THE FOLLOWING ITEMS, selected from news and medical information services, are presented not as an endorsement but for your reading and consideration.
Copaxone Impacts MRI Disease Activity and Burden
In the premiere issue of MS UPDATE, Barry Arnason, MD, reviewed the results of a T^sub 2^ magnetic resonance imaging (MRI) study of glatiramer acetate (Copaxone) in patients with relapsing-remitting multiple sclerosis (MS). A total of 239 patients with very active MS (based on gadolinium [GD]-enhanced lesions on brain MRIs) participated in the initial 9month, double-blind, placebo-controlled trial. The initial results were presented at the recent American Academy of Neurology annual meeting.
The results showed that glatiramer acetate 20 mg per day reduced the total number of enhancing lesions by 29% and the relapse rate by 33% when compared with placebo. However, the positive effects of glatiramer acetate on GD-enhanced lesions were less vigorous than those of the interferon betas (interferon beta 1-a [Avonex] and interferon beta 1-b [Betaseron]) and were not apparent for several months.
These findings suggest that the mechanism of action of glatiramer acetate is different than that of the interferon drugs, which have a rapid, anti-inflammatory, blood-brain barrier stabilizing effect.
All 225 patients who completed the double-blind phase of this study received glatiramer acetate during the 9-month, open-label extension phase. Of these, 217 patients (109 from the original glatiramer acetate group and 108 from the original placebo group) completed the 18-month follow-up study. The data from this portion of the study were presented at the recent European Committee for Treatment and Research in Multiple Sclerosis meeting.
In the group that originally received glatiramer acetate, the inhibitory effect of this agent on MRI activity and T^sub 2^ lesion load remained stable. In the group that originally received placebo, the use of glatiramer acetate was associated with a significant reduction in MRI activity and a stabilization of the T^sub 2^ lesion load. At the end of 18 months, the number of enhancing lesions was almost identical in both groups, independent of whether patients had received glatiramer acetate or placebo during initial double-blind treatment.
Interestingly, the pattern of the MRI findings and the magnitude of the effect observed during open-label treatment in the group originally randomized to placebo were similar to those observed in patients originally treated with glatiramer acetate during the doubleblind phase.
In addition, patients treated with glatiramer acetate in the original study continued to have a reduction in relapse rate, whereas patients who originally received placebo demonstrated a reduction in the relapse rate only during open-label treatment with glatiramer acetate.
This extension study confirms the positive effects of glatiramer acetate demonstrated on GD-enhanced and T^sub 2^ MRI as well as on disease exacerbations in patients with relapsingremitting MS. However, some of the T^sub 2^ MRI damage that occurred during placebo treatment persisted, despite the reduction in relapses and GD-enhanced MRI lesions that were observed during active treatment.
SOURCE: MS UPDATE
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