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Serial lactate determinations in tuberculous meningitis.

L M Tang1

  • 1Department of Neurology, Chang Gung Memorial Hospital, Taiwan, R.O.C.

Scandinavian Journal of Infectious Diseases
|January 1, 1988
PubMed
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High lactate levels in cerebrospinal fluid (CSF) are a consistent marker in tuberculous meningitis (TBM). These elevated lactate levels persist despite treatment, indicating a potential challenge in monitoring therapeutic response in TBM patients.

Area of Science:

  • Neurology
  • Infectious Diseases
  • Biochemistry

Background:

  • Tuberculous meningitis (TBM) is a severe form of tuberculosis affecting the central nervous system.
  • Cerebrospinal fluid (CSF) analysis is crucial for diagnosing and managing TBM.
  • Lactate is a metabolic byproduct that can indicate tissue hypoxia or altered metabolism.

Purpose of the Study:

  • To investigate lactate levels in the CSF of patients diagnosed with tuberculous meningitis.
  • To assess the correlation between CSF lactate concentration and the clinical stage or prognosis of TBM.
  • To evaluate the impact of antituberculous therapy on CSF lactate levels in the early stages of TBM.

Main Methods:

  • CSF samples were collected from 21 patients with culture-proven tuberculous meningitis.

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  • Lactate concentrations in CSF were measured.
  • Clinical staging and patient prognosis were assessed and correlated with lactate levels.

    • Main Results:

    • All 21 patients exhibited uniformly high CSF lactate levels (≥ 3.9 mmol/l).
    • CSF lactate concentration did not correlate with the clinical stage of TBM or patient prognosis.
    • Repeated CSF analyses showed persistently high lactate levels in the early disease phase, even with appropriate antituberculous therapy.

    Conclusions:

    • Elevated CSF lactate is a consistent biochemical finding in culture-proven tuberculous meningitis.
    • CSF lactate levels do not appear to be a reliable indicator of TBM severity or treatment outcome.
    • Persistently high CSF lactate despite therapy suggests potential limitations in using this marker to monitor early treatment response in TBM.