Recent progress in maintenance treatment of neuromyelitis optica spectrum disorder
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REVIEW
Recent progress in maintenance treatment of neuromyelitis optica spectrum disorder Trygve Holmøy1,2 · Rune Alexander Høglund1,2 · Zsolt Illes3,4 · Kjell‑Morten Myhr5,6 · Øivind Torkildsen5,6 Received: 14 July 2020 / Revised: 16 September 2020 / Accepted: 17 September 2020 © The Author(s) 2020
Abstract Background Treatment of neuromyelitis optica spectrum disorder (NMOSD) has so far been based on retrospective case series. The results of six randomized clinical trials including five different monoclonal antibodies targeting four molecules and three distinct pathophysiological pathways have recently been published. Methods Literature search on clinical trials and case studies in NMOSD up to July 10. 2020. Results We review mechanism of action, efficacy and side effects, and consequences for reproductive health from traditional immunosuppressants and monoclonal antibodies including rituximab, inebilizumab, eculizumab, tocilizumab and satralizumab. Conclusion In NMOSD patients with antibodies against aquaporin 4, monoclonal antibodies that deplete B cells (rituximab and inebilizumab) or interfere with interleukin 6 signaling (tocilizumab and satralizumab) or complement activation (eculizumab) have superior efficacy compared to placebo. Tocilizumab and rituximab were also superior to azathioprine in head-to-head studies. Rituximab, tocilizumab and to some extent eculizumab have well-known safety profiles for other inflammatory diseases, and rituximab and azathioprine may be safe during pregnancy. Keywords Neuromyelitis optica spectrum disorder · Demyelinating diseases · Treatment · Monoclonal antibodies
Introduction Neuromyelitis optica (NMO) was previously characterized by bilateral optic neuritis and transverse myelitis. After the discovery of antibodies against aquaporin 4 (AQP4-IgG), it was acknowledged that clinical presentation can be more diverse, and the term NMO spectrum disorder (NMOSD) * Trygve Holmøy [email protected] 1
Department of Neurology, Akershus University Hospital, Lørenskog, Norway
2
Institute of Clinical Medicine, University of Oslo, Oslo, Norway
3
Department of Neurology, Odense University Hospital, Odense, Denmark
4
Institute of Clinical Research, University of Southern Denmark, Odense, Denmark
5
Department of Clinical Medicine, University of Bergen, Bergen, Norway
6
Neuro‑SysMed, Department of Neurology, Haukeland University Hospital, Bergen, Norway
was introduced in 2007 [1]. In 2015, the International Panel for NMO Diagnosis decided to only use this unifying term [2]. In patients with AQP4-IgG, the diagnosis only requires one of the six core clinical criteria including optic neuritis and acute myelitis. In patients without AQP-4 IgG, it requires two core clinical characteristics disseminated in space, and at least one of these must be myelitis, optic neuritis, or area postrema syndrome supported by MRI [2]. Some AQP4-IgG-negative NMOSD patients may have antibodies against myelin oligodendrocyte glycoprotein (MOG-IgG). MOG-IgG-associated disease
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