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More MS news articles for January 2004

The effects of intramuscular interferon beta-Ia in patients at high risk for development of multiple sclerosis: a post hoc analysis of data from CHAMPS

Clin Ther. 2003 Nov; 25(11): 2865-74
O'Connor P; CHAMPS.
Division of Neurology, St. Michael's Hospital, University of Toronto, Toronto, Ontario, Canada.


In the Controlled High Risk Subjects Avonex Multiple Sclerosis Prevention Study (CHAMPS), intramuscular (IM) interferon beta-1a (IFNbeta-1a) delayed the development of clinically definite multiple sclerosis (CDMS) in patients with a single demyelinating event who had magnetic resonance imaging (MRI) evidence of previous subclinical disease activity (defined as >or=2 T2-weighted hyperintense lesions, 1 of which was periventricular or ovoid, on unenhanced MRI scans).


This post hoc analysis was conducted to assess the effects of IM IFNbeta-1a on delaying the development of CDMS in a subgroup of CHAMPS patients who met a more stringent definition of high risk than was used in that trial.


Patients from the overall CHAMPS population were included in the present analysis if they had >or=9 T2-weighted hyperintense lesions and >or=1 gadolinium-enhanced lesion on the baseline MRI scan.

The cumulative probability of developing CDMS in each treatment group was calculated using the Kaplan-Meier product-limit method and compared using the log-rank test.

The actual proportions of patients who developed CDMS in each treatment group were calculated and compared using the chi-square test.


Ninety-one patients met the more stringent definition of high risk and were included in the subgroup analysis.

Fifty-one patients (56.0%) received IFNbeta-1a 30 microg IM once weekly and 40 (44.0%) received placebo.

Baseline demographic and clinical characteristics were similar between the 2 groups.

Seventy-four patients (81.3%) were female, 80 (87.9%) were white, and the mean age was 33.0 years.

Overall, IM IFNbeta-1a reduced the rate of development of CDMS by 66% compared with the placebo group (P = 0.002, log-rank test) over the 3-year follow-up period.

At 2 years, the Kaplan-Meier estimate of the cumulative probability of developing CDMS was 21% in the IM IFNbeta-1a group and 56% in the placebo group, representing a 63% reduction in risk for CDMS with IFNbeta-1a (P = 0.002, log-rank test).

The results based on the actual proportions of patients developing CDMS were similar to the Kaplan-Meier estimates.


The results of this subgroup analysis are compatible with IM IFNbeta-1a reducing the risk of a second demyelinating event in patients meeting the more stringent definition of high risk.

Although the treatment effect of IFNbeta-1a was significant in both the overall CHAMPS population (44% risk reduction vs placebo; P = 0.002) and in this high-risk subgroup (66%), the results of the present analysis suggest that the magnitude of treatment benefit with IFNbeta-1a may be greater in patients with more disease activity, as measured by MRI parameters.