4.5 Article

GABAA receptor encephalitis associated with human parvovirus B19 virus infection Case report

期刊

MEDICINE
卷 100, 期 23, 页码 -

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LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MD.0000000000026324

关键词

encephalitis; gamma-aminobutyric acid type A receptor antagonists; human parvovirus B19

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  1. Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior - Brazil (CAPES) [001]

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This case study describes a 6-year-old boy hospitalized with super-refractory status epilepticus related to autoimmune encephalitis associated with B19 infection. Following immunosuppressive therapy, the patient achieved complete symptom remission, normal neurological examination, and appropriate neuropsychomotor development, highlighting the importance of early clinical suspicion and treatment.
Rationale: Human parvovirus B19 (B19) infection can produce a spectrum of clinical syndromes, including neurological manifestations, most notably encephalitis. Although symptoms suggestive of autoimmune disease in patients with B19 infection have been previously described, a clear association of autoimmune encephalitis with B19 infection has yet to be established. Patient concerns: We describe the case of a 6-year-old boy who was hospitalized due to status epilepticus, which evolved to super-refractory status epilepticus that was only mildly responsive to anticonvulsant drugs. Diagnosis: A cerebrospinal fluid study identified slight pleocytosis and B19 positivity. A subsequent autoimmunity cerebrospinal fluid study revealed the presence of anti-gamma-aminobutyric acid type A (GABA(A)) receptor antibodies. Interventions: After pulse therapy with methylprednisolone and continuous therapy with prednisolone with cyclosporine, the patient experiencing seizure persistence with disordered motor function manifestations and only minor improvement in consciousness, and so, plasmapheresis was performed. With continued immunosuppressive treatments with cyclosporine and prednisolone, the patient's clinical picture showed progressive improvement, with good control of seizures. Although the patient tolerated withdrawal of the anticonvulsant drugs well, he developed seizures when corticosteroid therapy withdrawal was attempted, so was started on azathioprine. Outcomes: After immunosuppressive therapy, the patient evolved with complete remission of symptoms, normal neurological examination and age-appropriate neuropsychomotor development. Lessons: The present case characteristics, together with previous findings, support the hypothesis that autoimmunity may be triggered by extensive antigen release due to degeneration of infected neurons. This case highlights the importance of early clinical suspicion and treatment.

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