“The neurological spectrum unified by a positive test for GFAP antibody is likely broader than the tip of the iceberg we are recognizing thus far,” Dr. Lennon says.
“Tests for the antibody need to be validated rigorously to avoid false positive results,” Dr. Lennon adds. “CSF yields greater sensitivity and specificity than serum. An optimized tissue-based immunofluorescence assay is recommended for screening, with confirmation by GFAP-transfected cell-based immunofluorescence assay.”
Dr. Robert P. Lisak from Wayne State University School of Medicine, Detroit, who wrote an editorial related to this report, tells Reuters Health by email, “If a physician sees a patient with the clinical features of the encephalomyelitis described in the report by Dr. Lennon and her colleagues who has the appropriate MRI and spinal fluid findings, they should strongly suspect their patient has this immune-mediated disorder and treat with corticosteroids and/or other immunosuppressive treatments.”2
“I am looking forward to the analysis of additional patients by Dr. Lennon and her colleagues who have this antibody to the epsilon isoform of glial acidic fibrillary protein as well as to their making antibody testing for this antibody available to the neurologic community,” he says.
“We are likely to see additional disorders proven to be immune mediated and likely autoimmune etiology,” Dr. Lisak adds.
References
- Fang B, McKeon A, Hinson SR, et al. Autoimmune glial fibrillary acidic protein astrocytopathy: A novel meningoencephalomyelitis. JAMA Neurol. 2016 Sep 12. doi: 10.1001/jamaneurol.2016.2549. [Epub ahead of print]
- Lisak RP. Expanding the range of diagnosable autoimmune encephalopathies and encephalomyelopathies. JAMA Neurol. 2016 Sep 12. doi: 10.1001/jamaneurol.2016.2970. [Epub ahead of print]
