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DOI: 10.1055/a-1219-7907
Aquaporin-4- und Myelin-Oligodendrozyten-Glykoprotein-Antikörper-assoziierte Optikusneuritis: Diagnose und Therapie
Aquaporin-4 and Myelin Oligodendrocyte Glycoprotein Antibody-Associated Optic Neuritis: Diagnosis and Treatment
Zusammenfassung
Die Optikusneuritis (ON) ist vielfach die erste Manifestation einer AQP4-Antikörper-vermittelten NMOSD (AQP4: Aquaporin-4, NMOSD: Neuromyelitis-optica-Spektrum-Erkrankung, Engl.: neuromyelitis optica spectrum disorders) oder einer Myelin-Oligodendrozyten-Glykoprotein-Antikörper-assoziierten Enzephalomyelitis (MOG-EM; auch MOG antibody associated disorders, MOGAD). Für beide Erkrankungen wurden in den vergangenen Jahren internationale Diagnosekriterien und Empfehlungen zu Indikation und Methodik der serologischen Testung vorgelegt. Seit Kurzem liegen zudem Ergebnisse aus 4 großen, internationalen Phase-III-Studien zur Behandlung der NMOSD vor. Mit dem den Komplementfaktor C5 blockierenden monoklonalen Antikörper Eculizumab wurde 2019 erstmalig ein Medikament zur Langzeitbehandlung der NMOSD, die bislang vornehmlich Off-Label mit Rituximab, Azathioprin und anderen Immunsuppressiva erfolgt, auf dem europäischen Markt zugelassen. Für die erst vor wenigen Jahren erstbeschriebene MOG-EM stehen inzwischen Daten aus mehreren retrospektiven Studien zur Verfügung, die eine Wirksamkeit von Rituximab und anderen Immunsuppressiva in der Schubprophylaxe auch in dieser Indikation nahelegen. Viele der zur Therapie der MS zugelassenen Medikamente sind entweder unwirksam oder können, wie z. B. Interferon-β, eine Verschlechterung des Krankheitsverlaufes bewirken. Beide Erkrankungen werden im Akutstadium mit hochdosierten Glukokortikoiden und Plasmapherese oder Immunadsorption behandelt. Diese Behandlung sollte möglichst rasch nach Symptombeginn eingeleitet werden. Insbesondere die MOG-EM ist durch eine oft ausgeprägte Steroidabhängigkeit gekennzeichnet, die ein langsames Ausschleichen der Steroidtherapie erfordert, und schließt viele Fälle der bislang meist als „idiopathisch“ klassifizierten „chronic relapsing inflammatory optic neuropathy“ (CRION) ein. Unbehandelt kann sowohl die NMOSD- als auch die MOG-EM-assoziierte ON zu schweren, persistierenden und oft bilateralen Visuseinschränkungen bis hin zur Erblindung führen. Beide Erkrankungen verlaufen meist relapsierend. Neben den Sehnerven sind häufig das Myelon sowie der Hirnstamm und, vor allem bei NMO-Patienten, das Dienzephalon betroffen; supratentorielle Hirnläsionen im kranialen MRT sind, anders als früher gedacht, kein Ausschlusskriterium, sondern häufig. In der vorliegenden Arbeit geben wir einen Überblick über Klinik, Diagnostik und Therapie dieser beiden wichtigen Differenzialdiagnosen der MS-assoziierten und idiopathischen ON.
Abstract
Optic neuritis (ON) is a frequent manifestation of aquaporin-4 (AQP4) antibody-mediated neuromyelitis optica spectrum disorders (NMOSD) and myelin oligodendrocyte glycoprotein antibody-associated encephalomyelitis (MOG-EM; also termed MOG antibody-associated disorders, MOGAD). The past few years have seen major advances in the diagnosis and treatment of these two relatively new entities: international diagnostic criteria for NMOSD and MOG-EM have been proposed, improved antibody assays developed, and consensus recommendations on the indications and methodology of serological testing published. Very recently, the results of four phase III trials assessing new treatment options for NMOSD have been presented. With eculizumab, a monoclonal antibody inhibiting complement factor C5, for the first time a relapse-preventing long-term treatment for NMOSD – which has so far mostly been treated off-label with rituximab, azathioprine, and other immunosuppressants – has been approved. Data from recent retrospective studies evaluating treatment responses in MOG-ON suggest that rituximab and other immunosuppressants are effective also in this entity. By contrast, many drugs approved for the treatment of multiple sclerosis (MS) have been found to be either ineffective or to cause disease exacerbation (e.g., interferon-β). Recent studies have shown that not only NMOSD-ON but also MOG-ON usually follows a relapsing course. If left untreated, both disorders can result in severe visual deficiency or blindness, though MOG-ON seems to have a better prognosis overall. Acute attacks are treated with high-dose intravenous methylprednisolone and, in many cases, plasma exchange (PEX) or immunoadsorption (IA). Early use of PEX/IA may prevent persisting visual loss and improve the long-term outcome. Especially MOG-ON has been found to be frequently associated with flare-ups, if steroids are not tapered, and to underlie many cases of “chronic relapsing inflammatory optic neuropathy” (CRION). Both NMOSD-ON and MOG-ON are often associated with simultaneous or consecutive attacks of myelitis and brainstem encephalitis; in contrast to earlier assumptions, supratentorial MRI brain lesions are a common finding and do not preclude the diagnosis. In this article, we review the current knowledge on the clinical presentation, epidemiology, diagnosis, and treatment of these two rare yet important differential diagnoses of both MS-associated ON und idiopathic autoimmune ON.
Schlüsselwörter
Optikusneuritis - Sehnervenentzündung - Neuromyelitis optica - Neuromyelitis-optica-Spektrum-Erkrankungen (NMOSD) - Myelin-Oligodendrozyten-Glykoprotein (MOG) - Aquaporin-4 (AQP4) - Antikörper - MyelitisKey words
optic neuritis - neuromyelitis optica - neuromyelitis optica spectrum disorders (NMOSD) - myelin oligodendrocyte glycoprotein (MOG) - Aquaporin-4 (AQP4) - antibodies - myelitisPublication History
Received: 04 June 2020
Accepted: 30 June 2020
Article published online:
17 November 2020
© 2020. Thieme. All rights reserved.
Georg Thieme Verlag KG
Rüdigerstraße 14, 70469 Stuttgart, Germany
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