ArticleFrontiers in neurology2026
Total cerebrospinal fluid IgA as a candidate adjunctive biomarker associated with autoimmune encephalitis: a retrospective case-control study.
Article in Frontiers in neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Autoimmune encephalitis (AE) is a rare but severe immune-mediated disease of the central nervous system. Early diagnosis remains challenging, and total cerebrospinal fluid (CSF) IgA is a routinely measurable parameter. However, its association with AE and its potential value as a candidate adjunctive biomarker remain unclear. Objective: To investigate whether total CSF IgA is independently associated with AE and to explore its potential as a candidate adjunctive biomarker for identifying AE cases. Methods: We conducted a single-center retrospective case-control study at the Second Affiliated Hospital of Soochow University (January 2010-June 2025), enrolling patients with autoimmune encephalitis and symptomatic controls with non-inflammatory, non-organic neurological disorders. Clinical, laboratory, and neuroimaging data were collected. Logistic regression was used to assess the independent association of total CSF IgA with autoimmune encephalitis and to construct a prediction model. Model performance was evaluated using receiver operating characteristic curves, calibration plots, decision curve analysis, and bootstrap internal validation. Results: A total of 101 patients with AE and 80 controls were included. Total CSF IgA levels were significantly higher in patients with AE than in controls (median 6.03 vs. 1.46 mg/L, Conclusion: Total CSF IgA was independently associated with AE, and a multivariable model combining CSF IgA with routine laboratory parameters showed excellent discrimination and good calibration in distinguishing AE from symptomatic controls. As a rapidly measurable parameter, it shows promise as a candidate adjunctive biomarker. However, its specificity in distinguishing AE from clinical mimics remains uncertain, warranting validation in larger, independent studies.
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