Abstract
High cerebrospinal fluid (CSF) concentrations of the chemokine CXCL13 have been associated with Lyme neuroborreliosis (LNB), and have recently been studied as a potential diagnostic marker. It has proven difficult to establish a reliable diagnostic cut-off, possibly in part due to heterogenicity of case–control groups. Our purpose was to investigate CSF CXCL13 concentrations in patients with similar clinical presentations, facial palsy. We retrospectively included patients with facial palsy associated with LNB (n = 21), or varicella zoster virus (VZV) (n = 26). Median CXCL13 concentrations were significantly higher in patients with LNB facial palsy compared to VZV facial palsy. Receiver-operating characteristic analyses yielded an optimal cut-off concentration at 34.5 pg/mL (sensitivity 85.7%, specificity of 84.6%), lower than that in previous studies. Although the analysis has potential, it is still not adequately established that CXCL13 provides additional, clinically useful, diagnostic information over current recommendations.
Highlights
Lyme neuroborreliosis (LNB) is a central nervous system (CNS) infection caused by the arthropod-borne spirochete Borrelia burgdorferi (Bb)
Median cerebrospinal fluid (CSF) concentrations of CXCL13 for facial palsy caused by LNB were 2041 pg/mL, for varicella zoster virus (VZV) facial palsy 8.5 pg/mL; only in one control sample, CXCL13 concentration exceeded the detection limit with a concentration of 9.0 pg/mL (Fig. 1)
CXCL13 was increased at 142 pg/mL. In this first comparative study on CXCL13 in patients with facial palsy caused by LNB and VZV, we can confirm significantly higher concentrations of CXCL13 in the CSF of patients with LNB compared to patients with reactivated VZV
Summary
Lyme neuroborreliosis (LNB) is a central nervous system (CNS) infection caused by the arthropod-borne spirochete Borrelia burgdorferi (Bb). Antibody production can be undetectable up to 6 weeks from emergence of symptoms, and can persist for several years after initial disease (Hansen and Lebech, 1992; Hammers-Berggren et al, 1993). Diagnosis of both early LNB and suspected reinfection is problematic, as the presence of lymphocytes in the CSF is non-specific to LNB. In an effort to improve diagnostics in CNS infections, high concentrations of the chemokine CXCL13 in CSF has emerged as a possible marker of LNB (Rupprecht et al, 2005). CXCL13 is produced in the CNS in a rapid response to infection, and is detectable before antibodies are present (Senel et al, 2010)
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