Title:Anti-NMDA Receptor Encephalitis: Efficacy of Treatment for Male Patients and miRNA Biomarker
VOLUME: 27 ISSUE: 24
Author(s):Hsiuying Wang*
Affiliation:Institute of Statistics, National Chiao Tung University, Hsinchu 30010
Keywords:anti-NMDA receptor encephalitis, immunotherapy, efficacy rate, treatment, chemokine 13, microRNA.
Abstract:
Background: Anti-N-methyl-D-aspartate (NMDA) receptor encephalitis is an
acute form of encephalitis. Treatments for the anti-NMDA receptor encephalitis usually include
steroids, intravenous immunoglobulin, plasma exchange, plasmapheresis, rituximab,
cyclophosphamide and tumor resection.
Objective: We aimed to compare the efficacy of the treatments including intravenous immunoglobulin,
plasma exchange, plasmapheresis, rituximab or cyclophosphamide for male anti-
NMDA receptor encephalitis patients without tumor and to discuss potential biomarkers for
this disease.
Method: The Fisher exact test and the contingency table analysis were used to analyze the
treatment efficacy for 43 male and 76 female patients. In addition, a hierarchical tree method
was adopted to analyze the difference in the treatment efficacy between male and female patients.
Results: The p-values of testing whether the efficacy rate of plasmapheresis (or plasma exchange)
for the male patient is greater than a threshold are significantly different from the pvalues
for the other two treatments. In addition, the hierarchical tree method shows that the
treatment strategy associating with early recovery is different for male and female patients.
Conclusion: The results revealed that the efficacy rate of plasmapheresis (or plasma exchange)
is not inferior to that of intravenous immunoglobulin and rituximab (or cyclophosphamide)
for male patients without tumor. In addition, B-cell attracting C-X-C motif
chemokine 13 (CXCL13) and microRNA let-7b have the potential to be the treatment response
biomarkers for anti-NMDA receptor encephalitis. They may not be useful prognostic
biomarkers for this encephalitis unless they are not biomarkers for other autoimmune encephalitides.