ReviewFrontiers in immunology2025
Anti-gamma-aminobutyric acid B receptor antibody-associated limbic encephalitis in relapsing polychondritis: a rare case report and literature review.
Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Myelin Oligodendrocyte Glycoprotein Antibody-Associated Cerebral Cortical Encephalitis: A Comparative Study With Antibody-Negative and Non-MOG Antibody-Positive Cortical Encephalitis in Chinese Adults.CNS neuroscience & therapeutics · 2026Article
- What should neurologists expect to observe in relapsing polychondritis and VEXAS?Frontiers in immunology · 2026Review
- Recurrent polychondritis complicated with demyelinating encephalopathy and limbic encephalitis: a case report and literature review.Frontiers in medicine · 2026Article
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7 authors.
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Abstract
Relapsing polychondritis (RP) is an immune-mediated disorder that primarily involves the targeting of cartilaginous tissues for inflammation and destruction. Limbic encephalitis (LE) is a rare central nervous system (CNS) manifestation of RP. We report the case of a 39-year-old man who was diagnosed with RP complicated by anti-gamma-aminobutyric acid B receptor (anti-GABABR) antibody-associated LE and presented with recurrent headaches, fever, bilateral auricular swelling, scleral injection, and cognitive impairment. Laboratory tests revealed positive anti-GABABR IgG antibodies in both the serum (titer 1:100) and the cerebrospinal fluid (CSF) (titer 1:1), along with CSF lymphocytic pleocytosis. A brain MRI revealed bilateral frontal and parietal subcortical and periventricular T2-weighted fluid-attenuated inversion recovery (T2-FLAIR) hyperintensities. Immunosuppressive therapy with high-dose methylprednisolone and cyclophosphamide induced rapid symptom resolution, and no relapse occurred during a follow-up period of 1 year. This case expands the spectrum of RP-associated LE, emphasizes the necessity of neuronal autoantibody screening in RP patients with neurological symptoms, and suggests potential pathogenic links involving antigenic cross-reactivity between cartilage and neural tissues and GABAergic metabolism dysregulation.
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