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Wando Mount Pleasant Library
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Elevated sTREM2 and NFL levels in patients with sepsis associated encephalopathy.
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- Author(s): Orhun, Günseli (AUTHOR); Esen, Figen (AUTHOR); Yilmaz, Vuslat (AUTHOR); Ulusoy, Canan (AUTHOR); Şanlı, Elif (AUTHOR); Yıldırım, Elif (AUTHOR); Gürvit, Hakan (AUTHOR); Ergin Özcan, Perihan (AUTHOR); Sencer, Serra (AUTHOR); Bebek, Nerses (AUTHOR); Tüzün, Erdem (AUTHOR)
- Source:
International Journal of Neuroscience. Mar2023, Vol. 133 Issue 3, p327-333. 7p. - Source:
- Additional Information
- Subject Terms:
- Abstract: Sepsis-associated encephalopathy (SAE) is a common manifestation of sepsis that may lead to cognitive decline. Our aim was to investigate whether the neurofilament light chain (NFL) and soluble triggering receptor expressed on myeloid cells 2 (sTREM2) could be utilized as prognostic biomarkers in SAE. In this prospective observational study, baseline serum levels of sTREM2 and cerebrospinal fluid (CSF) levels of sTREM2 and NFL were measured by ELISA in 11 SAE patients and controls. Patients underwent daily neurological examination. Brain magnetic resonance imaging (MRI) and standard electroencephalography (EEG) were performed. Cognitive dysfunction was longitudinally assessed after discharge in 4 SAE patients using the Mini-Mental State Examination (MMSE) and Addenbrooke's Cognitive Examination-Revised (ACE-R) tests. SAE patients showed higher CSF sTREM2 and NFL levels than controls. sTREM2 and NFL levels were not correlated with the severity measures of sepsis. Three months after discharge, 2 SAE patients displayed ACE-R scores congruent with mild cognitive impairment (MCI), persisting in one patient 12 months after discharge. SAE patients with MCI showed higher CSF NFL levels, bacteremia, and abnormal brain MRI. Patients with increased serum/CSF sTREM2 levels showed trends towards displaying poorer attention/orientation and visuo-spatial skills. sTREM2 and NFL levels may serve as a prognostic biomarker for cognitive decline in SAE. These results lend further support for the involvement of glial activation and neuroaxonal degeneration in the physiopathology of SAE. [ABSTRACT FROM AUTHOR]
- Abstract: Copyright of International Journal of Neuroscience is the property of Taylor & Francis Ltd and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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