Is disease activity prior to fingolimod initiation predictive of response? Fingolimod as a "common" first line treatment.


Journal

Revue neurologique
ISSN: 0035-3787
Titre abrégé: Rev Neurol (Paris)
Pays: France
ID NLM: 2984779R

Informations de publication

Date de publication:
Oct 2021
Historique:
received: 28 10 2020
accepted: 27 11 2020
pubmed: 28 2 2021
medline: 13 10 2021
entrez: 27 2 2021
Statut: ppublish

Résumé

In countries where fingolimod is available as first-line therapy without restrictions, we have an opportunity to observe long-term efficacy profile of this drug in treatment-naive patients according to their initial disease activity. We retrospectively analysed the data of RRMS patients treated with FTY, focusing on 2 groups: 17 highly active patients (HA) defined as follows: ≥2 relapses in the year before treatment initiation and either≥1 Gd-enhancing T1 lesion or a significant increase in T2 lesion load from a baseline MRI; and 37 "not highly active" (NHA). We reviewed treatment efficacy (defined as NEDA-3), reasons for discontinuation and treatment tolerance in both groups. Mean follow-up duration was 48.2 months, SD 18.4. Fingolimod efficiently reduced relapses (NHA 90.3% reduction, P<0.001, HA 84.9%, P<0.001), and new Gd enhancing lesions (NHA 85.4% reduction, P=0.019, HA 92.3%, P=0.043). The proportion of patients reaching NEDA-3 status was higher in the NHA group (NHA: 80% at 2 years and 66% at 4 years, HA: 58% at 2 years and 38% at 4 years, P=0.042). Fingolimod was discontinued in 20 cases, mainly because of lack of efficacy (n=15). FTY is efficient in reducing relapses and new Gd enhancing lesions in both HA and NHA patients although the probability of achieving NEDA-3 over time is higher in early-treated treatment-naive NHA patients.

Sections du résumé

BACKGROUND BACKGROUND
In countries where fingolimod is available as first-line therapy without restrictions, we have an opportunity to observe long-term efficacy profile of this drug in treatment-naive patients according to their initial disease activity.
METHODS METHODS
We retrospectively analysed the data of RRMS patients treated with FTY, focusing on 2 groups: 17 highly active patients (HA) defined as follows: ≥2 relapses in the year before treatment initiation and either≥1 Gd-enhancing T1 lesion or a significant increase in T2 lesion load from a baseline MRI; and 37 "not highly active" (NHA). We reviewed treatment efficacy (defined as NEDA-3), reasons for discontinuation and treatment tolerance in both groups.
RESULTS RESULTS
Mean follow-up duration was 48.2 months, SD 18.4. Fingolimod efficiently reduced relapses (NHA 90.3% reduction, P<0.001, HA 84.9%, P<0.001), and new Gd enhancing lesions (NHA 85.4% reduction, P=0.019, HA 92.3%, P=0.043). The proportion of patients reaching NEDA-3 status was higher in the NHA group (NHA: 80% at 2 years and 66% at 4 years, HA: 58% at 2 years and 38% at 4 years, P=0.042). Fingolimod was discontinued in 20 cases, mainly because of lack of efficacy (n=15).
CONCLUSIONS CONCLUSIONS
FTY is efficient in reducing relapses and new Gd enhancing lesions in both HA and NHA patients although the probability of achieving NEDA-3 over time is higher in early-treated treatment-naive NHA patients.

Identifiants

pubmed: 33637293
pii: S0035-3787(21)00040-0
doi: 10.1016/j.neurol.2020.11.009
pii:
doi:

Substances chimiques

Immunosuppressive Agents 0
Fingolimod Hydrochloride G926EC510T

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

935-940

Informations de copyright

Copyright © 2021 The Authors. Published by Elsevier Masson SAS.. All rights reserved.

Auteurs

V Pantazou (V)

Division of Neurology, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Rue du Bugnon 46, 1011 Lausanne, Switzerland; Laboratories of Neuroimmunology, Neuroscience Research Center , Lausanne University, Epalinges, Switzerland.

R Du Pasquier (R)

Division of Neurology, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Rue du Bugnon 46, 1011 Lausanne, Switzerland; Laboratories of Neuroimmunology, Neuroscience Research Center , Lausanne University, Epalinges, Switzerland.

C Pot (C)

Division of Neurology, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Rue du Bugnon 46, 1011 Lausanne, Switzerland; Laboratories of Neuroimmunology, Neuroscience Research Center , Lausanne University, Epalinges, Switzerland.

G Le Goff (G)

Division of Neurology, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Rue du Bugnon 46, 1011 Lausanne, Switzerland.

M Théaudin (M)

Division of Neurology, Department of Clinical Neurosciences, Lausanne University Hospital and University of Lausanne, Rue du Bugnon 46, 1011 Lausanne, Switzerland. Electronic address: marie.theaudin@chuv.ch.

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