Multiple sclerosis and related disorders · 2026
Calprotectin reveals distinct innate immune signatures in NMOSD, MOGAD, and multiple sclerosis.
СтатьяНаблюдательное исследованиеНазвание и аннотация: Перевод в очереди
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Johnsson Magnus, Lycke Jan, Novakova Lenka, Rosenstein Igal, Hafsteinsdottir Brynhildur, Malmeström Clas, Axelsson Markus
Аннотация
BACKGROUND: Granulocyte-mediated injury contributes to the immunopathology of aquaporin-4 neuromyelitis optica spectrum disease (AQP4-NMOSD) and myelin oligodendrocyte glycoprotein-associated disease (MOGAD), yet calprotectin, a myeloid-derived inflammatory marker, has not been evaluated in these disorders.
OBJECTIVE: To assess the diagnostic and activity-related potential of cerebrospinal fluid (CSF) and serum calprotectin concentrations in AQP4-NMOSD, MOGAD, seronegative or double-negative NMOSD (DNNMOSD) and RRMS.
METHODS: In this observational study, CSF and serum calprotectin were measured using a turbidimetric assay in patients with AQP4-NMOSD (n = 10), DNNMOSD (n = 6), MOGAD (n = 9), RRMS (n = 10), and healthy controls (HC; n = 8). Group comparisons, correlations with clinical and laboratory variables, and relapse analyses were performed.
RESULTS: Serum calprotectin was markedly elevated in AQP4-NMOSD, DNNMOSD, and MOGAD (p < 0.001), separating these disorders from RRMS and HCs (AUC = 1.0 at 1.18 mg/L). CSF calprotectin was detectable in all samples (range; 0.18-0.82 mg/L) and was significantly lower in patients with MOGAD compared with other groups (p = 0.025). In RRMS, serum and CSF calprotectin concentrations inversely correlated with time since last relapse, whereas no such relationship was observed in NMOSD or MOGAD.
CONCLUSION: Serum calprotectin shows promise as a diagnostic biomarker distinguishing NMOSD and MOGAD from RRMS and supports predominant systemic myeloid activation in these disorders.
OBJECTIVE: To assess the diagnostic and activity-related potential of cerebrospinal fluid (CSF) and serum calprotectin concentrations in AQP4-NMOSD, MOGAD, seronegative or double-negative NMOSD (DNNMOSD) and RRMS.
METHODS: In this observational study, CSF and serum calprotectin were measured using a turbidimetric assay in patients with AQP4-NMOSD (n = 10), DNNMOSD (n = 6), MOGAD (n = 9), RRMS (n = 10), and healthy controls (HC; n = 8). Group comparisons, correlations with clinical and laboratory variables, and relapse analyses were performed.
RESULTS: Serum calprotectin was markedly elevated in AQP4-NMOSD, DNNMOSD, and MOGAD (p < 0.001), separating these disorders from RRMS and HCs (AUC = 1.0 at 1.18 mg/L). CSF calprotectin was detectable in all samples (range; 0.18-0.82 mg/L) and was significantly lower in patients with MOGAD compared with other groups (p = 0.025). In RRMS, serum and CSF calprotectin concentrations inversely correlated with time since last relapse, whereas no such relationship was observed in NMOSD or MOGAD.
CONCLUSION: Serum calprotectin shows promise as a diagnostic biomarker distinguishing NMOSD and MOGAD from RRMS and supports predominant systemic myeloid activation in these disorders.