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Analysis of adenosine deaminase isoenzyme-2 (ADA2) in cerebrospinal fluid in the diagnosis of tuberculous meningitis
  1. S EINTRACHT
  1. Department of Chemical Pathology, South African Institute for Medical Research and University of the Witwatersrand, Johannesburg, South Africa
  2. Department of Neurology, Baragwanath Hospital and University of the Witwatersrand; and Department of Clinical Neurosciences, Guy's, King's and St Thomas' School of Medicine, King's College, London, UK
  3. Department of Community Health, University of the Witwatersrand; and Infectious Disease Epidemiology Unit, London School of Hygiene and Tropical Medicine, London, UK
  4. Department of Medical Microbiology, South African Institute for Medical Research and University of the Witwatersrand
  5. Department of Neurology, Baragwanath Hospital and University of the Witwatersrand
  1. Dr E Silber, Department of Neuroimmunology, 2nd Floor, Hodgkin Building, Guy's Hospital, London, SE1 9RT,UKeli.silber{at}kcl.ac.uk
  1. E SILBER
  1. Department of Chemical Pathology, South African Institute for Medical Research and University of the Witwatersrand, Johannesburg, South Africa
  2. Department of Neurology, Baragwanath Hospital and University of the Witwatersrand; and Department of Clinical Neurosciences, Guy's, King's and St Thomas' School of Medicine, King's College, London, UK
  3. Department of Community Health, University of the Witwatersrand; and Infectious Disease Epidemiology Unit, London School of Hygiene and Tropical Medicine, London, UK
  4. Department of Medical Microbiology, South African Institute for Medical Research and University of the Witwatersrand
  5. Department of Neurology, Baragwanath Hospital and University of the Witwatersrand
  1. Dr E Silber, Department of Neuroimmunology, 2nd Floor, Hodgkin Building, Guy's Hospital, London, SE1 9RT,UKeli.silber{at}kcl.ac.uk
  1. P SONNENBERG
  1. Department of Chemical Pathology, South African Institute for Medical Research and University of the Witwatersrand, Johannesburg, South Africa
  2. Department of Neurology, Baragwanath Hospital and University of the Witwatersrand; and Department of Clinical Neurosciences, Guy's, King's and St Thomas' School of Medicine, King's College, London, UK
  3. Department of Community Health, University of the Witwatersrand; and Infectious Disease Epidemiology Unit, London School of Hygiene and Tropical Medicine, London, UK
  4. Department of Medical Microbiology, South African Institute for Medical Research and University of the Witwatersrand
  5. Department of Neurology, Baragwanath Hospital and University of the Witwatersrand
  1. Dr E Silber, Department of Neuroimmunology, 2nd Floor, Hodgkin Building, Guy's Hospital, London, SE1 9RT,UKeli.silber{at}kcl.ac.uk
  1. H J KOORNHOF
  1. Department of Chemical Pathology, South African Institute for Medical Research and University of the Witwatersrand, Johannesburg, South Africa
  2. Department of Neurology, Baragwanath Hospital and University of the Witwatersrand; and Department of Clinical Neurosciences, Guy's, King's and St Thomas' School of Medicine, King's College, London, UK
  3. Department of Community Health, University of the Witwatersrand; and Infectious Disease Epidemiology Unit, London School of Hygiene and Tropical Medicine, London, UK
  4. Department of Medical Microbiology, South African Institute for Medical Research and University of the Witwatersrand
  5. Department of Neurology, Baragwanath Hospital and University of the Witwatersrand
  1. Dr E Silber, Department of Neuroimmunology, 2nd Floor, Hodgkin Building, Guy's Hospital, London, SE1 9RT,UKeli.silber{at}kcl.ac.uk
  1. D SAFFER
  1. Department of Chemical Pathology, South African Institute for Medical Research and University of the Witwatersrand, Johannesburg, South Africa
  2. Department of Neurology, Baragwanath Hospital and University of the Witwatersrand; and Department of Clinical Neurosciences, Guy's, King's and St Thomas' School of Medicine, King's College, London, UK
  3. Department of Community Health, University of the Witwatersrand; and Infectious Disease Epidemiology Unit, London School of Hygiene and Tropical Medicine, London, UK
  4. Department of Medical Microbiology, South African Institute for Medical Research and University of the Witwatersrand
  5. Department of Neurology, Baragwanath Hospital and University of the Witwatersrand
  1. Dr E Silber, Department of Neuroimmunology, 2nd Floor, Hodgkin Building, Guy's Hospital, London, SE1 9RT,UKeli.silber{at}kcl.ac.uk

https://doi.org/10.1136/jnnp.69.1.137

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    The outcome of tuberculous meningitis is influenced by the stage of disease at the start of treatment. Initiation of antituberculous therapy is often delayed because of the inadequacy of presently available laboratory tests. Management of patients with possible tuberculous meningitis would thus be advanced by the development of an accurate, reliable, and rapid diagnostic test, particularly if it could be applied in settings with poor recourses.

    Adenosine deaminase (ADA), an enzyme involved in purine catabolism, exists in at least three forms. ADA1 is a monomeric protein with a molecular mass of approximately 35 kDa and two ADA1molecules joined via a connecting protein form the dimeric ADA1+CP. The third isoenzyme ADA2 seems to be produced only by monocytes.1 Total CSF ADA has been suggested as a marker for tuberculous meningitis2 3; however, considerable variability and overlap, particularly with acute bacterial meningitis, has led some authors to question its clinical usefulness.4

    An increased proportion of ADA2 has been suggested to be a more specific means of diagnosing tuberculous effusions.2However, the use of CSF ADA2 in the diagnosis of tuberculous meningitis has not been described.

    Study subjects (all adults) were from a prospective cohort of patients undergoing a diagnostic lumbar puncture for suspected meningitis. Patient characteristics and investigations have previously been described in detail.5 In addition, CSF specimens from 10 patients at the Johannesburg Hospital were included (four tuberculous meningitis, four cryptococcal meningitis, two acute bacterial meningitis). Serum and CSF ADA analysis was performed on 11 specimens from patients with tuberculous meningitis (nine established by culture, two probable), nine with …

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