Contributions
Abstract: P769
Type: Poster
Abstract Category: Therapy - disease modifying - 30 Tools for detecting therapeutic response
Background: The No Evidence of Disease Activity (NEDA) is a desirable outcome measure for the treatment of relapsing-remitting multiple sclerosis (RRMS) [Giovannoni et al. Mult Scler Rel Disord 2015]. However, NEDA represents a stringent goal to achieve, especially with platform therapies [Rotstein et al. JAMA Neurol 2015]. Therefore, Minimal Evidence of Disease Activity (MEDA) has been proposed as a more realistic target that can be tolerated without any significantly increased risk of future disability worsening.
Objective: To investigate the effect of early NEDA or MEDA status on long-term disability outcome in patients with RRMS.
Methods: We collected data of patients with RRMS regularly attending 3 Italian MS Centres. Patients were considered eligible if they started Interferon Beta or Glatiramer Acetate as first treatment, had an Expanded Disability Status Scale (EDSS) score ≤4.0 and were followed for ≥5 years. They were classified in subgroups according to level of disease activity after the first year of treatment [Rio J et al. Mult Scler 2017]:
(i) NEDA, i.e. absence of relapses, of confirmed EDSS worsening and of magnetic resonance imaging (MRI) activity;
(ii) MEDA, i.e. either “1 relapse with ≤2 new T2 lesions” or “< 3 new T2 lesions or < 2 gadolinium-enhancing lesions”, in the absence confirmed EDSS worsening;
(iii) Evidence of disease activity (EDA), i.e. occurrence of ≥1 relapse with either confirmed EDSS worsening or ≥1 gadolinium-enhancing lesion or ≥3 new T2 lesions.
We ran a multivariable Cox regression model (stratified by Centre) to explore the long-term risk of reaching the disability milestone of EDSS≥6.0 according to one-year status (NEDA, MEDA or EDA).
Results: We analyzed 987 patients with mean age of 33.3±9.7 years and median EDSS score of 1.5. They were followed for a median time of 10 years (range 5 to 23). Of them, 423 (43%), 389 (39%) and 175 (18%) were classified at one year as having NEDA, MEDA and EDA, respectively. Overall, 182 (18%) patients reached EDSS≥6.0 after a median time of 9 years (range 2-22). The risk of reaching EDSS≥6.0 was higher in the event of one-year EDA (HR=1.95, p=0.002) and MEDA (HR=1.48, p=0.03) when compared to the NEDA status.
Conclusions: Our findings suggest that we should treat patients with RRMS to target the NEDA status as early as possible to prevent the risk of future irreversible disability. To further support this treatment approach, different definitions of MEDA need to be investigated.
Disclosure:
LP has received consulting and/or lecture fees and travel grant from Biogen, Genzyme, Merck Serono, Novartis, Roche and Teva.
RC has received consulting fees from Novartis, Biogen and lecture fees and/or travel grants from Novartis, Biogen, Genzyme and Sanofi-Aventis.
CP has served on scientific advisory boards for Actelion, Biogen, Genzyme, Hoffmann-La Roche Ltd,Merck-Serono, Novartis, Sanofi, Teva, and has received consulting and/or speaking fees, research support and travel grants from Allergan,Almirall,Biogen, Genzyme,Hoffmann-La Roche Ltd,Merck-Serono, Novartis, Sanofi and Teva.
CG has received lecture fees and/or consulting fees from Merck Serono, Biogen, Teva, Bayer Schering and Novartis.
CRM, ES and VT: nothing to disclose.
Abstract: P769
Type: Poster
Abstract Category: Therapy - disease modifying - 30 Tools for detecting therapeutic response
Background: The No Evidence of Disease Activity (NEDA) is a desirable outcome measure for the treatment of relapsing-remitting multiple sclerosis (RRMS) [Giovannoni et al. Mult Scler Rel Disord 2015]. However, NEDA represents a stringent goal to achieve, especially with platform therapies [Rotstein et al. JAMA Neurol 2015]. Therefore, Minimal Evidence of Disease Activity (MEDA) has been proposed as a more realistic target that can be tolerated without any significantly increased risk of future disability worsening.
Objective: To investigate the effect of early NEDA or MEDA status on long-term disability outcome in patients with RRMS.
Methods: We collected data of patients with RRMS regularly attending 3 Italian MS Centres. Patients were considered eligible if they started Interferon Beta or Glatiramer Acetate as first treatment, had an Expanded Disability Status Scale (EDSS) score ≤4.0 and were followed for ≥5 years. They were classified in subgroups according to level of disease activity after the first year of treatment [Rio J et al. Mult Scler 2017]:
(i) NEDA, i.e. absence of relapses, of confirmed EDSS worsening and of magnetic resonance imaging (MRI) activity;
(ii) MEDA, i.e. either “1 relapse with ≤2 new T2 lesions” or “< 3 new T2 lesions or < 2 gadolinium-enhancing lesions”, in the absence confirmed EDSS worsening;
(iii) Evidence of disease activity (EDA), i.e. occurrence of ≥1 relapse with either confirmed EDSS worsening or ≥1 gadolinium-enhancing lesion or ≥3 new T2 lesions.
We ran a multivariable Cox regression model (stratified by Centre) to explore the long-term risk of reaching the disability milestone of EDSS≥6.0 according to one-year status (NEDA, MEDA or EDA).
Results: We analyzed 987 patients with mean age of 33.3±9.7 years and median EDSS score of 1.5. They were followed for a median time of 10 years (range 5 to 23). Of them, 423 (43%), 389 (39%) and 175 (18%) were classified at one year as having NEDA, MEDA and EDA, respectively. Overall, 182 (18%) patients reached EDSS≥6.0 after a median time of 9 years (range 2-22). The risk of reaching EDSS≥6.0 was higher in the event of one-year EDA (HR=1.95, p=0.002) and MEDA (HR=1.48, p=0.03) when compared to the NEDA status.
Conclusions: Our findings suggest that we should treat patients with RRMS to target the NEDA status as early as possible to prevent the risk of future irreversible disability. To further support this treatment approach, different definitions of MEDA need to be investigated.
Disclosure:
LP has received consulting and/or lecture fees and travel grant from Biogen, Genzyme, Merck Serono, Novartis, Roche and Teva.
RC has received consulting fees from Novartis, Biogen and lecture fees and/or travel grants from Novartis, Biogen, Genzyme and Sanofi-Aventis.
CP has served on scientific advisory boards for Actelion, Biogen, Genzyme, Hoffmann-La Roche Ltd,Merck-Serono, Novartis, Sanofi, Teva, and has received consulting and/or speaking fees, research support and travel grants from Allergan,Almirall,Biogen, Genzyme,Hoffmann-La Roche Ltd,Merck-Serono, Novartis, Sanofi and Teva.
CG has received lecture fees and/or consulting fees from Merck Serono, Biogen, Teva, Bayer Schering and Novartis.
CRM, ES and VT: nothing to disclose.