scholarly journals Disease-Modifying Drugs Reduce Cortical Lesion Accumulation and Atrophy Progression in Relapsing-Remitting Multiple Sclerosis: Results from a 48-Month Extension Study

2015 ◽  
Vol 2015 ◽  
pp. 1-5 ◽  
Author(s):  
Francesca Rinaldi ◽  
Paola Perini ◽  
Matteo Atzori ◽  
Alice Favaretto ◽  
Dario Seppi ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Glatiramer Acetate ◽  
Reference Population ◽  
Cortical Atrophy ◽  
Cortical Lesion ◽  
Disease Modifying Drugs ◽  
Relapsing Remitting ◽  
The Mean ◽  
Disease Modifying ◽  
Relapsing Remitting Multiple Sclerosis

Cortical lesions (CLs) and atrophy are pivotal in multiple sclerosis (MS) pathology. This study determined the effect of disease modifying drugs (DMDs) on CL development and cortical atrophy progression in patients with relapsing-remitting MS (RRMS) over 48 months. Patients (n=165) were randomized to sc IFNβ-1a 44 μg, im IFNβ-1a 30 μg, or glatiramer acetate 20 mg. The reference population comprised 50 DMD-untreated patients with RRMS. After 24 months, 43 of the untreated patients switched to DMDs. The four groups of patients were followed up for an additional 24 months. At 48 months the mean standard deviation number of new CLs was significantly lower in patients treated with sc IFNβ-1a (1.4 ± 1.0, range 0–5) compared with im IFNβ-1a (2.3 ± 1.3, range 0–6,P=0.004) and glatiramer acetate (2.2 ± 1.5, range 0–7,P=0.03). Significant reductions in CL accumulation and new white matter and gadolinium-enhancing lesions were also observed in the 43 patients who switched to DMDs after 24 months, compared with the 24 months of no treatment. Concluding, this study confirms that DMDs significantly reduce CL development and cortical atrophy progression compared with no treatment.

Effect of disease-modifying drugs on cortical lesions and atrophy in relapsing–remitting multiple sclerosis

2011 ◽  
Vol 18 (4) ◽  
pp. 418-424 ◽  
Author(s):  
M Calabrese ◽  
V Bernardi ◽  
M Atzori ◽  
I Mattisi ◽  
A Favaretto ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Grey Matter ◽  
Reference Population ◽  
Cortical Atrophy ◽  
Cortical Lesions ◽  
Disease Modifying Drugs ◽  
Relapsing Remitting ◽  
Disease Modifying ◽  
Remitting Multiple Sclerosis ◽  
Relapsing Remitting Multiple Sclerosis

Objective: To measure the effects of disease-modifying drugs (DMDs) on the development of cortical lesions (CL) and cortical atrophy in patients with relapsing–remitting multiple sclerosis (RRMS). Methods: RRMS patients ( n = 165) were randomized to subcutaneous (sc) interferon (IFN) beta-1a (44 mcg three times weekly), intramuscular (im) IFN beta-1a (30 mcg weekly) or glatiramer acetate (GA; 20 mg daily). The reference population comprised 50 untreated patients. Clinical and MRI examinations were performed at baseline, 12 months and 24 months. Results: One hundred and forty-one treated patients completed the study. After 12 months, 37/50 (74%) of untreated patients developed ≥1 new CL (mean 1.6), compared with 30/47 (64%) of im IFN beta-1a-treated patients (mean 1.2, p = 0.021), 24/48 (50%) of GA-treated patients (mean 0.8, p = 0.001) and 12/46 (26%) of sc IFN beta-1a-treated patients (mean 0.4, p < 0.001). After 24 months, ≥1 new CL was observed in 41/50 (82%) of untreated (mean 3.0), 34/47 (72%) of im IFN beta-1a-treated (mean 1.6, p < 0.001), 30/48 (62%) of GA-treated (mean 1.3, p < 0.001) and 24/46 (52%) of sc IFN beta-1a-treated patients (mean 0.8, p < 0.001). Mean grey matter fraction decrease in DMD-treated patients at 24 months ranged from 0.7 to 0.8 versus 1.0 in untreated patients ( p = 0.023). Conclusions: Disease-modifying drugs significantly decreased new CL development and cortical atrophy progression compared with untreated patients, with faster and more pronounced effects seen with sc IFN beta-1a than with im IFN beta-1a or GA.

scholarly journals When to Initiate Disease-Modifying Drugs for Relapsing Remitting Multiple Sclerosis in Adults?

2011 ◽  
Vol 2011 ◽  
pp. 1-11 ◽  
Author(s):  
Mona Alkhawajah ◽  
Joel Oger
Keyword(s):  
Multiple Sclerosis ◽  
Decision Making ◽  
Glatiramer Acetate ◽  
Major Question ◽  
Disease Modifying Drugs ◽  
Relapsing Remitting ◽  
Disease Modifying ◽  
Remitting Multiple Sclerosis ◽  
Relapsing Remitting Multiple Sclerosis

For patients with Relapsing Remitting Multiple Scierosis Beta Interfaerons and Glatiramer Acetate were the first to be licensed for treatment. This review deals with one major question: when to initiate therapy? Through exploring the unique characteristics of the disease and treatement we suggest an approach that should be helpful in the process of decision-making.

Natalizumab strongly suppresses cortical pathology in relapsing–remitting multiple sclerosis

2012 ◽  
Vol 18 (12) ◽  
pp. 1760-1767 ◽  
Author(s):  
F Rinaldi ◽  
M Calabrese ◽  
D Seppi ◽  
M Puthenparampil ◽  
P Perini ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Reference Population ◽  
Cortical Atrophy ◽  
Cortical Lesion ◽  
Cognitive Disability ◽  
Cortical Lesions ◽  
Immunomodulatory Agents ◽  
Relapsing Remitting ◽  
Relevant Role ◽  
Cortical Pathology

Background: Since cortical pathology has been indicated to play a relevant role in the physical and cognitive disability of multiple sclerosis (MS) patients, this study aims to analyze the efficacy of natalizumab in slowing down its progression. Methods: A total of 120 relapsing–remitting MS patients completed a 2-year prospective study: 35 received natalizumab, 50 received interferon beta-1a or glatiramer acetate (immunomodulatory agents - IMA) and 35 remained untreated. Forty healthy subjects constituted the reference population. Clinical and magnetic resonance imaging (MRI) evaluations (including cortical lesions and atrophy) were performed at baseline and after 2 years. Results: Natalizumab significantly reduced accumulation of new cortical lesions (0.2±0.6,range 0–3) compared to immunomodulatory agents (1.3±1.1 togli spazio, range 1–6, p=0.001) and no treatment (2.9±1.5, range 1–8, p<0.001). The percentage of patients with new cortical lesions was also lower in natalizumab-treated patients (20%) compared to IMA-treated and untreated patients (68.0% and 74.2%; p<0.001 for both comparisons). Furthermore, the progression of cortical atrophy was significantly reduced by natalizumab (% change=1.7%) compared to IMA (3.7%, p=0.003) and no therapy (4.6%, p<0.001). Finally, a greater percentage (51.4%) of natalizumab-treated patients remained disease-free (no clinical or MRI evidence of disease activity or progression) compared to IMA-treated (18%, p=0.001) and untreated patients (5.7%, p<0.001). Conclusions: Natalizumab treatment significantly decreases cortical lesion accumulation and cortical atrophy progression in severe relapsing–remitting MS. While supporting the inflammatory origin of cortical lesions, our results highlight the significant impact of natalizumab on cortical pathology.

Residual disability after severe relapse in people with multiple sclerosis treated with disease-modifying therapy

2018 ◽  
Vol 25 (13) ◽  
pp. 1746-1753 ◽  
Author(s):  
Anat Achiron ◽  
Ida Sarova-Pinhas ◽  
David Magalashvili ◽  
Yael Stern ◽  
Aviva Gal ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Neurological Status ◽  
High Rate ◽  
High Dose ◽  
Disease Modifying Drugs ◽  
Disease Modifying Therapy ◽  
Disability Status ◽  
Relapsing Remitting ◽  
Disease Modifying ◽  
Relapsing Remitting Multiple Sclerosis

Background: The rate of post-relapse residual disability in patients with relapsing–remitting multiple sclerosis (RRMS) treated with disease-modifying drugs (DMD) has not been studied. Objective: To assess relapse residual disability in DMD-treated RRMS patients. Methods: We followed DMD-treated RRMS patients presenting with acute relapse who received high-dose steroids. Increases in Expanded Disability Status Scale (EDSS) of at least 2.0, 1.0–1.5 or 0.5 were defined as severe, moderate or mild relapses, respectively. The proportions of patients with post-relapse residual disability defined as the failure to regain pre-relapse neurological status at 1, 4 and 12 months were evaluated. Results: Out of 1672 relapses in DMD-treated RRMS patients, 17% were severe. In patients who presented with a severe relapse, we observed post-relapse residual disability of at least 1.0 EDSS point in 60.1%, 55.9% and 48.2% of patients at 1, 2 and 12 months of follow-up, respectively. Post-relapse residual disability of at least 2.0 EDSS points was observed in 37.4%, 30.7% and 20.7% of patients after 1, 2 and 12 months, respectively. Conclusion: A high rate of incomplete recovery was seen 12 months following severe relapse among RRMS patients and may contribute to the accumulation of long-term disability.

scholarly journals The results of two multicenter, open-label studies assessing efficacy, tolerability and safety of protiramer, a high molecular weight synthetic copolymeric mixture, in patients with relapsing–remitting multiple sclerosis

2008 ◽  
Vol 15 (2) ◽  
pp. 238-243 ◽  
Author(s):  
N De Stefano ◽  
M Filippi ◽  
C Confavreux ◽  
P Vermersch ◽  
M Simu ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Molecular Weight ◽  
Glatiramer Acetate ◽  
Average Molecular Weight ◽  
Weekly Dose ◽  
Pretreatment Period ◽  
Relapsing Remitting ◽  
The Mean ◽  
Remitting Multiple Sclerosis ◽  
Relapsing Remitting Multiple Sclerosis

Objective Two pilot studies were conducted to evaluate safety, tolerability, and efficacy of two doses of Protiramer (TV-5010) in patients with relapsing–remitting multiple sclerosis. Background Both glatiramer acetate and TV-5010 are synthetic copolymers comprised the same four amino acids in a defined molar ratio. TV-5010 has higher average molecular weight than Glatiramer acetate and might be hypothesized that glatiramoids with higher molecular weight might be more immunoreactive than lower molecular weight peptides, thus increasing therapeutic potential and allowing for less frequent dosing. Methods In the two separate studies, after a 10 week pretreatment period, TV-5010 was given subcutaneously once weekly at 15 mg and 30 mg for 36 weeks. The primary end point was a reduction in the number of magnetic resonance imaging active lesions (i.e., T1-weigthed gadolinium-enhancing and new T2-weighted lesions) between the pretreatment period and the end of study. Results Both TV-5010 doses were generally well tolerated. The treatment with TV-5010 at a dose of 15 mg/wk did not show any significant effect. In contrast, in patients treated with at a dose of 30 mg/wk, a significant reduction in the mean number of gadolinium-enhancing (−58.8%; P = 0.0013) and new T2-W (−50%; P = 0.0002) lesions was observed. However, a large decrease in the mean number of both gadolinium-enhancing (−55%) and new T2-W (−40%) lesions during the pretreatment period made difficult the interpretation of the efficacy assessments. Conclusions Further studies are needed to confirm these preliminary data on safety and efficacy of TV-5010 at a weekly dose of 30 mg.

Sign in / Sign up

Export Citation Format

Share Document