Contributions
Abstract: EP1575
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - Biomarkers
Background: Although evidence in clinically isolated syndrome (CIS) suggests that the presence of anti-myelin Abs can predict the clinical conversion to multiple sclerosis (MS), the relevance of anti-myelin antibodies (Abs) in MS patients remains largely unexplored.
Objective: To test the prognostic value of anti-myelin Abs in patients with MS in longer-term.
Methods: Sera were collected after the first clinical episode suggestive of MS and tested by Western blotting for the presence of anti-anti-myelin oligodendrocyte glycoprotein(MOG) and anti-myelin basic protein(MBP) IgM Ab. Patients were classified accordingly as anti-MOG+ve /anti-MOG-ve and anti-MBP+ve /anti-MBP-ve. We collected clinical data and considered as clinical endpoints: a) the number of patients with confirmed EDSS worsening of at least 1 point; b) the number of patients reaching EDSS=4.0. Possible risk factors for the reaching EDSS=4.0 were estimated using forward stepwise logistic regression and considering in the model the presence of MOG Abs, MBP Abs, age, sex, baseline EDSS, the involvement of ≥1 functional systems and the recovery after CIS.
Results: Out of 34 patients [18 (52.9%) women, mean age 30.7±8.0] 14 (41%)were anti-MOG+ve and 16 (47%) anti-MBP+ve at baseline. The mean follow-up (FU) was 17.9±2.9 years.
At the end of the FU, only 3 patients did not present a clinical relapse. One patient died during the observation period as consequence of serious infection.Thirty patients (88.2%) underwent MS specific treatment: 18 patients started interferon-beta, 7 glatiramer acetate, 2 dimethyl fumarate, 2 natalizumab and 1 fingolimod. Twenty-two patients (65%) presented an EDSS worsening: median EDSS baseline was 1.0 [0-1.5] median EDSS at FU was 2.5[1.5-5.875] (p< 0.001).
At the end of FU, anti-MBP+ve patients presented higher EDSS score and lower number of fully ambulatory patients compared to anti-MBP-ve (mean EDSS increase 3.4±2.4 vs.1.4±2.0 p=0.02, and 7 (44%) vs 14 (75%) p=0.04 respectively). No differences were found in patients anti-MOG+ve compared to patients anti-MOG-ve. Patients anti-MBP+ve showed an increased risk of reaching the EDSS=4.0 (OR 6, 95%CI 1.2-30, p=0.03).
Conclusion: We suggest that the presence of MBP IgM Abs after a first clinical episode increases long-term risk of disability and may represent a negative prognostic factor for disease course.
Disclosure: De Giglio L. received speaking onoraria from Genzyme and Novartis, travel grant from Biogen, Merk, Teva, consulting fee from Genzyme, Merk and Novartis.
Cortese A. received speaker honoraria from Biogen, Sanofi Genzyme; travel grants from Biogen, Merck, Sanofi Genzyme, Teva; advisory boards member honoraria from Biogen, Merck, Novartis, Teva.
Millefiorini E. received speaker honoraria from Biogen, Merck, Sanofi Genzyme, Novartis, Teva; travel grants from Biogen, Merck, Sanofi Genzyme, Teva, Novartis.
Berger T. and Reindl M. have received research grants (“BIG-WIG MS“, Austrian FederalMinistry ofScience, Research and Economy; Austrian Multiple Sclerosis Research Society) and institutional payments for antibody assays (Euroimmune, Germany) in the context of anti-myelin antibody research projects.
Pozzilli C. received consulting and lecture fees and research funding and travel grants from Almirall, Bayer, Biogen, Genzyme, Merck Serono, Novartis, Roche and Teva.Tommasini V. , Ianniello A. and Sgarlata E. declare no conflict of interest
Abstract: EP1575
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - Biomarkers
Background: Although evidence in clinically isolated syndrome (CIS) suggests that the presence of anti-myelin Abs can predict the clinical conversion to multiple sclerosis (MS), the relevance of anti-myelin antibodies (Abs) in MS patients remains largely unexplored.
Objective: To test the prognostic value of anti-myelin Abs in patients with MS in longer-term.
Methods: Sera were collected after the first clinical episode suggestive of MS and tested by Western blotting for the presence of anti-anti-myelin oligodendrocyte glycoprotein(MOG) and anti-myelin basic protein(MBP) IgM Ab. Patients were classified accordingly as anti-MOG+ve /anti-MOG-ve and anti-MBP+ve /anti-MBP-ve. We collected clinical data and considered as clinical endpoints: a) the number of patients with confirmed EDSS worsening of at least 1 point; b) the number of patients reaching EDSS=4.0. Possible risk factors for the reaching EDSS=4.0 were estimated using forward stepwise logistic regression and considering in the model the presence of MOG Abs, MBP Abs, age, sex, baseline EDSS, the involvement of ≥1 functional systems and the recovery after CIS.
Results: Out of 34 patients [18 (52.9%) women, mean age 30.7±8.0] 14 (41%)were anti-MOG+ve and 16 (47%) anti-MBP+ve at baseline. The mean follow-up (FU) was 17.9±2.9 years.
At the end of the FU, only 3 patients did not present a clinical relapse. One patient died during the observation period as consequence of serious infection.Thirty patients (88.2%) underwent MS specific treatment: 18 patients started interferon-beta, 7 glatiramer acetate, 2 dimethyl fumarate, 2 natalizumab and 1 fingolimod. Twenty-two patients (65%) presented an EDSS worsening: median EDSS baseline was 1.0 [0-1.5] median EDSS at FU was 2.5[1.5-5.875] (p< 0.001).
At the end of FU, anti-MBP+ve patients presented higher EDSS score and lower number of fully ambulatory patients compared to anti-MBP-ve (mean EDSS increase 3.4±2.4 vs.1.4±2.0 p=0.02, and 7 (44%) vs 14 (75%) p=0.04 respectively). No differences were found in patients anti-MOG+ve compared to patients anti-MOG-ve. Patients anti-MBP+ve showed an increased risk of reaching the EDSS=4.0 (OR 6, 95%CI 1.2-30, p=0.03).
Conclusion: We suggest that the presence of MBP IgM Abs after a first clinical episode increases long-term risk of disability and may represent a negative prognostic factor for disease course.
Disclosure: De Giglio L. received speaking onoraria from Genzyme and Novartis, travel grant from Biogen, Merk, Teva, consulting fee from Genzyme, Merk and Novartis.
Cortese A. received speaker honoraria from Biogen, Sanofi Genzyme; travel grants from Biogen, Merck, Sanofi Genzyme, Teva; advisory boards member honoraria from Biogen, Merck, Novartis, Teva.
Millefiorini E. received speaker honoraria from Biogen, Merck, Sanofi Genzyme, Novartis, Teva; travel grants from Biogen, Merck, Sanofi Genzyme, Teva, Novartis.
Berger T. and Reindl M. have received research grants (“BIG-WIG MS“, Austrian FederalMinistry ofScience, Research and Economy; Austrian Multiple Sclerosis Research Society) and institutional payments for antibody assays (Euroimmune, Germany) in the context of anti-myelin antibody research projects.
Pozzilli C. received consulting and lecture fees and research funding and travel grants from Almirall, Bayer, Biogen, Genzyme, Merck Serono, Novartis, Roche and Teva.Tommasini V. , Ianniello A. and Sgarlata E. declare no conflict of interest