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1. Mineralocorticoid Receptor Signaling in Peripheral Blood Cells in Patients with Multiple Sclerosis.

Author

Küstermann, Franziska, Busse, Kathy, Orthgieß, Johannes, Stoppe, Muriel, Haars, Sarah, and Then Bergh, Florian

Subjects
MONONUCLEAR leukocytes, GENE expression, MINERALOCORTICOID receptors, GENETIC regulation, TREATMENT effectiveness
Abstract

Multiple sclerosis (MS) is associated with alterations in neuroendocrine function, primarily the hypothalamic–pituitary–adrenal axis, including lower expression of the glucocorticoid receptor (GR) and its target genes in peripheral blood mononuclear cells (PBMC) or full blood. We previously found reduced mineralocorticoid receptor (MR) expression in MS patients' peripheral blood. MS is being treated with a widening variety of disease-modifying treatments (DMT), some of which have similar efficacy but different mechanisms of action; body-fluid biomarkers to support the choice of the optimal initial DMT and/or to indicate an unsatisfactory response before clinical activity are unavailable. Using cell culture of volunteers' PBMCs and subsequent gene expression analysis (microarray and qPCR validation), we identified the mRNA expression of OTUD1 to represent MR signaling. The MR and MR target gene expression levels were then measured in full blood samples. In 119 MS (or CIS) patients, the expression of both MR and OTUD1 was lower than in 42 controls. The expression pattern was related to treatment, with the MR expression being particularly low in patients treated with fingolimod. While MR signaling may be involved in the therapeutic effects of some disease-modifying treatments, MR and OTUD1 expression can complement the neuroendocrine assessment of MS disease course. If confirmed, such assessment may support clinical decision-making. [ABSTRACT FROM AUTHOR]

Published
2024
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3. Rituximab Treatment and Long-term Outcome of Patients With Autoimmune Encephalitis

Author

Thaler, Franziska S, Zimmermann, Luise, Urbanek, Christian, Pfefferkorn, Thomas, Philipsen, Alexandra, Piepgras, Johannes, von Podewils, Felix, Priller, Josef, Pröbstel, Anne-Katrin, Helena Rau, Johanna Maria, Räuber, Saskia Jania, Reimann, Gernot, Reinecke, Raphael, Sommer, Claudia, Ringelstein, Marius, Rohner, Hendrik, Rosenow, Felix, Rostásy, Kevin, Rüegg, Stephan, Schaumberg, Jens, Schmidt, Jens, Schmütz, Ina-Isabelle, Schreiber, Stephan, Schreyer, Gesa, Doppler, Kathrin, Schröder, Ina, Schuster, Simon, Seidel, Günter, Senel, Makbule, Siebenbrodt, Kai, Stammel, Oliver, Stangel, Martin, Stolze, Henning, Stoppe, Muriel, Storm Van's Gravesande, Karin, Penner, Loana, Sybre, Steffen, Tauber, Simone, Bergh, Florian Then, Trebst, Corinna, Trendelenburg, George, Trollmann, Regina, Tumani, Hayrettin, Türedi, Methab, von Mering, Matthias, Wagner, Judith, Lewerenz, Jan, Weissert, Robert, Wiendl, Heinz, Wildemann, Brigitte, Witt, Karsten, Wöpking, Sigrid, Wunderlich, Benjamin, Zieger, Lara, Roessling, Rosa, Finke, Carsten, Prüß, Harald, Melzer, Nico, Wandinger, Klaus-Peter, Kammermeier, Stefan, Leypoldt, Frank, Kümpfel, Tania, Encephalitis, German Network for Research on Autoimmune, Adelmann, Michael, Appeltshauser, Luise, Ayzenberg, Ilya, Baade-Büttner, Carolin, van Baalen, Andreas, Baatz, Sebastian, Balint, Bettina, Strippel, Christine, Bauer, Sebastian, Baumgartner, Annette, Benesch, Sonka, Berger, Robert, Berning, Sascha, Bernsen, Sarah, Bien, Christian, Bien, Corinna, Binder, Andreas, Bittner, Stefan, Bittner, Daniel, Blaes, Franz, Blaschek, Astrid, Dargvainiene, Justina, Dik, Andre, Dreesmann, Mona, Ebinger, Friedrich, Edelhoff, Lena, Ehrlich, Sven, Eisenhut, Katharina, Kraft, Andrea, Endres, Dominique, Entscheva, Marina, Faiss, Jürgen Hartmut, Fazeli, Walid Ahmad, Finke, Alexander, Fitzner, Dirk, Flotats-Bastardas, Marina, Paul, Friedemann, Friese, Manuel, Gallus, Marco, Sühs, Kurt-Wolfram, Gebhard, Marcel, Geis, Christian, Gorsler, Anna, Grau, Armin, Grauer, Oliver, Groß, Catharina, Gül, Halime, Handreka, Robert, Hansen, Niels, Häusler, Martin, Wickel, Jonathan, Havla, Joachim, Ha-Yeun, Chung, Heide, Wolfgang, Held, Valentin, Hellwig, Kerstin, Hillebrand, Philip, Hoffmann, Frank, Oy, Ulrich Hofstadt-van, Ismail, Fatme Seval, Jansen, Martina, Kaufmann, Max, Kellinghaus, Christoph, Knake, Susanne, Körtvelyessy, Peter, Kovac, Stjepana, Krämer, Markus, Krogias, Christos, Lehrich, Christoph, Linsa, Andreas, Lünemann, Jan, Markewitz, Robert, Malter, Michael, Melzer, Kristin Stefanie, Menge, Til, Meuth, Sven, Meyer Zu Hörste, Gerd, Mönig, Constanze, Mono, Marie-Luise, Nagel, Michael, Neumann-Haefelin, Tobias, and Obrocki, Jost

Subjects
Adult, Male, medicine.medical_specialty, immunology [Anti-N-Methyl-D-Aspartate Receptor Encephalitis], anti-GAD65 autoantibody, Disease, Real world evidence, Gastroenterology, immunology [Autoimmune Diseases of the Nervous System], pharmacology [Immunosuppressive Agents], anti-CASPR2 autoantibody, administration & dosage [Rituximab], Modified Rankin Scale, Internal medicine, Outcome Assessment, Health Care, immunology [Autoantibodies], Humans, Medicine, In patient, ddc:610, Registries, immunology [Encephalitis], anti-NMDA receptor autoantibody, Aged, Autoantibodies, Autoimmune encephalitis, pharmacology [Rituximab], biology, business.industry, Middle Aged, drug therapy [Encephalitis], Neurology, Cohort, administration & dosage [Immunosuppressive Agents], anti-leucine-rich glioma-inactivated 1 autoantibody, biology.protein, drug therapy [Autoimmune Diseases of the Nervous System], Female, Rituximab, Neurology (clinical), Antibody, drug therapy [Anti-N-Methyl-D-Aspartate Receptor Encephalitis], business, Immunosuppressive Agents, Follow-Up Studies, medicine.drug
Abstract

Background and ObjectivesTo determine the real-world use of rituximab in autoimmune encephalitis (AE) and to correlate rituximab treatment with the long-term outcome.MethodsPatients with NMDA receptor (NMDAR)-AE, leucine-rich glioma-inactivated-1 (LGI1)- AE, contactin-associated protein-like-2 (CASPR2)-AE, or glutamic acid decarboxylase 65 (GAD65) disease from the GErman Network for Research on AuToimmune Encephalitis who had received at least 1 rituximab dose and a control cohort of non–rituximab-treated patients were analyzed retrospectively.ResultsOf the 358 patients, 163 (46%) received rituximab (NMDAR-AE: 57%, CASPR2-AE: 44%, LGI1-AE: 43%, and GAD65 disease: 37%). Rituximab treatment was initiated significantly earlier in NMDAR- and LGI1-AE (median: 54 and 155 days from disease onset) compared with CASPR2-AE or GAD65 disease (median: 632 and 1,209 days). Modified Rankin Scale (mRS) scores improved significantly in patients with NMDAR-AE, both with and without rituximab treatment. Although being more severely affected at baseline, rituximab-treated patients with NMDAR-AE more frequently reached independent living (mRS score ≤2) (94% vs 88%). In LGI1-AE, rituximab-treated and nontreated patients improved, whereas in CASPR2-AE, only rituximab-treated patients improved significantly. No improvement was observed in patients with GAD65 disease. A significant reduction of the relapse rate was observed in rituximab-treated patients (5% vs 13%). Detection of NMDAR antibodies was significantly associated with mRS score improvement. A favorable outcome was also observed with early treatment initiation.DiscussionWe provide real-world data on immunosuppressive treatments with a focus on rituximab treatment for patients with AE in Germany. We suggest that early and short-term rituximab therapy might be an effective and safe treatment option in most patients with NMDAR-, LGI1-, and CASPR2-AE.Class of EvidenceThis study provides Class IV evidence that rituximab is an effective treatment for some types of AE.

Published
2021

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