Cerebrospinal fluid levels of the macrophage-specific biomarker sCD163 are diagnostic for Lyme neuroborreliosis: An observational cohort study

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Objectives: We aimed to investigate levels of the macrophage-specific marker, sCD163, in cerebrospinal fluid and plasma in patients with Lyme neuroborreliosis. We tested the diagnostic value of CSF-sCD163 and ReaScan-CXCL13 and analyzed if plasma-sCD163 could monitor treatment response. Methods: An observational cohort study: Cohort 1—Cerebrospinal fluid from adults with neuroborreliosis (n = 42), bacterial meningitis (n = 16), enteroviral meningitis (n = 29), and controls (n = 33); Cohort 2—Plasma from 23 adults with neuroborreliosis collected at diagnosis, three, and six months. sCD163 was determined using an in-house sandwich ELISA. ReaScan-CXCL13 measured semiquantitative concentrations of CXCL13, cut-off ≥ 250 pg/ml diagnosed neuroborreliosis. Receiver Operating Characteristics analyzed the diagnostic strength. A linear mixed model including follow-up as categorical fixed effect analyzed differences in plasma-sCD163. Results: CSF-sCD163 was higher in neuroborreliosis (643 µg/l) than in enteroviral meningitis (106 µg/l, p < 0.0001) and controls (87 µg/l, p < 0.0001), but not bacterial meningitis (669 µg/l, p = 0.9). The optimal cut-off was 210 µg/l, area under the curve (AUC) 0.85. ReaScan-CXCL13 had an AUC of 0.83. Combining ReaScan-CXCL13 with CSF-sCD163 increased AUC significantly to 0.89. Plasma-sCD163 showed little variation and was not elevated during the 6 months of follow-up. Conclusion: CSF-sCD163 is diagnostic for neuroborreliosis with an optimal cut-off of 210 µg/l. Combining ReaScan-CXCL13 with CSF-sCD163 increases AUC. Plasma-sCD163 cannot monitor treatment response.

OriginalsprogEngelsk
Artikelnummer117299
TidsskriftClinica Chimica Acta
Vol/bind543
Antal sider8
ISSN0009-8981
DOI
StatusUdgivet - 2023

Bibliografisk note

Funding Information:
This work was supported as part of NorthTick, an Interreg project supported by the North Sea Programme of the European Regional Development Fund of the European Union (grant number: J-no 38-2-7-19). Unrestricted grants from A.P. Møller Foundation (grant number: 20-L-0308) and by PERSIMUNE (grant number: DNRF126). MØ has received a research grant from Rigshospitalets Forskningspuljer. AML received a research grant from Lundbeck Foundation (grant number: R366-2021-127).

Funding Information:
The authors would like to thank nurse Pernille Mølbak and research nurse Annemette Hald from the Department of Infectious Diseases, Rigshospitalet for their excellent work including patients in this study. Further, we wish to acknowledge Fie Welling Paulsen for retrieving health-related information from medical records. As well as laboratory technicians Dorthe Hass, Department of Infectious Diseases, Rigshospitalet, Helle Ryom, Department of Clinical Biochemistry, Aarhus University Hospital, and MD Bo Bødker Jensen, Department of Clinical Microbiology, Rigshospitalet for their much-appreciated laboratory guidance, analysis, and help. This work was supported as part of NorthTick, an Interreg project supported by the North Sea Programme of the European Regional Development Fund of the European Union (grant number: J-no 38-2-7-19). Unrestricted grants from A.P. Møller Foundation (grant number: 20-L-0308) and by PERSIMUNE (grant number: DNRF126). MØ has received a research grant from Rigshospitalets Forskningspuljer. AML received a research grant from Lundbeck Foundation (grant number: R366-2021-127).

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© 2023 The Authors

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