TBM_Microdialysis_anonymised_data.xlsx (18.96 kB)

Data for: A pilot study of inflammatory mediators in brain extracellular fluid in paediatric tuberculous meningitis (TBM)

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posted on 26.02.2021, 09:33 by Nicholas Loxton, Ursula Rohlwink, Mvuwo Tshavhungwe, Lindizwe Dlamini, Muki Shey, Johannes Enslin, Anthony Figaji
This is the data linked to: A pilot study of inflammatory mediators in brain extracellular fluid in paediatric TBM (2021), PlosOne

Tuberculous meningitis (TBM) is the most fatal form of tuberculosis and frequently occurs in children. The inflammatory process initiates secondary brain injury processes that lead to death and disability. Much remains unknown about this cerebral inflammatory process, largely because of the difficulty in studying the brain. To date, studies have typically examined samples from sites distal to the site of disease, such as spinal cerebrospinal fluid (CSF) and blood. In this pilot study, we examined the feasibility of using direct brain microdialysis (MD) to detect inflammatory mediators in brain extracellular fluid (ECF) in TBM. MD was used to help guide neurocritical care in 7 comatose children with TBM by monitoring brain chemistry for up to 4 days. Remnant ECF fluid was stored for offline analysis. Samples of ventricular CSF, lumbar CSF and blood were collected at clinically indicated procedures for comparison. Inflammatory mediators were quantified using multiplex technology. All inflammatory markers, with the exception of interleukin (IL)-10 and IL-12p40, were detected in the ECF. Cytokine concentrations were generally lower in ECF than ventricular CSF in time-linked specimens. Individual cases showed ECF cytokine increases coinciding with marked increases in ECF glycerol or decreases in ECF glucose. Cytokine levels and glycerol were generally higher in patients with more severe disease. This is the first report of inflammatory marker analysis from samples derived directly from the brain and in high temporal resolution, demonstrating feasibility of cerebral MD to explore disease progression and possibly therapy response in TBM.


Reason for stand-alone publication:

This raw data which was analysed to put together the paper. It has been made public inline with PlosOne's publication requirements.

Funding

SARChI Chair of Clinical Neurosciences; Fund Number 443789 (Prof. Anthony Figaji)

Harry Crossley Research Fellowship (Nicholas Loxton)

South African Medical Research Council: National Medical Students Research Training Programme (Nicholas Loxton)

History

Department/Unit

Department of Surgery/Division of Neurosurgery