Journal
JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY
Volume 77, Issue 6, Pages 739-742Publisher
B M J PUBLISHING GROUP
DOI: 10.1136/jnnp.2005.077784
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Aim: To investigate whether the presence of serum antibodies against myelin oligodendrocyte glycoprotein (MOG) and myelin basic protein (MBP) in patients with a clinically isolated syndrome (CIS) predicts the interval to develop more frequently and earlier a first relapse (clinically definite multiple sclerosis: CDMS) than seronegative patients. Methods: Sera from 45 patients with a CIS and positive intrathecal IgG-synthesis were retrospectively tested for the presence of IgM antibodies against both MOG and MBP. Antibodies were detected by immunoblot using recombinant MOG (1-125) and human MBP antigen preparations. Clinical follow ups were performed retrospectively by telephone interviews and documented neurological examination. Results: Using the Cox proportional hazards model there was no significant increased risk for developing CDMS in anti-MOG and anti-MBP positive patients compared with negative. However regarding the median of the time span between CIS and CDMS over the whole follow up, antibody positive patients (MOG/MBP+/+) developed significantly earlier relapses (median 5.5 months (range 3-20)) than the antibody negative ones (median 25.0 months (range 7-43); p < 0.006). On testing sera from 56 apparently healthy students, quite high frequencies of anti-MOG and anti-MBP antibodies (21% and 28% respectively) were detected. This limited specificity of anti-MOG and anti-MBP antibodies has been seen earlier and restricts their diagnostic relevance in MS despite their role as a predictor of relapses after a CIS. Conclusions: This study confirms previous data only in a subanalysis indicating that patients with positive anti-MOG/MBP antibodies develop earlier relapses than patients who are antibody negative. However, the authors could not verify that the presence of these antibodies anticipates the overall risk of developing CDMS-according to study criteria-after a first demyelinating event within the study period of 21-106 months (mean 60 (SD 25)).
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