Format

Send to

Choose Destination
J Neurol. 2016 Mar;263(3):575-82. doi: 10.1007/s00415-015-7991-1. Epub 2016 Jan 25.

Efficacy of glatiramer acetate in neuromyelitis optica spectrum disorder: a multicenter retrospective study.

Author information

1
Department of Neurology, St. Josef Hospital, Ruhr University Bochum, Gudrunstr. 56, 44791, Bochum, Germany.
2
Department of Neurology, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
3
Institute of Clinical Neuroimmunology, Faculty of Medicine, Ludwig Maximilians University, Munich, Germany.
4
Department of Neurology and Stroke, and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany.
5
Department of Neurology, Hannover Medical School, Hannover, Germany.
6
Neurocure Clinical Research Center and Clinical and Experimental Multiple Sclerosis Research Center, Department of Neurology, Charité-Universitätsmedizin Berlin, Berlin, Germany.
7
Experimental and Clinical Research Center, Max Delbrueck Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, Berlin, Germany.
8
Department of Neurology, University of Essen, Essen, Germany.
9
Department of Neurology and Stroke, University of Tübingen, Tübingen, Germany.
10
Department of Neurology, Jena University Hospital, Jena, Germany.
11
Department of Neurology, Klinikum rechts der Isar, Technische Universität München, Munich, Germany.
12
Molecular Neuroimmunology Group, Department of Neurology, University of Heidelberg, Heidelberg, Germany.
13
Department of Neurology, St. Josef Hospital, Ruhr University Bochum, Gudrunstr. 56, 44791, Bochum, Germany. ingo.kleiter@rub.de.

Abstract

Glatiramer acetate (GA) is an approved therapy for relapsing-remitting multiple sclerosis, but its efficacy for the prevention of attacks in neuromyelitis optica spectrum disorder (NMOSD) remains unknown. We did a multicenter retrospective analysis of GA-treated patients with NMOSD, identified through a national registry. Annualized relapse rate and expanded disability status scale (EDSS) were the main outcome measures. We identified 23 GA-treated patients (21 female, 16 aquaporin-4 antibody-positive). GA was given for <6 months in seven patients; reasons for stopping were relapses (n = 3), confirmation of NMOSD (n = 2) and side effects (n = 2). Of 16 patients treated ≥ 6 months with GA (15 female, 11 aquaporin-4 antibody-positive), 14 experienced at least one relapse. There was no reduction in the mean annualized relapse rate in the total group (1.9 ± 1.1 before vs. 1.8 ± 1.4 during GA therapy), as well as in those patients who were aquaporin-4 antibody-positive, or had a history of prior immunotherapy or not. The median EDSS increased (2.5 start vs. 3.5 finish of GA, P < 0.05). GA therapy was discontinued in 15/16 patients; reasons were therapeutic inefficacy in 13 and post-injection skin reactions in two patients. We conclude that GA is not beneficial for preventing attacks in most patients with NMOSD, particularly in aquaporin-4 antibody-positive cases.

KEYWORDS:

Aquaporin-4 antibody; Devic’s disease; Glatiramer acetate; Myelitis; Neuromyelitis optica spectrum disorder; Optic neuritis

PMID:
26810718
DOI:
10.1007/s00415-015-7991-1
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Springer
Loading ...
Support Center