Contributions
Abstract: P1125
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - Biomarkers
Background: Risk of progressive multifocal leukoencephalopathy with natalizumab treatment is associated with the presence of anti-JC virus (JCV) antibodies.
Objective: To determine the predictive value of baseline anti-JCV antibody index for long-term stability of anti-JCV antibody status in MS patients.
Methods: MS patients from the MS centre of Medical University of Innsbruck, who had serum sampling for a time period of 4-6 years at intervals of 6±3 months, were included in this retrospective, longitudinal study. Anti-JCV antibody serological status and index were determined by 2-step second-generation anti-JCV antibody assay.
Results: 154 patients were included in this study. Median follow-up time was 63.7 months, with median 11 samples available per patient. At baseline, 111 (72.1%) patients were anti-JCV antibody positive. Baseline anti-JCV antibody index significantly correlated with age (R=0.22, p=0.005); there was no difference with respect to sex, disease duration or previously used disease-modifying treatment. During follow-up anti-JCV antibody status changed from negative to positive or vice versa in 17% of patients. In seronegative patients at baseline, baseline anti-JCV antibody index was significantly lower in those remaining seronegative at follow-up compared to those converting to seropositivity (median 0.16 vs. 0.24, p=0.002). In seropositive patients at baseline, index was higher in those remaining seropositive compared to those reverting to seronegativity (2.6 vs. 0.45, p< 10-7). Baseline anti-JCV antibody index >0.70 predicted stable positive serostatus (sensitivity 94.8%, specificity 94.7%) and < 0.20 stable negative serostatus (sensitivity 61.3%, specificity 97.6%).
Conclusions: In MS patients, anti-JCV antibody index remained relatively stable over 6-year follow-up with annual serostatus change of approximately 3%. Anti-JCV antibody index appears to be a good predictor for future serostatus change.
Disclosure:
The study was supported by Biogen.
H. Hegen has participated in meetings sponsored by, received speaker honoraria or travel funding from Bayer Schering, Biogen, Merck Serono and Novartis, and received honoraria for acting as consultant from Teva Pharmaceuticals Europe.
M. Auer reports no disclosures.
G. Bsteh reports no disclosures.
F. Di Pauli received travel funding and/or speaker honoraria from Biogen Idec and Genzyme.
F. Deisenhammer has participated in meetings sponsored by or received honoraria for acting as an advisor/ speaker for Bayer HealthCare, Biogen, Genzyme-Sanofi, Merck Serono, Novartis, and Teva-Ratiopharm. His institution has received financial support for participation in randomized controlled trials of IFNβ-1b (Betaferon, Bayer Schering Pharma), IFNβ -1a (Avonex, Biogen; Rebif, Merck Serono), glatiramer acetate (Copaxone, Teva Pharmaceuticals), natalizumab (Tysabri, Biogen), and fingolimod (Gilenya, Novartis) in MS.
T. Berger has participated as a consultant in meetings sponsored by and received honoraria (lectures, advisory boards, consultations) in the past 12 months from pharmaceutical companies marketing treatments for multiple sclerosis: Biogen, Merck Serono, Novartis, ratiopharm, Sanofi Aventis, and TEVA. Thomas Berger and his institution have received financial support by unrestricted research grants and clinical trial participation from Alexion, Bayer, Biogen, Merck Serono, Novartis, Octapharma, ratiopharm, Roche, and Sanofi Aventis.
Abstract: P1125
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - Biomarkers
Background: Risk of progressive multifocal leukoencephalopathy with natalizumab treatment is associated with the presence of anti-JC virus (JCV) antibodies.
Objective: To determine the predictive value of baseline anti-JCV antibody index for long-term stability of anti-JCV antibody status in MS patients.
Methods: MS patients from the MS centre of Medical University of Innsbruck, who had serum sampling for a time period of 4-6 years at intervals of 6±3 months, were included in this retrospective, longitudinal study. Anti-JCV antibody serological status and index were determined by 2-step second-generation anti-JCV antibody assay.
Results: 154 patients were included in this study. Median follow-up time was 63.7 months, with median 11 samples available per patient. At baseline, 111 (72.1%) patients were anti-JCV antibody positive. Baseline anti-JCV antibody index significantly correlated with age (R=0.22, p=0.005); there was no difference with respect to sex, disease duration or previously used disease-modifying treatment. During follow-up anti-JCV antibody status changed from negative to positive or vice versa in 17% of patients. In seronegative patients at baseline, baseline anti-JCV antibody index was significantly lower in those remaining seronegative at follow-up compared to those converting to seropositivity (median 0.16 vs. 0.24, p=0.002). In seropositive patients at baseline, index was higher in those remaining seropositive compared to those reverting to seronegativity (2.6 vs. 0.45, p< 10-7). Baseline anti-JCV antibody index >0.70 predicted stable positive serostatus (sensitivity 94.8%, specificity 94.7%) and < 0.20 stable negative serostatus (sensitivity 61.3%, specificity 97.6%).
Conclusions: In MS patients, anti-JCV antibody index remained relatively stable over 6-year follow-up with annual serostatus change of approximately 3%. Anti-JCV antibody index appears to be a good predictor for future serostatus change.
Disclosure:
The study was supported by Biogen.
H. Hegen has participated in meetings sponsored by, received speaker honoraria or travel funding from Bayer Schering, Biogen, Merck Serono and Novartis, and received honoraria for acting as consultant from Teva Pharmaceuticals Europe.
M. Auer reports no disclosures.
G. Bsteh reports no disclosures.
F. Di Pauli received travel funding and/or speaker honoraria from Biogen Idec and Genzyme.
F. Deisenhammer has participated in meetings sponsored by or received honoraria for acting as an advisor/ speaker for Bayer HealthCare, Biogen, Genzyme-Sanofi, Merck Serono, Novartis, and Teva-Ratiopharm. His institution has received financial support for participation in randomized controlled trials of IFNβ-1b (Betaferon, Bayer Schering Pharma), IFNβ -1a (Avonex, Biogen; Rebif, Merck Serono), glatiramer acetate (Copaxone, Teva Pharmaceuticals), natalizumab (Tysabri, Biogen), and fingolimod (Gilenya, Novartis) in MS.
T. Berger has participated as a consultant in meetings sponsored by and received honoraria (lectures, advisory boards, consultations) in the past 12 months from pharmaceutical companies marketing treatments for multiple sclerosis: Biogen, Merck Serono, Novartis, ratiopharm, Sanofi Aventis, and TEVA. Thomas Berger and his institution have received financial support by unrestricted research grants and clinical trial participation from Alexion, Bayer, Biogen, Merck Serono, Novartis, Octapharma, ratiopharm, Roche, and Sanofi Aventis.