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Widman, Guido [Author]; Golombeck, Kristin [Author]; Helmstaedter, Christoph [Author]; Wiendl, Heinz [Author]; Melzer, Nico [Author]; Elger, Christian E. [Author]; Hautzel, Hubertus [Author]; Gross, Catharina C. [Author]; Quesada, Carlos M. [Author]; Witt, Juri-Alexander [Author]; Rota Kops, Elena [Author]; Ermert, Johannes [Author]; Greschus, Susanne [Author]; Surges, Rainer [Author]

Treating a GAD65 Antibody-Associated Limbic Encephalitis with Basiliximab: A Case Study

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  • Media type: E-Article
  • Title: Treating a GAD65 Antibody-Associated Limbic Encephalitis with Basiliximab: A Case Study
  • Contributor: Widman, Guido [Author]; Golombeck, Kristin [Author]; Helmstaedter, Christoph [Author]; Wiendl, Heinz [Author]; Melzer, Nico [Author]; Elger, Christian E. [Author]; Hautzel, Hubertus [Author]; Gross, Catharina C. [Author]; Quesada, Carlos M. [Author]; Witt, Juri-Alexander [Author]; Rota Kops, Elena [Author]; Ermert, Johannes [Author]; Greschus, Susanne [Author]; Surges, Rainer [Author]
  • imprint: Frontiers Research Foundation, 2015
  • Published in: Frontiers in neurology 6, 167 (2015). doi:10.3389/fneur.2015.00167
  • Language: English
  • DOI: https://doi.org/10.3389/fneur.2015.00167
  • ISSN: 1664-2295
  • Origination:
  • Footnote: Diese Datenquelle enthält auch Bestandsnachweise, die nicht zu einem Volltext führen.
  • Description: Background: Antibodies (ABs) against the 65-kDa isoform of the intracellular enzymeglutamate decarboxylase (GAD65) have been found in limbic encephalitis (LE) andother neurological conditions. The direct significance of anti-GAD65-ABs for epilepsyis unclear. However, in histological preparations from biopsies of resective epilepsysurgeries, predominantly cytotoxic T-lymphocytes were detected making close contactsto neurons. Activated T-lymphocytes can, in turn, be selectively controlled by therapeuticinterleukin-2 receptor Abs, such as basiliximab.Case presentation: We report of a 25-year-old male patient with epilepsy since theage of 18 and displaying clinical signs of LE and a high titer of GAD65 ABs in cerebro-spinal fluid (CSF) and serum. Monthly, repetitive, intravenous cortisone pulse therapiesthat were initially administered for 6 months failed to improve his condition. Subsequentflow-cytometry analysis of CSF showed especially an increased fraction of activatedHLA-DR+CD8+T-lymphocytes (fCD8+TL) when compared to controls. Thus, a second,intravenous cortisone pulse therapy with an additional basiliximab dose of 20 mg/monthwas started. After 3 months, the fCD8+TL in the CSF normalized; after 6 months, thepsychological impulse-control deficits normalized; and after 11 months the patientwas seizure free. However, 7 weeks later, seizures and, later on, psychological deficitsrecurred and fCD8+TL was once again present in the CSF. Flumazenil PET, magneticresonance imaging-volumetry, and neuropsychological changes during therapy aredescribed.Conclusion: The correlation of the fCD8+TL in the CSF with clinical and paraclinical measures of disease activity combined with the unambiguous response to basiliximabstrongly argues in favor of the putative pathogenic role fCD8+TL in anti-GAD65 LE. The clinical relapse at the end of the observation period might be due to the formation ofhuman anti-drug ABs, a well-known complication of therapy with chimeric ABs.
  • Access State: Open Access