Glial fibrillary acidic protein antibody-associated astrocytopathy presents isolated spinal cord enhancement: A case report

胶质纤维酸性蛋白抗体相关性星形胶质细胞病表现为孤立性脊髓强化:病例报告

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Abstract

RATIONALE: Glial fibrillary acidic protein antibody-associated astrocytopathy (GFAP-A) is an autoimmune central nervous system inflammatory disorder diagnosed via cerebrospinal fluid (CSF) glial fibrillary acidic protein-immunoglobulin G detection. Clinically, it typically presents with meningoencephalitis or myelitis, accompanied by periventricular perivascular enhancement on brain magnetic resonance imaging (MRI) (findings that guide most routine diagnoses). Yet isolated spinal cord abnormalities (with negative brain MRI) in GFAP-A remain rarely reported, especially when occurring in patients with comorbidities like diabetes mellitus and active infection; these overlapping conditions often mask GFAP-A's typical features, consequently increasing the risk of clinical misdiagnosis. By reporting this atypical case, the study aims to supplement the existing imaging spectrum of GFAP-A and provide practical diagnostic references for complex clinical scenarios where underlying diseases obscure classic GFAP-A manifestations. It further carries significance in emphasizing the critical role of CSF GFAP-immunoglobulin G detection: this biomarker enables accurate identification of such atypical cases, directly addressing the misdiagnosis risk highlighted earlier. PATIENT CONCERNS: A 47-year-old Chinese male patient with a 13-year history of type 2 diabetes mellitus was admitted to the hospital due to fever and headache. Initially, the patient was diagnosed with upper respiratory tract infection based on positive Mycoplasma pneumoniae and parainfluenza virus antibodies; however, his symptoms persisted and worsened after treatment with moxifloxacin combined with oseltamivir. DIAGNOSES: Emergency CSF examination showed increased pressure, elevated protein level, and monocytosis. Subsequent examination results revealed positive glial fibrillary acidic protein antibodies in the CSF; combined with lumbar MRI showing linear enhancement on the surface of the cauda equina nerves (and negative brain MRI findings), the patient was diagnosed with GFAP-A. INTERVENTIONS: The patient received anti-infection treatment, intracranial pressure reduction, and blood glucose control. OUTCOMES: After receiving the treatment, the patient's symptoms improved and he was discharged. At the 2-month follow-up after discharge, the patient still had postural tremor in both upper limbs, but no pathological reflexes were elicited. LESSONS: This case confirms that GFAP-A can be detected with positive spinal cord MRI findings alone, while negative brain MRI findings. Its key clinical significance lies in emphasizing the diagnostic value of CSF glial fibrillary acidic protein antibody detection for atypical cases, providing a new reference for the imaging spectrum of GFAP-A.

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