Contributions
Abstract: P587
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - Biomarkers
Background: Acute myelitis could be the clinical presentation of an idiopathic acute transverse myelitis (IATM), a first clinical episode of relapsing-remitting multiple sclerosis (RRMS), considered as a clinically isolated syndrome (CIS) or a subsequent relapse of RRMS.
Objective: To investigate axonal, glial and immune response biomarkers in cerebrospinal fluid (CSF) samples from patients with acute myelitis.
Methods: Levels of NFL, GFAP, YKL-40, MCP-1 and cytokines (IL-6, IL-7, IL-12 and IL-16) were analysed in CSF samples collected during the acute phase of an acute myelitis. Fifteen MS patients (10 CIS and 5 RRMS) and 38 IATM (8 aquaporin-4 negative longitudinally extensive transverse myelitis (LETM) were included. Twenty-four patients suffering from neurological conditions (5 inflammatory and 19 non-inflammatory) were also evaluated.
Results: Levels of NFL, YKL-40 and GFAP were significantly higher in LETM (NFL: 5693 ng/L (3792 - 17264); GFAP: 279 ng/L (108 - 4870); YKL-40: 229 ng/mL (146 - 309) vs CIS (NFL: 1325 ng/L (762 - 2224), p = 0.006; GFAP: 70 ng/L (70 - 82), p = 0.02; YKL-40: 61 ng/mL (39 - 113), p = 0.001). Levels of IL-7 and IL-16 were significantly higher in CIS (IL-7: 5.6 pg/mL (4.1 - 6.8); IL-16: 175 pg/mL (59 - 197) vs IATM (IL-7: 0.2 pg/mL (0.1 - 0.4), p < 0.0001; IL-16: 2.9 pg/mL (1.6 - 5.4), p < 0.0001) and LETM (IL-7: 0.2 pg/mL (0.2 - 0.5), p = 0.001; IL-16: 5.5 pg/mL (3.1 - 18.7), p = 0.001). However, the highest levels were found in RRMS (IL-7: 8.2 pg/mL (5 - 16), IL-16: 248 pg/mL (125 - 295).
Conclusions: Patients with idiopathic LETM showed a higher astrocytic and axonal damage than MS patients. CSF levels of IL-7 and IL-16 were higher in acute myelitis related to MS.
Disclosure: M.Alba Mañé-Martinez: received research support from the Fundació Hospital Universitari de Tarragona Joan XXIII and Fundació Institut d"Investigació Biomèdica de Bellvitge (IDIBELL), and received research support, funding for travel and congress expenses from Biogen Idec, Teva Pharmaceutical Industries LTD, Sanofi-Aventis, Merck Serono, Novartis and Bayer Schering Pharma.
Álvaro Cobo-Calvo: received research support, funding for travel and congress expenses from Biogen Idec, Teva Pharmaceutical Industries LTD, Sanofi-Aventis, Merck Serono, Novartis and Bayer Schering Pharma.
Bob Olsson: nothing to disclose
Laura Bau: received research support, funding for travel and congress expenses from Biogen Idec, Teva Pharmaceutical Industries LTD, Sanofi-Aventis, Merck Serono, Novartis and Bayer Schering Pharma.
Ulf Andreasson: nothing to disclose
Lucia Romero-Pinel: received research support, funding for travel and congress expenses from Biogen Idec, Teva Pharmaceutical Industries LTD, Sanofi-Aventis, Merck Serono, Novartis and Bayer Schering Pharma.
Kaj Blennow: has served on Advisory Boards for Innogenetics, Belgium.
Henrik Zetterberg: nothing to disclose.
Sergio Martinez-Yelamos: received honoraria compensation to participate in Advisory Boards, collaborations as a consultant and scientific communications from Biogen Idec, Teva Pharmaceutical Industries LTD, Sanofi-Aventis, Merck Serono, Novartis and Bayer Schering Pharma, and received research support, funding for travel and congress expenses from Biogen Idec, Teva Pharmaceutical Industries LTD, Sanofi-Aventis, Merck Serono, Novartis and Bayer Schering Pharma.
Abstract: P587
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - Biomarkers
Background: Acute myelitis could be the clinical presentation of an idiopathic acute transverse myelitis (IATM), a first clinical episode of relapsing-remitting multiple sclerosis (RRMS), considered as a clinically isolated syndrome (CIS) or a subsequent relapse of RRMS.
Objective: To investigate axonal, glial and immune response biomarkers in cerebrospinal fluid (CSF) samples from patients with acute myelitis.
Methods: Levels of NFL, GFAP, YKL-40, MCP-1 and cytokines (IL-6, IL-7, IL-12 and IL-16) were analysed in CSF samples collected during the acute phase of an acute myelitis. Fifteen MS patients (10 CIS and 5 RRMS) and 38 IATM (8 aquaporin-4 negative longitudinally extensive transverse myelitis (LETM) were included. Twenty-four patients suffering from neurological conditions (5 inflammatory and 19 non-inflammatory) were also evaluated.
Results: Levels of NFL, YKL-40 and GFAP were significantly higher in LETM (NFL: 5693 ng/L (3792 - 17264); GFAP: 279 ng/L (108 - 4870); YKL-40: 229 ng/mL (146 - 309) vs CIS (NFL: 1325 ng/L (762 - 2224), p = 0.006; GFAP: 70 ng/L (70 - 82), p = 0.02; YKL-40: 61 ng/mL (39 - 113), p = 0.001). Levels of IL-7 and IL-16 were significantly higher in CIS (IL-7: 5.6 pg/mL (4.1 - 6.8); IL-16: 175 pg/mL (59 - 197) vs IATM (IL-7: 0.2 pg/mL (0.1 - 0.4), p < 0.0001; IL-16: 2.9 pg/mL (1.6 - 5.4), p < 0.0001) and LETM (IL-7: 0.2 pg/mL (0.2 - 0.5), p = 0.001; IL-16: 5.5 pg/mL (3.1 - 18.7), p = 0.001). However, the highest levels were found in RRMS (IL-7: 8.2 pg/mL (5 - 16), IL-16: 248 pg/mL (125 - 295).
Conclusions: Patients with idiopathic LETM showed a higher astrocytic and axonal damage than MS patients. CSF levels of IL-7 and IL-16 were higher in acute myelitis related to MS.
Disclosure: M.Alba Mañé-Martinez: received research support from the Fundació Hospital Universitari de Tarragona Joan XXIII and Fundació Institut d"Investigació Biomèdica de Bellvitge (IDIBELL), and received research support, funding for travel and congress expenses from Biogen Idec, Teva Pharmaceutical Industries LTD, Sanofi-Aventis, Merck Serono, Novartis and Bayer Schering Pharma.
Álvaro Cobo-Calvo: received research support, funding for travel and congress expenses from Biogen Idec, Teva Pharmaceutical Industries LTD, Sanofi-Aventis, Merck Serono, Novartis and Bayer Schering Pharma.
Bob Olsson: nothing to disclose
Laura Bau: received research support, funding for travel and congress expenses from Biogen Idec, Teva Pharmaceutical Industries LTD, Sanofi-Aventis, Merck Serono, Novartis and Bayer Schering Pharma.
Ulf Andreasson: nothing to disclose
Lucia Romero-Pinel: received research support, funding for travel and congress expenses from Biogen Idec, Teva Pharmaceutical Industries LTD, Sanofi-Aventis, Merck Serono, Novartis and Bayer Schering Pharma.
Kaj Blennow: has served on Advisory Boards for Innogenetics, Belgium.
Henrik Zetterberg: nothing to disclose.
Sergio Martinez-Yelamos: received honoraria compensation to participate in Advisory Boards, collaborations as a consultant and scientific communications from Biogen Idec, Teva Pharmaceutical Industries LTD, Sanofi-Aventis, Merck Serono, Novartis and Bayer Schering Pharma, and received research support, funding for travel and congress expenses from Biogen Idec, Teva Pharmaceutical Industries LTD, Sanofi-Aventis, Merck Serono, Novartis and Bayer Schering Pharma.