Aktuelle Neurologie 2005; 32 - P571
DOI: 10.1055/s-2005-919602

Anti-myelin antibodies and the risk of relapse in patients with a primary demyelinating event

S Rauer 1, B Euler 1, T Berger 1, M Reindl 1
  • 1Freiburg; Innsbruck, A

According to Berger et al. the presence of antimyelin antibodies may predict a clinically definite multiple sclerosis after a first demyelinating event (NEJM 349, 2003). Sera from 45 patients with a clinically isolated syndrome (CIS) and positive oligoclonal bands in cerebrospinal fluid (CSF) were retrospectively tested for the presence of IgM antibodies against both myelin oligodendrocyte glycoprotein (MOG) and myelin basic protein (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. Within 12 months 2 (14%) out of 14 patients of the antibody negative group (MOG/MBP –/–) compared to 7 (47%) out of 15 patients of the antibody positive group (MOG/MBP +/+) revealed CDMS (p=0.068). Albeit not significant this result shows a trend to an increased risk of developing a relapse within 12 months after a CIS in patients who are MOG/MBP positive than compared to antibody negative patients. In addition, we measured 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 one (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; however, it may diminish their clinical value as a predictor of relapses after a CIS. In conclusion, this study only partly could confirm previous data indicating that the presence of anti-myelin antibodies may anticipate clinically definite multiple sclerosis after a first demyelinating event.