
Contributions
Abstract: EP1280
Type: ePoster
Abstract Category: Clinical aspects of MS - 1 Diagnosis and differential diagnosis
Background: Serum anti-myelin oligodendrocyte glycoprotein antibodies (MOG-IgG) have been described in different CNS inflammatory disorders. We report longitudinal clinical, MRI and CSF data of a series of patients seronegative for anti-aquaporin-4 antibody (AQP4-IgG) and positive for MOG-IgG.
Methods: A commercial cell-based assay was used to analyze AQP4-IgG, while a live-cells (HEK293A) immunofluorescence assay was used for the detection of MOG-IgG with a positive titer cut-off set at 1:160. Consecutive serum samples referred to Verona University Neuropathology Laboratory for AQP4-IgG/MOG-IgG testing were analyzed between March 2014 and April 2017.
Results: Among 444 tested patients, 22 MOG-IgG positive cases (13 females) were identified. In the 4 weeks before the onset, 10 patients had fever, upper respiratory tract and/or gastrointestinal infection and one received anti-influenza vaccination. Three cases had serological evidence of a recent infection with HSV1, Borrelia Burgdorferi, and Cytomegalovirus. Clinical presentation included optic neuritis in 10 cases, myelitis in 10, both in one and confusion and lethargy in one subject. In addition, cerebellar and/or brainstem signs were present in two patients. Eleven patients experienced relapses. Spinal cord MRI showed short lesions in 11 patients, and longitudinally extensive lesions in 3 subjects. Seven patients had CSF pleocytosis and/or increased protein level, while 4 had CSF oligoclonal bands. Recovery was partial in 17 cases, complete in 3, and absent in 2. Of 6 patients retested for MOG-IgG after 3-168 months from the index event in absence of relapses, 4 resulted negative while 2 were positive, at a lower titer compared to initial test.
Conclusion: Serum MOG-IgG are associated with neurological syndromes usually characterized by involvement of the spinal cord and optic nerve. In rare cases a syndrome resembling viral or autoimmune encephalitis can also be the presenting feature. MOG-IgG are preceded or accompanied by an acute infection and followed by relapses in half of cases. Most patients have neurological sequelae. It is essential to test MOG-IgG in the acute phase since antibody titer tends to decrease in non-relapsing patients.
Disclosure:
Dr.ssa Mariotto is supported by the EAN Research Fellowship.
Dr. Capra received consulting fees from Novartis, Biogen-Idec and lecture fees and/or travel grants from Novartis, Biogen-Idec, Genzyme and Sanofi-Aventis. The Neurological Research Laboratory (Medical University of Innsbruck and Tirol Kliniken) receives payments for antibody assays (AQP4- and anti-neuronal antibodies) and AQP4 antibody validation experiments organized by Euroimmun (Germany).
Research studies of Prof. Markus Reindl are supported by the following research grants: Bridge I project EDNA (FFG and Euroimmun) and “BIG-WIG MS” from the Austrian Federal Ministry of Science, Research and Economy.
Dr. Gajofatto received travel support to attend scientific meeting by Almirall, Biogen, Merck, and Novartis.
Sergio Ferrari, Chiara Mancinelli, Roberto Bombardi, Luigi Zuliani, Marco Zoccarato, Raffaella Tanel, Adriana Bonora, Alberto Polo, Antonino Pavone, Luisa Grazian, Daniela Alberti, Alessia Farinazzo, Kathrin Schanda, Elia Sechi, Daniele Urso, Rachele Delogu, Janes Francesco, Maria Donata Benedetti, Salvatore Monaco have nothing to disclose.
Abstract: EP1280
Type: ePoster
Abstract Category: Clinical aspects of MS - 1 Diagnosis and differential diagnosis
Background: Serum anti-myelin oligodendrocyte glycoprotein antibodies (MOG-IgG) have been described in different CNS inflammatory disorders. We report longitudinal clinical, MRI and CSF data of a series of patients seronegative for anti-aquaporin-4 antibody (AQP4-IgG) and positive for MOG-IgG.
Methods: A commercial cell-based assay was used to analyze AQP4-IgG, while a live-cells (HEK293A) immunofluorescence assay was used for the detection of MOG-IgG with a positive titer cut-off set at 1:160. Consecutive serum samples referred to Verona University Neuropathology Laboratory for AQP4-IgG/MOG-IgG testing were analyzed between March 2014 and April 2017.
Results: Among 444 tested patients, 22 MOG-IgG positive cases (13 females) were identified. In the 4 weeks before the onset, 10 patients had fever, upper respiratory tract and/or gastrointestinal infection and one received anti-influenza vaccination. Three cases had serological evidence of a recent infection with HSV1, Borrelia Burgdorferi, and Cytomegalovirus. Clinical presentation included optic neuritis in 10 cases, myelitis in 10, both in one and confusion and lethargy in one subject. In addition, cerebellar and/or brainstem signs were present in two patients. Eleven patients experienced relapses. Spinal cord MRI showed short lesions in 11 patients, and longitudinally extensive lesions in 3 subjects. Seven patients had CSF pleocytosis and/or increased protein level, while 4 had CSF oligoclonal bands. Recovery was partial in 17 cases, complete in 3, and absent in 2. Of 6 patients retested for MOG-IgG after 3-168 months from the index event in absence of relapses, 4 resulted negative while 2 were positive, at a lower titer compared to initial test.
Conclusion: Serum MOG-IgG are associated with neurological syndromes usually characterized by involvement of the spinal cord and optic nerve. In rare cases a syndrome resembling viral or autoimmune encephalitis can also be the presenting feature. MOG-IgG are preceded or accompanied by an acute infection and followed by relapses in half of cases. Most patients have neurological sequelae. It is essential to test MOG-IgG in the acute phase since antibody titer tends to decrease in non-relapsing patients.
Disclosure:
Dr.ssa Mariotto is supported by the EAN Research Fellowship.
Dr. Capra received consulting fees from Novartis, Biogen-Idec and lecture fees and/or travel grants from Novartis, Biogen-Idec, Genzyme and Sanofi-Aventis. The Neurological Research Laboratory (Medical University of Innsbruck and Tirol Kliniken) receives payments for antibody assays (AQP4- and anti-neuronal antibodies) and AQP4 antibody validation experiments organized by Euroimmun (Germany).
Research studies of Prof. Markus Reindl are supported by the following research grants: Bridge I project EDNA (FFG and Euroimmun) and “BIG-WIG MS” from the Austrian Federal Ministry of Science, Research and Economy.
Dr. Gajofatto received travel support to attend scientific meeting by Almirall, Biogen, Merck, and Novartis.
Sergio Ferrari, Chiara Mancinelli, Roberto Bombardi, Luigi Zuliani, Marco Zoccarato, Raffaella Tanel, Adriana Bonora, Alberto Polo, Antonino Pavone, Luisa Grazian, Daniela Alberti, Alessia Farinazzo, Kathrin Schanda, Elia Sechi, Daniele Urso, Rachele Delogu, Janes Francesco, Maria Donata Benedetti, Salvatore Monaco have nothing to disclose.