Clinica chimica acta; international journal of clinical chemistry · 2015
Increased levels of CSF CD59 in neuromyelitis optica and multiple sclerosis.
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Uzawa Akiyuki, Mori Masahiro, Uchida Tomohiko, Masuda Hiroki, Ohtani Ryohei, Kuwabara Satoshi
Аннотация
BACKGROUND: Complement activation is important in multiple sclerosis (MS) and is essential for anti-aquaporin 4 antibodies to damage the central nervous system in neuromyelitis optica (NMO). Little is known about the role of cerebrospinal fluid (CSF) regulators of complement activation in NMO and MS. We determined whether CSF CD59, which is a complement regulator and C5b-9 formation inhibitor, is involved in the pathogenesis of NMO and MS.
METHODS: We analyzed CSF levels of CD59 in 30 patients with NMO, 22 patients with MS, and 24 patients with non-inflammatory neurological disorders (NINDs). Possible correlations between CSF CD59 levels and the clinical and laboratory variables in patients with NMO and MS were also reviewed.
RESULTS: CSF CD59 levels in patients with NMO and MS were higher than those in patients with NINDs (p<0.001), and those in patients with NMO decreased after treatment. No significant correlations were found between CSF CD59 levels and clinical and laboratory parameters in NMO and MS.
CONCLUSION: High CSF CD59 levels in NMO and MS may reflect inflammation, damage, and/or complement activation in the central nervous system.
METHODS: We analyzed CSF levels of CD59 in 30 patients with NMO, 22 patients with MS, and 24 patients with non-inflammatory neurological disorders (NINDs). Possible correlations between CSF CD59 levels and the clinical and laboratory variables in patients with NMO and MS were also reviewed.
RESULTS: CSF CD59 levels in patients with NMO and MS were higher than those in patients with NINDs (p<0.001), and those in patients with NMO decreased after treatment. No significant correlations were found between CSF CD59 levels and clinical and laboratory parameters in NMO and MS.
CONCLUSION: High CSF CD59 levels in NMO and MS may reflect inflammation, damage, and/or complement activation in the central nervous system.