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CSF neuromarkers predict outcomes in tuberculous meningitis

09 Jul 2017

Cerebrospinal fluid (CSF) neuromarkers show potential as biomarkers for injury severity and for predicting mortality in patients with tuberculous meningitis (TBM), according to a recent study. An elevation in CSF neuromarkers particularly suggests ongoing brain injury regardless of a decline in inflammation markers achieved with treatment.

The study included 44 children with TBM and hydrocephalus (median age 3.3 years), 11 with fatty filum (median age 2.8 years) and nine with pulmonary tuberculosis (pTB; median age 3.7 years). Blood and CSF collected on admission and at different time points over 3 weeks were analysed for neuromarkers S100B, neuron-specific enolase (NSE) and glial fibrillary acidic protein (GFAP), and multiple inflammatory markers.

Of the patients with TBM, seven (16 percent) died and 16 (36 percent) had disabilities. Neuromarkers and inflammatory markers in CSF, but not in serum, were elevated on admission and for up to 3 weeks. Initial and highest concentrations in week 1 of S100B and NSE were associated with poor outcome, as were highest concentration overall and an increasing profile over time in S100B, NSE and GFAP.

In patients who died, combined neuromarker concentrations increased over time while inflammatory markers decreased.

Cerebral infarcts were particularly linked to the highest overall neuromarker concentrations and an increasing profile over time. Tuberculomas demonstrated an association with increased IL-12p40, IP-10 and MCP-1 concentrations, while infarcts were found to be related to elevated TNF-α, MIP-1α, IL-6 and IL-8.

The most common form of central nervous system TB, TBM is associated with very high morbidity and mortality. TBM commonly presents as a subacute disease with symptoms that may persist for weeks prior to diagnosis. Characteristic CSF findings of TBM include a lymphocytic-predominant pleiocytosis, elevated protein and low glucose. [J Infect Dis 2005;192:2054–2058; Scand J Infect Dis 2002;34:811–814]

Treatment should be initiated in patients with suspected TBM as soon as clinical suspicion is supported by initial CSF studies. Empiric treatment should include at least four first-line drugs, preferably isoniazid, rifampin, pyrazinamide, and streptomycin or ethambutol. Furthermore, there is evidence suggesting that adjunctive treatment with corticosteroids can improve mortality in TBM patients. [Tuberc Res Treat 2011;doi:10.1155/2011/798764]

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Most Read Articles
Roshini Claire Anthony, 4 days ago

The combined use of piperacillin and tazobactam does not appear to be a suitable alternative to meropenem for patients with bloodstream infections caused by ceftriaxone-resistant Escherichia coli (E. coli) or Klebsiella pneumoniae (K. pneumoniae), according to results of the MERINO* trial.

Tristan Manalac, 19 May 2018
Taking oral antibiotics appears to increase the risk of nephrolithiasis, according to a recent study. Moreover, the risk seems to be compounded for individuals with recent antibiotic exposure and those who were exposed at a younger age.
2 days ago
Patients with inflammatory bowel disease are at increased risk of developing acute myocardial infarction (AMI) or heart failure, although the prevalence of traditional risk factors for such cardiovascular disorders appears to be low, as reported in a recent study.
3 days ago
Early renin-angiotensin-aldosterone system (RAAS) blockade with renin-angiotensin system inhibitors (RASI) leads to better short- and long-term renal outcomes in systemic lupus erythematosus (SLE) patients with antiphospholipid-associated nephropathy (aPLN), according to a study, adding that this renal protective effect is independent of RASI’s antihypertensive and antiproteinuric effects.