More MS news articles for August 2000

Interferon-Beta-1a Impedes Development of MS Lesions

http://www.medscape.com/reuters/prof/2000/08/08.14/20000814clin013.html

WESTPORT, Aug 14 (Reuters Health) - Weekly injections of interferon-beta-1a (IFN-beta-1a) slow the accumulation of T1 hypointense lesions detected by MRI in the brain of patients with relapsing-remitting multiple sclerosis (MS), according to the results of a multicenter study.

In the study, at baseline, 80 patients treated with IFN-beta-1a were similar to 80 placebo-treated subjects in terms of most major clinical and magnetic resonance characteristics. Dr. Jack H. Simon, of the University of Colorado Health Sciences Center, in Denver, and colleagues with the Multiple Sclerosis Collaborative Research Group report the course of T1 hypointense lesions in these two groups in the July 25th issue of Neurology.

After 2 years, the median increment in T1 hypointense lesions was 124.5 cubic millimeters among placebo-treated patients, compared with 40 cubic millimeters for the IFN-beta-1a-treated subjects. The change from baseline, 29.1%, was significant for the placebo group, but not for the treatment group, which changed by 11.8%.

Dr. Simon and his associates observed "some correlation" between change in T1 hypointense lesions and change in Expanded Disability Status Scale scores and between the lesions and cumulative number of relapses after 2 years.

Although this appears to be the first time that T1 lesions analysis has been used as a formal treatment outcome measure, the increase in T1 lesion volumes paralleled cumulative enhancing lesions, T2 hyperintense lesions, and cerebral atrophy. According to the investigators, the T1 hypointense lesions' more severe damage-specific nature compared with T2 hyperintense lesions suggests that the T1 lesion "may be a robust and important outcome measure."

The investigators conclude that treatment with IFN-beta-1a "brings the most active disease patients to the range of MR outcomes observed in patients with less active disease."

Neurology 2000;55:185-192.