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From the Department of Neurology (Dr. Polman), Free University Hospital, Amsterdam, the Netherlands; Department of Neurology (Dr. Kappos), University Hospital, Basel, Switzerland; Schering AG (Drs. Dahlke, Graf, and Bogumil, K. Beckmann), Berlin, Germany; Department of Neurological Science (Dr. Pozzilli), University La Sapienza, Rome, Italy; and Department of Clinical Neurology (Dr. Thompson), Institute of Neurology, London, UK
Address correspondence and reprint requests to Dr. C.H. Polman, Department of Neurology, Vrije Universiteit Medical Center, PO Box 7057, 1007 MB Amsterdam, the Netherlands; e-mail: ch.polman{at}vumc.nl
Background: There is little information regarding the potential of interferon beta (IFNß) to induce or exacerbate autoimmune disease. Existing data from uncontrolled studies are contradictory and do not differentiate between autoimmune dysfunction, which is frequent in patients with multiple sclerosis (MS), and untoward drug effects.
Objective: To evaluate the impact of IFNß on hepatic, thyroid, and other markers of autoimmunity using data from the European placebo-controlled double-blind, multicenter study of IFNß-1b in patients with secondary progressive MS (SPMS).
Methods: Serum samples obtained at baseline and at 6-month intervals for 24 months were analyzed for the following autoantibodies (AAbs): antinuclear (ANA), antimitochondrial (AMA), smooth muscle (SMA), liver kidney microsome (LKM), thyroid microsome (TPO), and human thyroglobulin (TG). AAb status at baseline and during treatment was related to respective laboratory and clinical deviations.
Results: The analysis of AAb data included 355 patients receiving IFNß-1b and 353 receiving placebo. There was no difference between treatment groups in de novo AAb positivity. A greater proportion of women were AAb positive at baseline and during treatment. No association was found between liver enzyme elevations and ANA, AMA, or SMA antibody formation in either treatment group. Laboratory-based thyroid alterations during the study were significantly related to TG/TPO status at baseline but were not associated with IFNß-1b treatment. Adverse events possibly indicative of other diseases with autoimmune links were not associated with respective AAb status.
Conclusion: Interferon beta-1b treatment did not induce autoantibody formation in this population of patients with secondary progressive multiple sclerosis.
Additional material related to this article can be found on the Neurology Web site. Go to www.neurology.org and scroll down the Table of Contents for the March 22 issue to find the title link for this article.
*See the Appendix for a list of Group members.
Drs. Dahlke, Graf, Beckmann, and Bogumil are employees of Schering AG. Drs. Dahlke and Bogumil have equity interest in the company. Drs. Polman, Kappos, Pozzilli, and Thompson have received honoraria from Schering AG for consultancy and delivering lectures at scientific meetings. In addition, their departments have received financial compensation in excess of 10,000 USD from Schering AG for participation in research on interferon beta in multiple sclerosis.
Received May 26, 2004. Accepted in final form November 23, 2004.
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