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- W1992460922 abstract "Current treatment options for first-line immunotherapy in relapsing-remitting multiple sclerosis (MS) are recombinant interferon-β and glatiramer acetate. However, these therapies are only partially effective and certain patients may fail to respond. For this reason, it is important to elaborate alternative treatment strategies. Induction therapy represents a more aggressive approach in which powerful drugs are used right from the beginning to tackle the disease process hard and early. Natalizumab is a powerful monoclonal antibody approved for the treatment of relapsing-remitting MS and is known to silence disease activity.We describe here the early outcome at 1 month and at 6 months of three patients treated with natalizumab for relapsing-remitting MS.All three patients had a high disease activity before the initiation of natalizumab, with 4, 8 and 5 gadolinium-enhancing lesions on brain MRI respectively. On the MRI scans made at 1 month after the first infusion, and at 6 months, there was no more gadolinium-enhancement and no new T2-lesion. Clinically, they did not experience any relapse.In these three cases, natalizumab showed a dramatic efficacy: the patients became disease activity free right from the first infusion. To our knowledge, natalizumab is not classically used as an induction therapy, unlike mitoxantrone. However, this treatment has potential hematological and cardiac toxicity and its use can be limited. Thus, in JC virus negative patients, natalizumab could be an interesting alternative treatment.Our report suggests that induction strategy with natalizumab may be applicable in patients with aggressive multiple sclerosis. A study of more similar cases may be interesting to confirm these preliminary results." @default.
- W1992460922 created "2016-06-24" @default.
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- W1992460922 date "2014-01-01" @default.
- W1992460922 modified "2023-10-01" @default.
- W1992460922 title "Traitement d’induction dans la sclérose en plaques : place du natalizumab" @default.
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- W1992460922 doi "https://doi.org/10.1016/j.neurol.2013.06.004" @default.
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