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From the Experimental Neuroimaging Section (Drs. Frank and Bash, B. Lewis), Laboratory of Diagnostic Radiology Research, and Neuroimmunology Branch (Drs. Richert and McFarland, R. Stone and T. Howard), National Institute for Neurological Disorders and Stroke, NIH, Uniformed Services University of Health Sciences (Dr. Bash), Bethesda, and Johns Hopkins University (Dr. Calabresi), Baltimore, MD, and Cleveland Clinic (Dr. Stone), OH.
Address correspondence and reprint requests to Dr. J.A. Frank, Experimental Neuroimaging Section, Laboratory of Diagnostic Radiology Research, 10 Center Drive, MSC 1074, Bldg. 10, Rm. B1N256, Bethesda, MD 20892-1074; e-mail: jafrank{at}helix.nih.gov
Objective: To determine the effect of interferon-ß-1b (IFNß-1b) treatment on total contrast-enhancing lesions (CEL), white matter lesion load (WMLL), and cerebral atrophy (CA) in patients with relapsingremitting multiple sclerosis (RRMS) using serial monthly MRI.
Methods: An open-label baseline-vs-treatment crossover trial was conducted with 30 RRMS patients monitored during a 6-month baseline and up to 36 months on treatment with IFNß-1b. Monthly MRI exams and neurologic exams using the Expanded Disability Status Scale (EDSS) were performed.
Results: The percentage changes from baseline for years 1, 2, and 3 on IFNß-1b were as follows: brain volume (BV) = -1.35, -1.48, and -1.68%; CEL = -76.5, -60.1, and -54.7%; WMLL = -12.2, -9.8, and -10.4%. There was no difference in the BV, CEL, or WMLL for between-year comparisons, and the decrease in BV from year 1 to years 2 and 3 was less than the change from baseline to year 1. EDSS did increase (p < 0.001) when comparing the last 3 months of baseline (2.8 ± 2.1) and the last 3 months on IFNß-1b (3.6 ± 2.1). Eleven patients developed neutralizing antibody (NAb) during the study. The effect of IFNß-1b on CEL and WMLL was significantly reduced in NAb+ patients compared with NAb- patients (p < 0.003).
Conclusion: IFNß-1b decreases contrast-enhancing lesions and white matter lesion load over 3 years on therapy and slows the progression in cerebral atrophy during years 2 and 3.
Received July 2, 2003. Accepted in final form November 3, 2003.
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 9 issue to find the title link for this article.
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