Contributions
Abstract: EP1850
Type: ePoster
Abstract Category: Therapy - symptomatic - 35 Enhancing CNS plasticity
Background: New demyelinating lesions may or may not be associated with clinical symptoms depending on the extent of inflammation and individual network plasticity properties. In animal models and relapsing remitting MS, Fingolimod (FTY720) has been proven to reduce neuroinflammation and modulate glutamate-mediated neurotransmission by enhancing synaptic plasticity and compensating for demyelinating damage.
Objective: This study aimed at retrospectively observing whether treatment with FTY720 can attenuate the clinical expression of new lesions.
Methods: 103 patients with relapsing-remitting MS switching for inefficacy from first-line injectable therapy with IFNβ-1a to FTY720 and treated for at least 12 months were included. For each patient, the occurrence of new gadolinium (Gd+) enhancing lesions was evaluated during IFNβ-1a and FTY720 treatment. The number of asymptomatic active lesions was compared for the two treatments.
Results: Treatment with FTY720 was associated with a significantly lower number of Gd+ lesions (p=0.01) and higher rate of asymptomatic lesions compared with IFNβ-1a therapy (88% vs 30.9%, p=< 0.025). Assuming a linear trend between T2 active lesion accrual and annualised relapse rate (ARR), we found that treatment with FTY720 was associated with an increase of 0.04 in the ARR for each new T2 lesion and of 0.06 for each new active lesion against treatment with IFNβ-1a, which was associated with an increase of 0.29 and 0.33, respectively.
Conclusion: FTY720 limits the clinical expression of new Gd+ enhancing lesions, possibly modulating brain network plasticity in patients with suboptimal response to previous immunomodulating treatments, as well as causing an overall reduction in neuroinflammation.
Disclosure: Dr. Signoriello has received personal compensation for activities with Biogen Idec, Roche, Merck Serono, Novartis as a consultant and speaker; has received support for travelling from Biogen Idec, Merck Serono, Novartis, Teva, Roche, Genzyme.
Dr. Landi received funding for traveling from Novartis, Teva, Merck Serono, Almirall, Biogen, Genzyme. She is involved as sub-investigator in clinical trials for Novartis, Merck Serono, Teva, Biogen, Roche.
Dr. Monteleone received consultation fees from Almirall.
Dr. Buttari received funding for traveling from Novartis, Teva, Merck Serono, Almirall, Biogen.
Dr. Marfia received funding for traveling from Teva, Genzyme, Biogen and she is involved as principal investigator in clinical trials for Novartis, Merck Serono, Teva, Biogen, Roche.
Dr. Lus has received personal compensation for activities with Biogen Idec, Merck Serono, Novartis, Sanofi-Aventis Pharmaceuticals, Teva neuroscience as a consultant and speaker; has received research support from Biogen Idec, Merck Serono, and Novartis.
Dr. Centonze acted as an Advisory Board member of Merck-Serono, Teva, Bayer Schering, Biogen, Novartis, Almirall, GW Pharmaceuticals, Genzyme, Roche, and received funding for traveling and honoraria for speaking or consultation fees from Merck Serono, Teva, Novartis, Bayer Schering, Sanofi-aventis, Biogen, Almirall, Genzyme.
The other authors declare that there is no conflict of interest.
Abstract: EP1850
Type: ePoster
Abstract Category: Therapy - symptomatic - 35 Enhancing CNS plasticity
Background: New demyelinating lesions may or may not be associated with clinical symptoms depending on the extent of inflammation and individual network plasticity properties. In animal models and relapsing remitting MS, Fingolimod (FTY720) has been proven to reduce neuroinflammation and modulate glutamate-mediated neurotransmission by enhancing synaptic plasticity and compensating for demyelinating damage.
Objective: This study aimed at retrospectively observing whether treatment with FTY720 can attenuate the clinical expression of new lesions.
Methods: 103 patients with relapsing-remitting MS switching for inefficacy from first-line injectable therapy with IFNβ-1a to FTY720 and treated for at least 12 months were included. For each patient, the occurrence of new gadolinium (Gd+) enhancing lesions was evaluated during IFNβ-1a and FTY720 treatment. The number of asymptomatic active lesions was compared for the two treatments.
Results: Treatment with FTY720 was associated with a significantly lower number of Gd+ lesions (p=0.01) and higher rate of asymptomatic lesions compared with IFNβ-1a therapy (88% vs 30.9%, p=< 0.025). Assuming a linear trend between T2 active lesion accrual and annualised relapse rate (ARR), we found that treatment with FTY720 was associated with an increase of 0.04 in the ARR for each new T2 lesion and of 0.06 for each new active lesion against treatment with IFNβ-1a, which was associated with an increase of 0.29 and 0.33, respectively.
Conclusion: FTY720 limits the clinical expression of new Gd+ enhancing lesions, possibly modulating brain network plasticity in patients with suboptimal response to previous immunomodulating treatments, as well as causing an overall reduction in neuroinflammation.
Disclosure: Dr. Signoriello has received personal compensation for activities with Biogen Idec, Roche, Merck Serono, Novartis as a consultant and speaker; has received support for travelling from Biogen Idec, Merck Serono, Novartis, Teva, Roche, Genzyme.
Dr. Landi received funding for traveling from Novartis, Teva, Merck Serono, Almirall, Biogen, Genzyme. She is involved as sub-investigator in clinical trials for Novartis, Merck Serono, Teva, Biogen, Roche.
Dr. Monteleone received consultation fees from Almirall.
Dr. Buttari received funding for traveling from Novartis, Teva, Merck Serono, Almirall, Biogen.
Dr. Marfia received funding for traveling from Teva, Genzyme, Biogen and she is involved as principal investigator in clinical trials for Novartis, Merck Serono, Teva, Biogen, Roche.
Dr. Lus has received personal compensation for activities with Biogen Idec, Merck Serono, Novartis, Sanofi-Aventis Pharmaceuticals, Teva neuroscience as a consultant and speaker; has received research support from Biogen Idec, Merck Serono, and Novartis.
Dr. Centonze acted as an Advisory Board member of Merck-Serono, Teva, Bayer Schering, Biogen, Novartis, Almirall, GW Pharmaceuticals, Genzyme, Roche, and received funding for traveling and honoraria for speaking or consultation fees from Merck Serono, Teva, Novartis, Bayer Schering, Sanofi-aventis, Biogen, Almirall, Genzyme.
The other authors declare that there is no conflict of interest.