Abstract Details

Title Nivolumab-Induced Limbic Encephalitis Associated with Glutamic Acid Decarboxylase 65 Antibodies

Topic Autoimmune Neurology

Presentation(s) P8 - Poster Session 8 (11:45 AM-12:45 PM)

Poster/Presentation
Number 9-003

Objective Immune checkpoint inhibitor (ICI) therapies have improved the overall survival rates of patients with various advanced malignancies. ICIs target and block immune inhibitory receptors, including programmed cell death protein 1 (PD-1), cytotoxic T-lymphocyte associated antigen 4 (CTLA-4) and programmed cell death ligand 1 (PD-L1) expressed by both tumoral cells and healthy tissues. Systemic and neurological immune-related adverse events (irAEs) are well-known side effects of ICI. We report a case of autoimmune limbic encephalitis secondary to the intracellular antigen Glutamic Acid Decarboxylase (GAD) 65 in the context of nivolumab therapy for stage IV melanoma in a 40-year-old female. Treatment included high doses of intravenous methylprednisolone, five sessions of plasma exchange and cyclophosphamide without any improvement.
In contrast to our patient, there are three cases in the literature reporting of ICI induced anti-GAD 65 limbic encephalitis, all having responded to immunotherapy.
We hypothesize that the anti-GAD 65 antibodies in the reported patients may be associated with neuronal cell surface antibodies to GABAa or GABAb receptors vs anti-GAD 65, which are intraneuronal antigens and are known to be resistant to immunotherapy.

Background

Design/Methods na

Results na

Conclusions na

Authors/Disclosures
Al-alya Alsabah, MD PRESENTER	Dr. Alsabah has nothing to disclose.
Robert Altman, MD (Jewish General Hospital)	Dr. Altman has nothing to disclose.

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