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Autoimmune glial fibrillar acidic protein astrocytopathy mimicking tuberculous meningitis
Hidehiro Someko1, Toshiaki Shiojiri2
1General Internal Medicine, Asahi General Hospital, Asahi, Chiba, Japan someko@med.kitasato-u.ac.jp.
Abstract:
Autoimmune glial fibrillar acidic protein (GFAP) astrocytopathy typically presents as acute or subacute meningoencephalitis with or without myelitis. We describe a case of autoimmune GFAP astrocytopathy that mimicked tuberculous meningitis. A man in his 70s was referred to our hospital with lethargy persistent for 2 months, appetite loss for 1 month and fever with headache for 10 days. The cerebrospinal fluid test revealed lymphocytic pleocytosis with elevated adenosine deaminase (ADA). Laboratory investigations ruled out microbial and neoplastic causes. Empirical therapy for tuberculous meningitis combined with corticosteroid improved the patient's condition. Culture for Mycobacterium tuberculosis failed to show microbial growth despite 1 month of incubation. The cerebrospinal fluid was examined for GFAP antibody and returned positive result. Antituberculous agents were discontinued, and corticosteroid was administered until patient's symptoms resolved completely. Thus, clinicians should consider autoimmune GFAP astrocytopathy as one of the differential diagnoses of lymphocytic meningitis with elevated ADA.
Insights
Autoimmune GFAP astrocytopathy can mimic tuberculous meningitis. Early identification and treatment with corticosteroids are crucial for managing this rare neurological condition.
Area of Science:
- Neurology
- Immunology
Background:
- Autoimmune glial fibrillar acidic protein (GFAP) astrocytopathy is an inflammatory condition affecting the central nervous system.
- It often presents with meningoencephalitis or myelitis, posing diagnostic challenges.
Observation:
- A case report details a 70-year-old male with symptoms mimicking tuberculous meningitis, including lethargy, appetite loss, fever, and headache.
- Cerebrospinal fluid analysis showed lymphocytic pleocytosis and elevated adenosine deaminase (ADA), initially suggesting tuberculosis.
- Despite empirical anti-tuberculosis treatment, the patient's condition improved with corticosteroids.
Findings:
- Cultures for Mycobacterium tuberculosis were negative.
- Positive GFAP antibody testing confirmed autoimmune GFAP astrocytopathy.
- Discontinuation of anti-tuberculosis therapy and continued corticosteroid treatment led to complete symptom resolution.
Implications:
- Autoimmune GFAP astrocytopathy should be considered in the differential diagnosis of lymphocytic meningitis with elevated ADA.
- This highlights the importance of considering autoimmune etiologies even with suggestive infectious markers.
- Prompt diagnosis and appropriate immunosuppressive therapy can lead to favorable outcomes in GFAP astrocytopathy.
