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000824547 1001_ $$0P:(DE-HGF)0$$aWidman, Guido$$b0$$eCorresponding author
000824547 245__ $$aTreating a GAD65 Antibody-Associated Limbic Encephalitis with Basiliximab: A Case Study
000824547 260__ $$aLausanne$$bFrontiers Research Foundation$$c2015
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000824547 520__ $$aBackground: 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.
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000824547 7001_ $$0P:(DE-HGF)0$$aGolombeck, Kristin$$b1
000824547 7001_ $$0P:(DE-Juel1)132313$$aHautzel, Hubertus$$b2$$ufzj
000824547 7001_ $$0P:(DE-HGF)0$$aGross, Catharina C.$$b3
000824547 7001_ $$0P:(DE-HGF)0$$aQuesada, Carlos M.$$b4
000824547 7001_ $$0P:(DE-HGF)0$$aWitt, Juri-Alexander$$b5
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000824547 7001_ $$0P:(DE-HGF)0$$aGreschus, Susanne$$b8
000824547 7001_ $$0P:(DE-HGF)0$$aSurges, Rainer$$b9
000824547 7001_ $$0P:(DE-HGF)0$$aHelmstaedter, Christoph$$b10
000824547 7001_ $$0P:(DE-HGF)0$$aWiendl, Heinz$$b11
000824547 7001_ $$0P:(DE-HGF)0$$aMelzer, Nico$$b12
000824547 7001_ $$0P:(DE-HGF)0$$aElger, Christian E.$$b13
000824547 773__ $$0PERI:(DE-600)2564214-5$$a10.3389/fneur.2015.00167$$gVol. 6$$p167$$tFrontiers in neurology$$v6$$x1664-2295$$y2015
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