Contributions
Abstract: P1169
Type: Poster
Abstract Category: Therapy - disease modifying - Immunomodulation/Immunosuppression
Objectives: To compare the effects of natalizumab (NAT) and fingolimod (FTY) on clinical and MRI measures in relapsing-remitting (RR) MS after two years of treatment.
Background: NAT and FTY reduce clinical and MRI disease activity in RRMS, but comparative studies are limited.
Methods: Fifty-four RRMS patients starting natalizumab (NAT) (n=28) or fingolimod (FTY) (n=26) underwent 3T brain scans, and clinical evaluation (including EDSS and evaluation of clinical relapses) at baseline (T0), year 1 (Y1) and year 2 (Y2). T2, T1 and cortical lesion volumes (LV), brain, white matter (WM), gray matter (GM) and deep GM volumes were measured. Between- and within-group analyses were performed using two- and paired-sample t-tests.
Results: At T0, the two groups were matched for demographic, clinical and MRI variables. Both drugs significantly reduced clinical relapses at Y1 and Y2, with a greater reduction at Y1 in NAT vs FTY patients (0.23 vs 0.04, p=0.04). NAT vs FTY patients formed also a lower number of new T2 lesions at Y1 (1.81 vs 0.79, p=0.04). In NAT patients, EDSS, T2 and cortical LV remained stable at Y1 and Y2, T1 LV decreased at Y1 (p=0.03) and remained stable at Y2. In FTY patients, EDSS and cortical LV decreased significantly at Y1 (p=0.008 and p=0.0001, respectively), while T2 and T1 LV significantly increased at Y1 (p< 0.0001 and p=0.0001, respectively), and remained stable at Y2. At Y1, thalamic atrophy significantly occurred in both groups (p=0.03 for NAT patients and p=0.002 for FTY patients, respectively); NAT patients had also volume loss of the pallidus (p=0.02), while FTY patients showed significant atrophy of caudate nuclei (p=0.03). At Y2 vs Y1, a significant brain atrophy occurred in both groups (p=0.03 for NAT group and p=0.02 for FTY group). NAT patients also had significant GM atrophy (p=0.01). In the direct comparisons of longitudinal differences between patients" subgroups, a significant increased T2 and T1 LV (p< 0.0001 for both comparisons) and a decreased cortical LV (p=0.01) was found in FTY vs NAT patients.
Conclusions: NAT and FTY reduce disease activity in RRMS. NAT could have a more significant effect on WM inflammatory lesion accumulation, while both drugs seems to prevent significant regional atrophy.
Disclosure: Drs Preziosa, Riccitelli, Rodegher, Moiola, and Falini have nothing to disclose.
Dr Rocca received speakers honoraria from Biogen Idec, Novartis and ExceMed and receives research support from the Italian Ministry of Health and Fondazione Italiana Sclerosi Multipla.
Prof. Comi has received consulting fees for participating on advisory boards from Novartis, Teva Pharmaceutical Ind. Ltd, Sanofi, Genzyme, Merck Serono, Bayer, Actelion and honorarium for speaking activities for Novartis, Teva Pharmaceutical Ind. Ltd, Sanofi, Genzyme, Merck Serono, Bayer, Biogen, Excemed.
Prof. Filippi is Editor-in-Chief of the Journal of Neurology; serves on scientific advisory boards for Teva Pharmaceutical Industries; has received compensation for consulting services and/or speaking activities from Biogen Idec, Excemed, Novartis, and Teva Pharmaceutical Industries; and receives research support from Biogen Idec, Teva Pharmaceutical Industries, Novartis, Italian Ministry of Health, Fondazione Italiana Sclerosi Multipla, Cure PSP, Alzheimer´s Drug Discovery Foundation (ADDF), the Jacques and Gloria Gossweiler Foundation (Switzerland), and ARiSLA (Fondazione Italiana di Ricerca per la SLA).
Abstract: P1169
Type: Poster
Abstract Category: Therapy - disease modifying - Immunomodulation/Immunosuppression
Objectives: To compare the effects of natalizumab (NAT) and fingolimod (FTY) on clinical and MRI measures in relapsing-remitting (RR) MS after two years of treatment.
Background: NAT and FTY reduce clinical and MRI disease activity in RRMS, but comparative studies are limited.
Methods: Fifty-four RRMS patients starting natalizumab (NAT) (n=28) or fingolimod (FTY) (n=26) underwent 3T brain scans, and clinical evaluation (including EDSS and evaluation of clinical relapses) at baseline (T0), year 1 (Y1) and year 2 (Y2). T2, T1 and cortical lesion volumes (LV), brain, white matter (WM), gray matter (GM) and deep GM volumes were measured. Between- and within-group analyses were performed using two- and paired-sample t-tests.
Results: At T0, the two groups were matched for demographic, clinical and MRI variables. Both drugs significantly reduced clinical relapses at Y1 and Y2, with a greater reduction at Y1 in NAT vs FTY patients (0.23 vs 0.04, p=0.04). NAT vs FTY patients formed also a lower number of new T2 lesions at Y1 (1.81 vs 0.79, p=0.04). In NAT patients, EDSS, T2 and cortical LV remained stable at Y1 and Y2, T1 LV decreased at Y1 (p=0.03) and remained stable at Y2. In FTY patients, EDSS and cortical LV decreased significantly at Y1 (p=0.008 and p=0.0001, respectively), while T2 and T1 LV significantly increased at Y1 (p< 0.0001 and p=0.0001, respectively), and remained stable at Y2. At Y1, thalamic atrophy significantly occurred in both groups (p=0.03 for NAT patients and p=0.002 for FTY patients, respectively); NAT patients had also volume loss of the pallidus (p=0.02), while FTY patients showed significant atrophy of caudate nuclei (p=0.03). At Y2 vs Y1, a significant brain atrophy occurred in both groups (p=0.03 for NAT group and p=0.02 for FTY group). NAT patients also had significant GM atrophy (p=0.01). In the direct comparisons of longitudinal differences between patients" subgroups, a significant increased T2 and T1 LV (p< 0.0001 for both comparisons) and a decreased cortical LV (p=0.01) was found in FTY vs NAT patients.
Conclusions: NAT and FTY reduce disease activity in RRMS. NAT could have a more significant effect on WM inflammatory lesion accumulation, while both drugs seems to prevent significant regional atrophy.
Disclosure: Drs Preziosa, Riccitelli, Rodegher, Moiola, and Falini have nothing to disclose.
Dr Rocca received speakers honoraria from Biogen Idec, Novartis and ExceMed and receives research support from the Italian Ministry of Health and Fondazione Italiana Sclerosi Multipla.
Prof. Comi has received consulting fees for participating on advisory boards from Novartis, Teva Pharmaceutical Ind. Ltd, Sanofi, Genzyme, Merck Serono, Bayer, Actelion and honorarium for speaking activities for Novartis, Teva Pharmaceutical Ind. Ltd, Sanofi, Genzyme, Merck Serono, Bayer, Biogen, Excemed.
Prof. Filippi is Editor-in-Chief of the Journal of Neurology; serves on scientific advisory boards for Teva Pharmaceutical Industries; has received compensation for consulting services and/or speaking activities from Biogen Idec, Excemed, Novartis, and Teva Pharmaceutical Industries; and receives research support from Biogen Idec, Teva Pharmaceutical Industries, Novartis, Italian Ministry of Health, Fondazione Italiana Sclerosi Multipla, Cure PSP, Alzheimer´s Drug Discovery Foundation (ADDF), the Jacques and Gloria Gossweiler Foundation (Switzerland), and ARiSLA (Fondazione Italiana di Ricerca per la SLA).