Contributions
Abstract: P664
Type: Poster
Abstract Category: Therapy - disease modifying - 26 Immunomodulation/Immunosuppression
Background: Natalizumab and fingolimod were approved for treatment of active relapsing-remitting multiple sclerosis (RRMS) in Austria in 2006 and 2011, respectively. No randomized head-to-head studies comparing natalizumab and fingolimod are available.
Objectives: To compare patients who started with natalizumab or fingolimod in a nationwide observational cohort using prospectively collected data.
Methods: We included all patients starting treatment with natalizumab or fingolimod documented in the Austrian MS Treatment Registry (AMSTR) from 2011 and staying on therapy for at least 24 months. We used propensity scores for several matching methods and as a covariate in multivariate models to correct for the bias of this non-randomised registry study.
Results: The study cohort includes 588 RRMS patients. 10 patients did not produce a propensity score in the common support region, thus leaving 578 cases for final analyses, 332 in the fingolimod and 246 in the natalizumab group. Mean annualized relapse rates (ARR) during the 24 months observation period were 0.19 under fingolimod and 0.12 under natalizumab treatment (p = 0.005). No statistical significant differences were found analysing the log-transformed ARR, probability for experiencing a relapse, EDSS progression and EDSS regression. The hazard ratio for switching treatment from fingolimod comparing with natalizumab was 0.36 (95% CI: 0.247-0.523), p< 0.001.
Conclusions: The generalized linear model (GLM) for relapse count as Poisson distributed dependent variable and propensity score as covariate showed a statistically significant reduction for the mean relapse count in the natalizumab group compared with fingolimod. This effect was smaller in the analyses of log transformed ARR with propensity score matching, loosing statistical significance although showing the same direction for the effect. We assume, that the GLM was the more sensitive model analysing this question.
Disclosure:
Michael Guger received support and honoraria for research, consultation, lectures and education from Allmirall, Bayer, Biogen, Genzyme, Merck, Novartis, Octapharma, Sanofi Aventis, Roche and TEVA ratiopharm.
Christian Enzinger received funding for travel and speaker honoraria from Biogen, Bayer Schering, Merck Serono, Novartis, Shire, Genzyme and Teva Pharmaceutical Industries Ltd./sanofi-aventis, research support from Merck Serono, Biogen, and Teva Pharmaceutical Industries Ltd./sanofi-aventis and serving on scientific advisory boards for Bayer Schering, Biogen, Merck Serono, Novartis, Roche and Teva Pharmaceutical Industries Ltd./sanofi- Aventis.
Dr. Leutmezer has received funding for travel and speaker honoraria from Biogen, Bayer Schering Pharma, Merck Serono, Novartis, Genzyme, Santhera and Teva Pharmaceutical Industries Ltd./sanofi-aventis.
Dr. Kraus received support for research, consultation, and education from Allmirall, Bayer, Biogen-Idec, Biotest, Genzyme, Medtronic, Merck-Serono, Novartis, Octapharma, Sanofi-Aventis, TEVA ratiopharm.
Thomas Berger has participated in meetings sponsored by and received honoraria (lectures, advisory boards, consultations) from pharmaceutical companies marketing treatments for multiple sclerosis: Almirall, Bayer, Biogen, Genzyme, Merck, Novartis, Octapharma, ratiopharm, Roche, Sanofi Aventis, TEVA.
His institution has received financial support in the last 12 months by unrestricted research grants (Biogen, Bayer, Merck, Novartis, ratiopharm, Sanofi Aventis) and for participation in clinical trials in multiple sclerosis sponsored by Alexion, Bayer, Biogen, Merck, Novartis, Octapharma, Roche, Sanofi Aventis, TEVA.
Abstract: P664
Type: Poster
Abstract Category: Therapy - disease modifying - 26 Immunomodulation/Immunosuppression
Background: Natalizumab and fingolimod were approved for treatment of active relapsing-remitting multiple sclerosis (RRMS) in Austria in 2006 and 2011, respectively. No randomized head-to-head studies comparing natalizumab and fingolimod are available.
Objectives: To compare patients who started with natalizumab or fingolimod in a nationwide observational cohort using prospectively collected data.
Methods: We included all patients starting treatment with natalizumab or fingolimod documented in the Austrian MS Treatment Registry (AMSTR) from 2011 and staying on therapy for at least 24 months. We used propensity scores for several matching methods and as a covariate in multivariate models to correct for the bias of this non-randomised registry study.
Results: The study cohort includes 588 RRMS patients. 10 patients did not produce a propensity score in the common support region, thus leaving 578 cases for final analyses, 332 in the fingolimod and 246 in the natalizumab group. Mean annualized relapse rates (ARR) during the 24 months observation period were 0.19 under fingolimod and 0.12 under natalizumab treatment (p = 0.005). No statistical significant differences were found analysing the log-transformed ARR, probability for experiencing a relapse, EDSS progression and EDSS regression. The hazard ratio for switching treatment from fingolimod comparing with natalizumab was 0.36 (95% CI: 0.247-0.523), p< 0.001.
Conclusions: The generalized linear model (GLM) for relapse count as Poisson distributed dependent variable and propensity score as covariate showed a statistically significant reduction for the mean relapse count in the natalizumab group compared with fingolimod. This effect was smaller in the analyses of log transformed ARR with propensity score matching, loosing statistical significance although showing the same direction for the effect. We assume, that the GLM was the more sensitive model analysing this question.
Disclosure:
Michael Guger received support and honoraria for research, consultation, lectures and education from Allmirall, Bayer, Biogen, Genzyme, Merck, Novartis, Octapharma, Sanofi Aventis, Roche and TEVA ratiopharm.
Christian Enzinger received funding for travel and speaker honoraria from Biogen, Bayer Schering, Merck Serono, Novartis, Shire, Genzyme and Teva Pharmaceutical Industries Ltd./sanofi-aventis, research support from Merck Serono, Biogen, and Teva Pharmaceutical Industries Ltd./sanofi-aventis and serving on scientific advisory boards for Bayer Schering, Biogen, Merck Serono, Novartis, Roche and Teva Pharmaceutical Industries Ltd./sanofi- Aventis.
Dr. Leutmezer has received funding for travel and speaker honoraria from Biogen, Bayer Schering Pharma, Merck Serono, Novartis, Genzyme, Santhera and Teva Pharmaceutical Industries Ltd./sanofi-aventis.
Dr. Kraus received support for research, consultation, and education from Allmirall, Bayer, Biogen-Idec, Biotest, Genzyme, Medtronic, Merck-Serono, Novartis, Octapharma, Sanofi-Aventis, TEVA ratiopharm.
Thomas Berger has participated in meetings sponsored by and received honoraria (lectures, advisory boards, consultations) from pharmaceutical companies marketing treatments for multiple sclerosis: Almirall, Bayer, Biogen, Genzyme, Merck, Novartis, Octapharma, ratiopharm, Roche, Sanofi Aventis, TEVA.
His institution has received financial support in the last 12 months by unrestricted research grants (Biogen, Bayer, Merck, Novartis, ratiopharm, Sanofi Aventis) and for participation in clinical trials in multiple sclerosis sponsored by Alexion, Bayer, Biogen, Merck, Novartis, Octapharma, Roche, Sanofi Aventis, TEVA.