari, Italy – sequence: 17 givenname: Guillermo surname: Izquierdo fullname: Izquierdo, Guillermo organization: Hospital Universitario Virgen Macarena, Sevilla, Spain – sequence: 18 givenname: Alessandra surname: Lugaresi fullname: Lugaresi, Alessandra organization: Department of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy – sequence: 19 givenname: Alexandre surname: Prat fullname: Prat, Alexandre organization: Hopital Notre Dame, Montreal, QC, Canada – sequence: 20 givenname: Marc surname: Girard fullname: Girard, Marc organization: Hopital Notre Dame, Montreal, QC, Canada – sequence: 21 givenname: Pierre surname: Duquette fullname: Duquette, Pierre organization: Hopital Notre Dame, Montreal, QC, Canada – sequence: 22 givenname: Pierre surname: Grammond fullname: Grammond, Pierre organization: Centres intégrés de santé et de services sociaux de Chaudière-Appalache, Levis, QC, Canada – sequence: 23 givenname: Raed surname: Alroughani fullname: Alroughani, Raed organization: Amiri Hospital, Qurtoba, Kuwait City, Kuwait – sequence: 24 givenname: Eugenio surname: Pucci fullname: Pucci, Eugenio organization: Azienda Sanitaria Unica Regionale Marche AV3, Macerata, Italy – sequence: 25 givenname: Patrizia surname: Sola fullname: Sola, Patrizia organization: Nuovo Ospedale Civile Sant'Agostino-Estense, Modena, Italy – sequence: 26 givenname: Raymond surname: Hupperts fullname: Hupperts, Raymond organization: Zuyderland Ziekenhuis, Sittard, Netherlands – sequence: 27 givenname: Jeannette surname: Lechner-Scott fullname: Lechner-Scott, Jeannette organization: University of Newcastle, Newcastle, NSW, Australia – sequence: 28 givenname: Murat surname: Terzi fullname: Terzi, Murat organization: Medical Faculty, 19 Mayis University, Kurupelit, Samsun, Turkey – sequence: 29 givenname: Vincent surname: Van Pesch fullname: Van Pesch, Vincent organization: Cliniques Universitaires Saint-Luc, Brussels, Belgium – sequence: 30 givenname: Csilla surname: Rozsa fullname: Rozsa, Csilla organization: Jahn Ferenc Teaching Hospital, Budapest, Hungary – sequence: 31 givenname: François surname: Grand'Maison fullname: Grand'Maison, François organization: Neuro Rive-Sud, Greenfield Park, QC, Canada – sequence: 32 givenname: Cavit surname: Boz fullname: Boz, Cavit organization: KTÜ Medical Faculty Farabi Hospital, Karadeniz Technical University, Trabzon, Turkey – sequence: 33 givenname: Franco surname: Granella fullname: Granella, Franco organization: University of Parma, Parma, Italy – sequence: 34 givenname: Mark surname: Slee fullname: Slee, Mark organization: Flinders University, Adelaide, SA, Australia – sequence: 35 givenname: Daniele surname: Spitaleri fullname: Spitaleri, Daniele organization: Azienda Ospedaliera San Giuseppe Moscati di Avellino, Avellino, Italy – sequence: 36 givenname: Javier surname: Olascoaga fullname: Olascoaga, Javier organization: Hospital Universitario Donostia, San Sebastián, Spain – sequence: 37 givenname: Roberto surname: Bergamaschi fullname: Bergamaschi, Roberto organization: C Mondino National Neurological Institute, Pavia, Italy – sequence: 38 givenname: Freek surname: Verheul fullname: Verheul, Freek organization: Groene Hart Ziekenhuis, Gouda, Netherlands – sequence: 39 givenname: Steve surname: Vucic fullname: Vucic, Steve organization: Westmead Hospital, Sydney, NSW, Australia – sequence: 40 givenname: Pamela surname: McCombe fullname: McCombe, Pamela organization: Royal Brisbane and Women's Hospital, Brisbane, QLD, Australia – sequence: 41 givenname: Suzanne surname: Hodgkinson fullname: Hodgkinson, Suzanne organization: Liverpool Hospital, Sydney, NSW, Australia – sequence: 42 givenname: Jose Luis surname: Sanchez-Menoyo fullname: Sanchez-Menoyo, Jose Luis organization: Hospital de Galdakao-Usansolo, Galdakao, Spain – sequence: 43 givenname: Radek surname: Ampapa fullname: Ampapa, Radek organization: Nemocnice Jihlava, Jihlava, Czech Republic – sequence: 44 givenname: Magdolna surname: Simo fullname: Simo, Magdolna organization: Semmelweis University Budapest, Budapest, Hungary – sequence: 45 givenname: Tunde surname: Csepany fullname: Csepany, Tunde organization: University of Debrecen, Faculty of Medicine, Department of Neurology, Debrecen, Hungary – sequence: 46 givenname: Cristina surname: Ramo fullname: Ramo, Cristina organization: Hospital Germans Trias i Pujol, Badalona, Spain – sequence: 47 givenname: Edgardo surname: Cristiano fullname: Cristiano, Edgardo organization: Hospital Italiano, Buenos Aires, Argentina – sequence: 48 givenname: Michael surname: Barnett fullname: Barnett, Michael organization: Brain and Mind Centre, Camperdown, NSW, Australia – sequence: 49 givenname: Helmut surname: Butzkueven fullname: Butzkueven, Helmut organization: Department of Medicine, University of Melbourne, Melbourne, VIC, Australia – sequence: 50 givenname: Alasdair surname: Coles fullname: Coles, Alasdair organization: Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK |
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| Snippet | Alemtuzumab, an anti-CD52 antibody, is proven to be more efficacious than interferon beta-1a in the treatment of relapsing-remitting multiple sclerosis, but... Summary Background Alemtuzumab, an anti-CD52 antibody, is proven to be more efficacious than interferon beta-1a in the treatment of relapsing-remitting... Background Alemtuzumab, an anti-CD52 antibody, is proven to be more efficacious than interferon beta-1a in the treatment of relapsing-remitting multiple... |
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| SubjectTerms | Adult Alemtuzumab Antibodies, Monoclonal, Humanized - therapeutic use Clinical medicine Clinical trials Cohort Studies Data entry Databases, Bibliographic - statistics & numerical data Disability Evaluation Female Fingolimod Hydrochloride - therapeutic use Humans Immunologic Factors - therapeutic use Immunotherapy Interferon Interferon-beta - therapeutic use Male Medical research Multiple sclerosis Multiple Sclerosis, Relapsing-Remitting - drug therapy Natalizumab - therapeutic use Neurology Pharmaceutical industry Quality Studies Treatment Outcome Young Adult |
| Title | Treatment effectiveness of alemtuzumab compared with natalizumab, fingolimod, and interferon beta in relapsing-remitting multiple sclerosis: a cohort study |
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