Contributions
Abstract: P262
Type: Poster
Abstract Category: Clinical aspects of MS - Diagnosis and differential diagnosis
Background: Considerable efforts have been devoted to the search of diagnostic serological and cerebrospinal fluid (CSF) markers of inflammatory demyelinating CNS disorders. Recently, the presence of circulating anti-myelin oligodendrocyte glycoprotein antibodies (MOG-abs) has been described in patients with multiple sclerosis (MS), acute disseminated encephalomyelitis, acute myelitis (AM), optic neuritis (ON), and neuromyelitis optica spectrum disorders (NMOSD), particularly in anti-aquaporin
4 antibody (AQP4-ab) seronegative cases. To date, several areas of uncertainty still remain regarding the actual significance of MOG-abs detection, including the appropriate clinical setting in which the test is indicated, in addition to its diagnostic and predictive value.
Goals:
- To assess serum MOG-abs status of AQP4-ab negative patients with an initial suspect of NMOSD
- To analyze the association between the presence of MOG-abs and clinical, MRI, and laboratory findings
- To determine a MOG-abs positive clinically significant titre cut-off
- To clarify if MOG-abs positivity is associated with a distinct demyelinating condition
Methods: We identified stored serum samples of patients with suspected NMOSD sent to Verona Neuropathology laboratory between 03/2014 and 03/2016 for AQP4-abs assay resulting to be negative. Live-cells (HEK293A) staining immunofluorescence assay was used for the detection of MOG-abs. We retrospectively collected and analyzed clinical, MRI and CSF data of tested patients and divided them in five groups based on the final diagnosis:
1) NMOSD;
2) isolated ON and/or AM (ION/AM);
3) MS or clinically isolated syndrome (CIS) suggestive of MS;
4) other inflammatory CNS disorders;
5) non-inflammatory conditions.
Results: We analyzed the samples of 157 eligible patients with the following final diagnosis: 4 NMOSD, 75 ION/AM, 58 CIS/MS, 13 other inflammatory disorders, and 7 non-inflammatory conditions. Of these, 29 were MOG-abs positive with 1:20 titre in 9, 1:40 in 10, 1:80 in 5, and ≥1:160 in 5 cases. All patients with a titre ≥1:160 had a final diagnosis of ION/AM while patients with lower titres had CIS/MS in 10 cases, ION/AM in 13, and another inflammatory disorder in one.
Conclusions: MOG-abs testing should be included in the diagnostic evaluation of patients with ON and/or AM who are anti-AQP4 abs negative, as high titre positivity seems to identify a subgroup of cases not related to MS, NMOSD, or other definite inflammatory disorders.
Disclosure:
S. Mariotto, S. Ferrari, S. Monaco, M.D. Benedetti, M. Turatti, D. Alberti, A. Farinazzo, R. Capra, L. Deotto, A. Bonora, A. Pavone, A. Polo, M.R. Bianchi, R. Bombardi, K. Shanda: nothing to disclose
M. Calabrese: Advisory Board membership: Bayer-Schering, Genzyme, Biogen Idec. Payment for development of educational presentations including service on speakers bureaus: Biogen-Elan, Genzyme, TEVA, Bayer-Schering. Travel/accomodation expenses covered or reimbursed: Novartis Pharma, Genzyme, Biogen Idec, Merck Serono, Bayer-Schering, TEVA
N. De Rossi: presentations for Biogen, TEVA; travel support to attend scientific meetings by Biogen, Merck Serono, TEVA
M. Cadaldini: travel support to attend scientific meetings by Merck Serono, Bayer, Genzyme, TEVA
M. Reindl: funded by the project BIG WIG MS from the Austrian Federal Ministery of Sciences
A. Gajofatto:travel support to attend scientific meetings by Almirall, Biogen, Merck, and Novartis
Abstract: P262
Type: Poster
Abstract Category: Clinical aspects of MS - Diagnosis and differential diagnosis
Background: Considerable efforts have been devoted to the search of diagnostic serological and cerebrospinal fluid (CSF) markers of inflammatory demyelinating CNS disorders. Recently, the presence of circulating anti-myelin oligodendrocyte glycoprotein antibodies (MOG-abs) has been described in patients with multiple sclerosis (MS), acute disseminated encephalomyelitis, acute myelitis (AM), optic neuritis (ON), and neuromyelitis optica spectrum disorders (NMOSD), particularly in anti-aquaporin
4 antibody (AQP4-ab) seronegative cases. To date, several areas of uncertainty still remain regarding the actual significance of MOG-abs detection, including the appropriate clinical setting in which the test is indicated, in addition to its diagnostic and predictive value.
Goals:
- To assess serum MOG-abs status of AQP4-ab negative patients with an initial suspect of NMOSD
- To analyze the association between the presence of MOG-abs and clinical, MRI, and laboratory findings
- To determine a MOG-abs positive clinically significant titre cut-off
- To clarify if MOG-abs positivity is associated with a distinct demyelinating condition
Methods: We identified stored serum samples of patients with suspected NMOSD sent to Verona Neuropathology laboratory between 03/2014 and 03/2016 for AQP4-abs assay resulting to be negative. Live-cells (HEK293A) staining immunofluorescence assay was used for the detection of MOG-abs. We retrospectively collected and analyzed clinical, MRI and CSF data of tested patients and divided them in five groups based on the final diagnosis:
1) NMOSD;
2) isolated ON and/or AM (ION/AM);
3) MS or clinically isolated syndrome (CIS) suggestive of MS;
4) other inflammatory CNS disorders;
5) non-inflammatory conditions.
Results: We analyzed the samples of 157 eligible patients with the following final diagnosis: 4 NMOSD, 75 ION/AM, 58 CIS/MS, 13 other inflammatory disorders, and 7 non-inflammatory conditions. Of these, 29 were MOG-abs positive with 1:20 titre in 9, 1:40 in 10, 1:80 in 5, and ≥1:160 in 5 cases. All patients with a titre ≥1:160 had a final diagnosis of ION/AM while patients with lower titres had CIS/MS in 10 cases, ION/AM in 13, and another inflammatory disorder in one.
Conclusions: MOG-abs testing should be included in the diagnostic evaluation of patients with ON and/or AM who are anti-AQP4 abs negative, as high titre positivity seems to identify a subgroup of cases not related to MS, NMOSD, or other definite inflammatory disorders.
Disclosure:
S. Mariotto, S. Ferrari, S. Monaco, M.D. Benedetti, M. Turatti, D. Alberti, A. Farinazzo, R. Capra, L. Deotto, A. Bonora, A. Pavone, A. Polo, M.R. Bianchi, R. Bombardi, K. Shanda: nothing to disclose
M. Calabrese: Advisory Board membership: Bayer-Schering, Genzyme, Biogen Idec. Payment for development of educational presentations including service on speakers bureaus: Biogen-Elan, Genzyme, TEVA, Bayer-Schering. Travel/accomodation expenses covered or reimbursed: Novartis Pharma, Genzyme, Biogen Idec, Merck Serono, Bayer-Schering, TEVA
N. De Rossi: presentations for Biogen, TEVA; travel support to attend scientific meetings by Biogen, Merck Serono, TEVA
M. Cadaldini: travel support to attend scientific meetings by Merck Serono, Bayer, Genzyme, TEVA
M. Reindl: funded by the project BIG WIG MS from the Austrian Federal Ministery of Sciences
A. Gajofatto:travel support to attend scientific meetings by Almirall, Biogen, Merck, and Novartis