Immune reconstitution inflammatory syndrome after withdrawal of Natalizumab?

• Verfasst von: Lenhard, Thorsten [VerfasserIn]
• Verfasst von: Biller, Armin [VerfasserIn]
• Verfasst von: Müller, Wolf C. [VerfasserIn]
• Verfasst von: Metz, Imke [VerfasserIn]
• Verfasst von: Schönberger, J. [VerfasserIn]
• Verfasst von: Wildemann, Brigitte [VerfasserIn]
• Titel: Immune reconstitution inflammatory syndrome after withdrawal of Natalizumab?
• Verf.angabe: T. Lenhard, A. Biller, W. Mueller, I. Metz, J. Schönberger, B. Wildemann
• E-Jahr: 2010
• Jahr: August 30, 2010
• Umfang: 3 S.
• Fussnoten: Gesehen am 13.03.2023
• Titel Quelle: Enthalten in: Neurology
• Ort Quelle: Philadelphia, Pa. : Wolters Kluwer, 1951
• Jahr Quelle: 2010
• Band/Heft Quelle: 75(2010), 9 vom: Aug., Seite 831-833
• ISSN Quelle: 1526-632X
• DOI: doi:10.1212/WNL.0b013e3181f07362
• Datenträger: Online-Ressource
• Sprache: eng
• K10plus-PPN: 1839016159

Abstract

Natalizumab, a humanized monoclonal antibody directed against the very late activating antigen-4, prevents lymphocyte transmigration across endothelium in multiple sclerosis (MS).1 It is undefined whether cessation of treatment carries the risk of disease exacerbation. A postwithdrawal rebound in T2-weighted lesional activity has been described after short-term exposure, whereas another study reported stable findings up to 14 months after discontinuation of natalizumab.2 We report a patient who developed dramatic clinical and radiologic worsening as a consequence of natalizumab withdrawal after prolonged therapy. Several features were reminiscent of an immune reconstitution inflammatory syndrome (IRIS). - - ### Case report. - - A 30-year-old woman had been diagnosed with relapsing-remitting MS in 1999 and had received glatiramer acetate and interferon-β as disease-modifying agents before natalizumab was started as escalating therapy because of continuing relapses (3-4/year; Expanded Disability Status Scale score [EDSS] 5). Natalizumab effectively reduced disease activity to 3 mild clinical events within a treatment period of almost 2 years (22 infusions). A cranial MRI 4 months after institution of therapy showed no new or active lesions (figure, A and B). In November 2008, natalizumab was discontinued because of a wish to have children. At that time, the disease was clinically stable. The patient was able to manage her everyday life with mild support and was employed half-time as an office clerk (EDSS 5). Within 9 weeks after natalizumab withdrawal, she progressively developed high-grade tetraparesis despite repeated IV steroid pulses (methylprednisolone 8.5 g in total). This coincided with multiple new T2-weighted and gadolinium-enhancing lesions in …