Magnetization transfer ratio in new MS lesions before and during therapy with IFN beta-1a

Citation
M. Kita et al., Magnetization transfer ratio in new MS lesions before and during therapy with IFN beta-1a, NEUROLOGY, 54(9), 2000, pp. 1741-1745
Citations number
34
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
NEUROLOGY
ISSN journal
00283878 → ACNP
Volume
54
Issue
9
Year of publication
2000
Pages
1741 - 1745
Database
ISI
SICI code
0028-3878(20000509)54:9<1741:MTRINM>2.0.ZU;2-W
Abstract
Objective: The authors examined the effect of 6.0 MIU interferon beta-1a (I FN beta-1a) administered IM each week on the evolution of monthly magnetiza tion transfer ratio (MTR) within new gadolinium-enhancing (Gd+) lesions in patients with very early relapsing-remitting (RR) MS. Background: IFN beta is an effective disease-modifying treatment for patients with RRMS. Among o ther effects, it has been shown to decrease the number of new Gd+ and T2-we ighted lesions. MTR is a putative marker for irreversible tissue damage and evolution of MTR within a lesion may reflect recovery of tissue damage. It is not known whether IFN beta-1a affects the recovery phase of lesions. Me thods: Eight untreated patients with RRMS who completed up to 14 monthly br ain MRI sessions elected to initiate treatment with IFN beta-1a. Four out o f eight patients developed new Gd+ lesions during treatment. MTR of lesions at the time of appearance and subsequent rate of change of monthly MTR wer e compared before and after treatment (stratified Mann-Whitney test). Resul ts: The difference between MTR at appearance of 47 new Gd+ lesions before t reatment versus 23 new Gd+ lesions during treatment was not significant. Tw enty-two of 47 new Gd+ lesions before treatment and 11 of 23 new Gd+ lesion s after treatment were monitored for up to 6 months. After appearance of ne w Gd+ lesions, the rate of increase in MTR was faster during therapy (p = 0 .037). Conclusion: MTR abnormalities within new Gd+ lesions evolve at a fas ter rate during treatment with IFN beta-1a than before initiating therapy. This is consistent with the hypothesis that IFN beta-1a promotes resolution of new Gd+ lesions.