Abstract

AbstractObjectivesTo examine the chemokine profile in the cerebrospinal fluid (CSF) of patients with glial fibrillary acidic protein astrocytopathy (GFAP‐A), central nervous system immune‐related adverse event (CNS‐irAE), neurosarcoidosis (NS), neuromyelitis optica spectrum disorders (NMOSD), multiple sclerosis (MS), and human T‐cell leukemia virus‐1 (HTLV‐1)‐associated myelopathy (HAM).MethodsThe study included 38 patients presenting to St. Marianna University Hospital between May 2013 and November 2021 with GFAP‐A, CNS‐irAE, NMOSD, MS, NS, HAM and noninflammatory neurological diseases (NIND). We recorded the age, sex, duration of disease, brain/spinal lesions on magnetic resonance imaging (MRI), blood data, and measured chemokines (CXCL9, −10, −13, CCL3, −4, −17, −20, −22) in CSF. In patients with GFAP‐A, clinical symptoms, and CSF CXCL10 levels were compared before and after steroid treatment.ResultsPatients with GFAP‐A had higher CSF levels of CXCL10, CXCL13, and CCL22 (10736.1 [8786.7–149079.0] pg/ml (p < .05), 378.4 [239.9–412.2] pg/ml (p < .01) and 159.9 [130.5–413.9] pg/ml (p < .01), respectively). The CSF levels of CXCL10 improved from 10736.1 [8786.7–149079.0] pg/ml to 1879.0 [783.9–4360.0] pg/ml in patients with GFAP‐A by steroid therapy.ConclusionCSF CXCL10 levels were particularly high in GFAP‐A, and changes in levels after treatment correlated with clinical improvements, suggesting CXCL10 involvement in GFAP‐A pathogenesis.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.