We aimed to evaluate fingolimod effectiveness in a real-world sample of RRMS patients.Ī retrospective, multicentre study in patients treated with fingolimod, whom clinical and radiological data were collected in the 2 years preceding and following the initiation of fingolimod. These results support an in situ effect of GA therapy inside the CNS and suggest potential neuroprotective effects of GA.įingolimod is the first oral agent approved for treatment of relapsing-remitting multiple sclerosis (RRMS). Our data shows that treatment with GA leads to axonal metabolic recovery and protection from sub-lethal axonal injury. NAA/Cr was measured in a large central brain volume of interest (VOI) as well as the normal appearing white matter (NAWM) within the VOI.
A small group of four treatment naïve RRMS patients, electing to remain untreated, served as controls. In a pilot study to investigate the effect of GA on axonal injury, we performed combined brain magnetic resonance imaging (MRI) and MRS studies in 18 treatment naïve RRMS patients initiating therapy with GA at baseline and annually for two years on therapy. Brain proton magnetic resonance spectroscopy (MRS) allows in vivo examination of axonal integrity by quantifying the resonance intensity of the neuronal marker N-acetylaspartate (NAA). Currently, there is paucity ofin vivo human data linking the well-established peripheral immunologic effects of therapy with GA to its potential effects inside the central nervous system (CNS). Glatiramer acetate (GA) is a disease-modifying therapy for relapsing-remitting multiple sclerosis (RRMS) with several putative mechanisms of action. This study shows a low rate of relapses and EDSS progression in RRMS patients on GA for up to 22 years. Adverse events were similar to those reported in short-term clinical trials. Of the 18 remaining patients in October 2004 (average disease duration 23 years), 17% with baseline EDSS scores < 4.0 reached EDSS ≥ 4.0 and 28% with baseline scores < 6.0 reached EDSS ≥ 6.0. Annualized relapse rate decreased to 0.1 ± 0.2 from 2.9 ± 1.4 prestudy ( P < 0.0001). A majority (57%) maintained improved or unchanged EDSS scores. Only 10/28 (36%) patients with baseline EDSS <4.0 had a last observed value ≥ 4.0 and 8/34 (24%) with entry EDSS < 6.0 reached EDSS ≥ 6.0. Mean EDSS score increased 0.9 ± 1.9 from the pretreatment score (3.0 ± 1.8 P = 0.076). At GA initiation, disease durations ranged from 0-20 years (median 6.0 years) and at data cut-off (October 2004), GA therapy duration ranged from 1-22 years (median 12.0 years). Kurtzke expanded disability status scale (EDSS) was measured every six months, relapses were reported at occurrence and patients self-reported adverse events (AEs). To evaluate the safety and efficacy of long-term glatiramer acetate (GA) therapy, 46 patients with relapsing-remitting multiple sclerosis (RRMS) were treated for up to 22 years in an ongoing, open-label study.