Contributions
Abstract: P662
Type: Poster Sessions
Abstract Category: Clinical aspects of MS - MS Variants
Background: Although some clinical differences in AQP4-IgG-positive NMOSD between Japan and UK have been reported, the similarity and difference of the MOG-IgG-positive CNS inflammatory disorders between Asian and western countries was hardly investigated.
Goal: To elucidate the similarity and difference of demographic, clinical, laboratory and radiological features of patients with MOG-IgG-positive CNS inflammatory disorders between Japan and Germany.
Methods: We retrospectively collected and compared data of patients seropositive for MOG-IgG who were seen in two Japanese centers (Chiba University Hospital and Saitama medical center) and two German centers (NeuroCure Clinical Research Center, Charité and Ludwig Maximilians University Hospital, Munich). Antibodies to MOG-IgG were tested by cell-based assays.
Results: A total of 80 patients seropositive for MOG-IgG were included. Fifty-one were from Japanese cohort (31 from Chiba and 20 from Saitama) and 29 were from German (14 from Charité and 15 from Munich). Female ratios were similar (62.7% and 62.1% in the Japanese and German cohort, respectively). While all patients were Asian in the Japanese cohort, 82.8%, 6.90%, and 10.3% were Caucasian, Asian, and others, respectively, in the German cohort. Mean (±SD) age at disease onset was similar (40.5±18.0 and 38.0±14.5 in the Japanese and German cohort, respectively). Meanwhile, disease duration was shorter in the Japanese cohort (mean±SD, 2.9±5.1 yrs) than the German cohort (5.7±6.0 yrs) (P< 0.001). Lesion location at disease onset exhibited a similar distribution in both cohorts. The number of total attacks tended to be lower in the Japanese cohort (2.4±2.4 times) than in the German cohort (3.3±2.8 times) (P=0.079), and EDSS score was lower in the Japanese cohort (2.2±1.8) than the German cohort (2.4±1.3) (P< 0.001). To prevent attack, 35.3% and only 7.8% were treated with prednisolone and immunomodulators, respectively, in the Japanese cohort. In contrast, only 6.9% and 48.3% were treated with prednisolone and immunomodulators including rituximab and azathioprine, respectively, in the German cohort. None of the Japanese patients and 7.41% of the German patients had CSF oligoclonal bands, and 11.8% of Japanese patients and 31.0% of German patients had long spinal cord lesions.
Conclusion: Except for a lower total attack number, EDSS, and percentages of patients treated with rituximab/azathioprine, comparatively similar features were seen in the two cohorts.
Disclosure: Masahiro Mori: nothing to disclose.
Alexander U. Brandt: AUB is cofounder and shareholder of Motognosis and Nocturne. He is named as inventor on several patent applications regarding MS serum biomarkers, OCT image analysis and perceptive visual computing.
Joachim Havla: reports a grant for OCT research from the Friedrich-Baur-Stiftung, personal fees and non-financial support from Merck, Novartis, Roche, Bayer Healthcare, Santhera, Biogen, Sanofi Genzyme and non-financial support of the Guthy-Jackson Charitable Foundation, all outside the submitted work.Satoru Tanaka: nothing to disclose.
Jia Liu: nothing to disclose.
Hanna Zimmermann: Received a research grant from Novartis and speaking fees from Teva, unrelated to this work.Satoru Oji: nothing to disclose.
Akiyuki Uzawa: nothing to disclose.
Felix Schmidt: F. Schmidt received speaker honoraria from Genzyme.
Judith Bellmann-Strobl: has received travel grants and speaking fees from Bayer Healthcare, Biogen Idec, Merck Serono, sanofi-aventis/Genzyme, Teva Pharmaceuticals, and Novartis.
Klemens Ruprecht: was supported by the German Ministry of Education and Research (BMBF/KKNMS, Competence Network Multiple Sclerosis) and has received research support from Novartis and Merck Serono as well as speaking fees and travel grants from Guthy Jackson Charitable Foundation, Bayer Healthcare, Biogen Idec, Merck Serono, sanofi-aventis/Genzyme, Teva Pharmaceuticals, Roche and Novartis.
Nadja Borisow: nothing to disclose.
Hiroki Masuda: nothing to disclose.
Ryohei Ohtani: nothing to disclose.
Kyoichi Nomura: nothing to disclose.
Satoshi Kuwabara: serves as an asociate editor of Journal of Neurology, Neurosurgery, and Psychiatry, and an editorual board membaer of Journal of the Neurological Sciences, and received a grant from Japanese Agency of Medical Research and Development.
Edgar Meinl: received honorarium from Roche, Novartis and Genzyme, and grant support from Novartis and Genzyme.
Tania Kümpfel: received travel expenses and personal compensations from Bayer Healthcare, Teva Pharma, Merck, Novartis Pharma, Sanofi-Aventis/Genzyme, Roche and Biogen as well as grant support from Bayer-Schering AG, Novartis and Chugai Pharma, unrelated to this work.
Friedemann Paul: This work is supported by Bundesministerium für Bildung und Forschung Förderkennzeichen 01DR17013. F Paul serves on the scientific advisory board for Novartis; received speaker honoraria and travel funding from Bayer, Novartis, Biogen Idec, Teva, Sanofi-Aventis/Genzyme, Merck Serono, Alexion, Chugai, MedImmune, and Shire; is an academic editor for PLoS ONE; is an associate editor for Neurology® Neuroimmunology & Neuroinflammation; consulted for SanofiGenzyme, Biogen Idec, MedImmune, Shire, and Alexion; and received research support from Bayer, Novartis, Biogen Idec, Teva, Sanofi-Aventis/Genzyme, Alexion, Merck Serono, German Research Council, Werth Stiftung of the City of Cologne, German Ministry of Education and Research, Arthur Arnstein Stiftung Berlin, EU FP7 Framework Program, Arthur Arnstein Foundation Berlin, Guthy Jackson Charitable Foundation, and National Multiple Sclerosis of the USA.
Abstract: P662
Type: Poster Sessions
Abstract Category: Clinical aspects of MS - MS Variants
Background: Although some clinical differences in AQP4-IgG-positive NMOSD between Japan and UK have been reported, the similarity and difference of the MOG-IgG-positive CNS inflammatory disorders between Asian and western countries was hardly investigated.
Goal: To elucidate the similarity and difference of demographic, clinical, laboratory and radiological features of patients with MOG-IgG-positive CNS inflammatory disorders between Japan and Germany.
Methods: We retrospectively collected and compared data of patients seropositive for MOG-IgG who were seen in two Japanese centers (Chiba University Hospital and Saitama medical center) and two German centers (NeuroCure Clinical Research Center, Charité and Ludwig Maximilians University Hospital, Munich). Antibodies to MOG-IgG were tested by cell-based assays.
Results: A total of 80 patients seropositive for MOG-IgG were included. Fifty-one were from Japanese cohort (31 from Chiba and 20 from Saitama) and 29 were from German (14 from Charité and 15 from Munich). Female ratios were similar (62.7% and 62.1% in the Japanese and German cohort, respectively). While all patients were Asian in the Japanese cohort, 82.8%, 6.90%, and 10.3% were Caucasian, Asian, and others, respectively, in the German cohort. Mean (±SD) age at disease onset was similar (40.5±18.0 and 38.0±14.5 in the Japanese and German cohort, respectively). Meanwhile, disease duration was shorter in the Japanese cohort (mean±SD, 2.9±5.1 yrs) than the German cohort (5.7±6.0 yrs) (P< 0.001). Lesion location at disease onset exhibited a similar distribution in both cohorts. The number of total attacks tended to be lower in the Japanese cohort (2.4±2.4 times) than in the German cohort (3.3±2.8 times) (P=0.079), and EDSS score was lower in the Japanese cohort (2.2±1.8) than the German cohort (2.4±1.3) (P< 0.001). To prevent attack, 35.3% and only 7.8% were treated with prednisolone and immunomodulators, respectively, in the Japanese cohort. In contrast, only 6.9% and 48.3% were treated with prednisolone and immunomodulators including rituximab and azathioprine, respectively, in the German cohort. None of the Japanese patients and 7.41% of the German patients had CSF oligoclonal bands, and 11.8% of Japanese patients and 31.0% of German patients had long spinal cord lesions.
Conclusion: Except for a lower total attack number, EDSS, and percentages of patients treated with rituximab/azathioprine, comparatively similar features were seen in the two cohorts.
Disclosure: Masahiro Mori: nothing to disclose.
Alexander U. Brandt: AUB is cofounder and shareholder of Motognosis and Nocturne. He is named as inventor on several patent applications regarding MS serum biomarkers, OCT image analysis and perceptive visual computing.
Joachim Havla: reports a grant for OCT research from the Friedrich-Baur-Stiftung, personal fees and non-financial support from Merck, Novartis, Roche, Bayer Healthcare, Santhera, Biogen, Sanofi Genzyme and non-financial support of the Guthy-Jackson Charitable Foundation, all outside the submitted work.Satoru Tanaka: nothing to disclose.
Jia Liu: nothing to disclose.
Hanna Zimmermann: Received a research grant from Novartis and speaking fees from Teva, unrelated to this work.Satoru Oji: nothing to disclose.
Akiyuki Uzawa: nothing to disclose.
Felix Schmidt: F. Schmidt received speaker honoraria from Genzyme.
Judith Bellmann-Strobl: has received travel grants and speaking fees from Bayer Healthcare, Biogen Idec, Merck Serono, sanofi-aventis/Genzyme, Teva Pharmaceuticals, and Novartis.
Klemens Ruprecht: was supported by the German Ministry of Education and Research (BMBF/KKNMS, Competence Network Multiple Sclerosis) and has received research support from Novartis and Merck Serono as well as speaking fees and travel grants from Guthy Jackson Charitable Foundation, Bayer Healthcare, Biogen Idec, Merck Serono, sanofi-aventis/Genzyme, Teva Pharmaceuticals, Roche and Novartis.
Nadja Borisow: nothing to disclose.
Hiroki Masuda: nothing to disclose.
Ryohei Ohtani: nothing to disclose.
Kyoichi Nomura: nothing to disclose.
Satoshi Kuwabara: serves as an asociate editor of Journal of Neurology, Neurosurgery, and Psychiatry, and an editorual board membaer of Journal of the Neurological Sciences, and received a grant from Japanese Agency of Medical Research and Development.
Edgar Meinl: received honorarium from Roche, Novartis and Genzyme, and grant support from Novartis and Genzyme.
Tania Kümpfel: received travel expenses and personal compensations from Bayer Healthcare, Teva Pharma, Merck, Novartis Pharma, Sanofi-Aventis/Genzyme, Roche and Biogen as well as grant support from Bayer-Schering AG, Novartis and Chugai Pharma, unrelated to this work.
Friedemann Paul: This work is supported by Bundesministerium für Bildung und Forschung Förderkennzeichen 01DR17013. F Paul serves on the scientific advisory board for Novartis; received speaker honoraria and travel funding from Bayer, Novartis, Biogen Idec, Teva, Sanofi-Aventis/Genzyme, Merck Serono, Alexion, Chugai, MedImmune, and Shire; is an academic editor for PLoS ONE; is an associate editor for Neurology® Neuroimmunology & Neuroinflammation; consulted for SanofiGenzyme, Biogen Idec, MedImmune, Shire, and Alexion; and received research support from Bayer, Novartis, Biogen Idec, Teva, Sanofi-Aventis/Genzyme, Alexion, Merck Serono, German Research Council, Werth Stiftung of the City of Cologne, German Ministry of Education and Research, Arthur Arnstein Stiftung Berlin, EU FP7 Framework Program, Arthur Arnstein Foundation Berlin, Guthy Jackson Charitable Foundation, and National Multiple Sclerosis of the USA.