Background: Fingolimod is a modulator of Central and peripheral sphingosine pathways, which is currently approved for treatment of Multiple Sclerosis (MS). In animal models it reduces inflammation, but it is also able to potentiate glutamatergic transmission and synaptic plasticity. We aimed to explore whether Fingolimod is able to modify the clinical expression of new demyelinating lesions with respect to IFNβâ1a in relapsing remitting MS (RRMS) patients suboptimal responders to IFNβâ1a. Methods: 103 patients with RRMS switching for inefficacy from IFNβâ1a to Fingolimod and treated for at least 12 months were included. Annualised Relapse Rate (ARR), EDSS and the number of new brain and spinal gadolinium enhancing (Gd +) and T2 lesions were retrospectively assessed in the whole group during each treatment period. The likelihood of co-occurrence of new Gd + lesions and clinical relapses during IFNβâ1a and Fingolimod treatment was analysed. Results: The mean duration of treatment with IFNβâ1a and Fingolimod was 3.14 (SD 1.6) and 3.22 years (SD 1.1) respectively. Significant reduction of ARR (p <.001), total number of Gd + and T2 lesions (p <.001) was found switching from IFNβâ1a to Fingolimod. Gd + lesions occurring during treatment with Fingolimod were more likely to be asymptomatic compared with IFNβâ1a (88% vs 30.9%, p = <.025). Conclusion: Fingolimod reduces clinical and radiological inflammation in MS. Additionally, it limits the clinical expression of new Gd + lesions, possibly reducing local inflammatory processes and improving brain network plasticity in patients with suboptimal response to IFNβâ1a.
Fingolimod reduces the clinical expression of active demyelinating lesions in MS
Elisabetta, Signoriello;Giuseppe, Di Iorio;Giacomo, Lus;
2018
Abstract
Background: Fingolimod is a modulator of Central and peripheral sphingosine pathways, which is currently approved for treatment of Multiple Sclerosis (MS). In animal models it reduces inflammation, but it is also able to potentiate glutamatergic transmission and synaptic plasticity. We aimed to explore whether Fingolimod is able to modify the clinical expression of new demyelinating lesions with respect to IFNβâ1a in relapsing remitting MS (RRMS) patients suboptimal responders to IFNβâ1a. Methods: 103 patients with RRMS switching for inefficacy from IFNβâ1a to Fingolimod and treated for at least 12 months were included. Annualised Relapse Rate (ARR), EDSS and the number of new brain and spinal gadolinium enhancing (Gd +) and T2 lesions were retrospectively assessed in the whole group during each treatment period. The likelihood of co-occurrence of new Gd + lesions and clinical relapses during IFNβâ1a and Fingolimod treatment was analysed. Results: The mean duration of treatment with IFNβâ1a and Fingolimod was 3.14 (SD 1.6) and 3.22 years (SD 1.1) respectively. Significant reduction of ARR (p <.001), total number of Gd + and T2 lesions (p <.001) was found switching from IFNβâ1a to Fingolimod. Gd + lesions occurring during treatment with Fingolimod were more likely to be asymptomatic compared with IFNβâ1a (88% vs 30.9%, p = <.025). Conclusion: Fingolimod reduces clinical and radiological inflammation in MS. Additionally, it limits the clinical expression of new Gd + lesions, possibly reducing local inflammatory processes and improving brain network plasticity in patients with suboptimal response to IFNβâ1a.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.