Frontiers in immunology · 2026
Case Report: Recurrent anti-glutamic acid decarboxylase 65 antibody-associated encephalitis in a child.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
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Tian Pingping, Li Juan, Liu Yong, Ding Xiufang, Zhang Hongwei
Аннотация
OBJECTIVE: To explore the clinical characteristics of recurrent pediatric anti-glutamic acid decarboxylase 65 (GAD65) antibody-associated autoimmune encephalitis and to enhance understanding of this disease.
METHODS: We conducted a retrospective analysis of the clinical data of a pediatric patient with recurrent anti-GAD65 antibody-associated encephalitis.
RESULTS: The patient was a 7-year-old boy who presented with slurred speech and epileptic seizures in June 2024. Brain magnetic resonance imaging(MRI)demonstrated multiple abnormal signal intensities in the bilateral frontal, temporal, parietal, and occipital cortical regions. Electroencephalogram (EEG) revealed focal epileptiform discharges and status epilepticus. His clinical condition improved following treatment with methylprednisolone and intravenous immunoglobulin. In November 2024, the child presented with a decline in mental status, generalized weakness, increased somnolence, reduced mobility and social interaction, gait instability, as well as accompanying headache and vomiting. Brain MRI demonstrated inflammatory involvement of the right cerebellar hemisphere. The cerebrospinal fluid (CSF) analysis revealed a white blood cell count of 17×106/L. Anti- GAD antibody IgG was positive in both serum and cerebrospinal fluid, with a titer of 1:100.The diagnosis of anti-GAD65 antibody-associated encephalitis was well-established. The clinical symptoms of the child showed improvement following the administration of methylprednisolone and immunoglobulin therapy. Following discharge, monthly administration of immunoglobulin therapy was initiated. In February 2025, the child presented with tremors in the right foot, a repeat MRI scan of the cranial revealed an increase in multiple abnormal signals within the brain compared to prior imaging studies, indicating the presence of new lesions. Concurrently, testing for anti-GAD65 antibodies was positive, with titers of 1:1 in CSF and 1:32 in serum. These findings were interpreted as indicative of a relapse of anti-GAD65 antibody-associated encephalitis. Following the administration of a repeat methylprednisolone pulse therapy, the child's symptoms showed improvement, and sequential treatment with rituximab was subsequently initiated. During the follow-up visit in September 2025, the pediatric patient remained asymptomatic with no evidence of disease recurrence.
CONCLUSIONS: We present a detailed case report of recurrent anti-GAD65 antibody-associated encephalitis in a pediatric patient, characterized by complex and variable clinical manifestations. Rituximab demonstrated therapeutic effectiveness in managing this recurrent condition.
METHODS: We conducted a retrospective analysis of the clinical data of a pediatric patient with recurrent anti-GAD65 antibody-associated encephalitis.
RESULTS: The patient was a 7-year-old boy who presented with slurred speech and epileptic seizures in June 2024. Brain magnetic resonance imaging(MRI)demonstrated multiple abnormal signal intensities in the bilateral frontal, temporal, parietal, and occipital cortical regions. Electroencephalogram (EEG) revealed focal epileptiform discharges and status epilepticus. His clinical condition improved following treatment with methylprednisolone and intravenous immunoglobulin. In November 2024, the child presented with a decline in mental status, generalized weakness, increased somnolence, reduced mobility and social interaction, gait instability, as well as accompanying headache and vomiting. Brain MRI demonstrated inflammatory involvement of the right cerebellar hemisphere. The cerebrospinal fluid (CSF) analysis revealed a white blood cell count of 17×106/L. Anti- GAD antibody IgG was positive in both serum and cerebrospinal fluid, with a titer of 1:100.The diagnosis of anti-GAD65 antibody-associated encephalitis was well-established. The clinical symptoms of the child showed improvement following the administration of methylprednisolone and immunoglobulin therapy. Following discharge, monthly administration of immunoglobulin therapy was initiated. In February 2025, the child presented with tremors in the right foot, a repeat MRI scan of the cranial revealed an increase in multiple abnormal signals within the brain compared to prior imaging studies, indicating the presence of new lesions. Concurrently, testing for anti-GAD65 antibodies was positive, with titers of 1:1 in CSF and 1:32 in serum. These findings were interpreted as indicative of a relapse of anti-GAD65 antibody-associated encephalitis. Following the administration of a repeat methylprednisolone pulse therapy, the child's symptoms showed improvement, and sequential treatment with rituximab was subsequently initiated. During the follow-up visit in September 2025, the pediatric patient remained asymptomatic with no evidence of disease recurrence.
CONCLUSIONS: We present a detailed case report of recurrent anti-GAD65 antibody-associated encephalitis in a pediatric patient, characterized by complex and variable clinical manifestations. Rituximab demonstrated therapeutic effectiveness in managing this recurrent condition.