L’induction thérapeutique dans les formes très inflammatoires de sclérose en plaques rémittente récurrente (SEP-RR) est une stratégie intéressante, jusqu’à maintenant limitée à la mitoxantrone.

Nous rapportons l’évolution clinico-radiologique rapidement favorable de trois patientes ayant une forme très active de SEP-RR, dès le premier mois après l’initiation du traitement par natalizumab.

Chez les trois patientes décrites, le natalizumab a montré une efficacité précoce, avec disparition du rehaussement des lésions par le gadolinium sur l’IRM réalisée un mois après l’initiation du traitement. Une stratégie d’induction par natalizumab pourrait être une option intéressante chez les patients ayant une forme agressive de SEP-RR.

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 1month and at 6months 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 1month after the first infusion, and at 6months, 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.