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Previous Volume 356:371-378 January 25, 2007 Number 4 Next

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ABSTRACT

Background Patients with a single episode of neurologic dysfunction and brain magnetic resonance imaging (MRI) scans suggestive of multiple sclerosis are at high risk for clinically definite multiple sclerosis, but the outcome for individual patients is unpredictable. An increased risk of progression to clinically definite multiple sclerosis in patients with serum antibodies against myelin oligodendrocyte glycoprotein (MOG) and myelin basic protein (MBP) has been reported.

Methods We measured serum anti-MOG and anti-MBP IgG and IgM antibodies in 462 patients with a first clinical event suggestive of multiple sclerosis and at least two clinically silent lesions on brain MRI. The patients were participating in a multicenter trial of treatment with interferon beta-1b. Antibodies were assessed by Western blot analysis at baseline, and the results compared with the time and rate of progression to clinically definite multiple sclerosis or a diagnosis of multiple sclerosis as defined by an international panel (the McDonald criteria). Regular visits were scheduled for the assessment of neurologic impairment and for MRI before treatment and at months 3, 6, 9, 12, 18, and 24.

Results No associations were found between the presence of anti-MOG and anti-MBP IgM and IgG antibodies and progression to clinically definite multiple sclerosis or a diagnosis of multiple sclerosis according to the McDonald criteria, either in the entire cohort or in any subgroups of the study population.

Conclusions Serum antibodies against MOG and MBP, as detected by Western blot analysis, are not associated with an increased risk of progression to clinically definite multiple sclerosis in patients who have had a clinically isolated syndrome suggestive of multiple sclerosis.

Source Information

From the Departments of Research and Neurology, University Hospital, Basel, Switzerland (J.K., M.M., R.L., L.K.); Schering, Berlin (C.P., L.B., S.D., R.S.); the Department of Neurology, University Hospital, Bonn, Germany (C.P.); Clinique Neurologique, Rennes, France (G.E.); the Multiple Sclerosis Research Clinic, Ottawa Hospital, Ottawa (M.S.F.); the Department of Neurology, Heinrich-Heine-Universität, Düsseldorf, Germany (H.-P.H.); the Departments of Neurology (C.H.P.) and Neuroradiology (F.B.), Vrije Universiteit Medical Center, Amsterdam; the Institute of Neurology, National Hospital for Neurology and Neurosurgery, London (D.H.M.); and the Clinical Neuroimmunology Unit, Hospital Vall d'Hebron, Barcelona (X.M.).

Drs. Kuhle and Pohl contributed equally to this article.

Address reprint requests to Dr. Kappos at the Outpatient Clinic Neurology–Neurosurgery and Clinical Neuroimmunology Laboratory, Departments of Neurology and Research, University Hospital, Petersgraben 4, CH-4031 Basel, Switzerland, or at lkappos{at}uhbs.ch.

Full Text of this Article

Related Letters:

Lack of Association between Antimyelin Antibodies and Progression to Multiple Sclerosis
Berger T., Reindl M., Kappos L., Kuhle J., Sandbrink R.
Extract | Full Text | PDF  
N Engl J Med 2007; 356:1888-1889, May 3, 2007. Correspondence

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