title: Changes in vitamin C and oxidative stress status during the treatment of tuberculous meningitis.
abstract: BACKGROUND
  Tuberculosis (TB) is associated with oxidative stress and is traditionally linked to vitamin C deficiency.
  
  
  OBJECTIVE
  To evaluate the time course of the oxidative stress marker, malondialdehyde (MDA), and vitamin C status during the clinical treatment of tuberculous meningitis (TBM).
  
  
  METHODS
  MDA and vitamin C reduction/oxidation (redox) status were spectrophotometrically measured at admission and during hospital treatment in cerebrospinal fluid (CSF) and serum from 27 TBM patients and 20 controls.
  
  
  RESULTS
  Baseline CSF and serum MDA levels in TBM patients were higher than in controls (both P < 0.05), and remained elevated throughout the study. CSF MDA steadily increased from baseline 0.66 ± 0.24 mol/l to 1.02 ± 0.33 μmol/l at the end of the sixth week of treatment (P < 0.05), and then returned to baseline levels. Baseline CSF and serum total vitamin C were lower in TBM patients than in controls, but were soon normalised. CSF and serum ascorbate, reduced/oxidised vitamin C ratios and ascorbate CSF/serum ratio were markedly decreased in TBM patients (P < 0.05), and showed no improvement during treatment.
  
  
  CONCLUSIONS
  These results indicate increased local and systemic oxidative stress, accompanied by impaired redox status, but not total vitamin C deficiency, which persisted during conventional clinical treatment of TBM.
authors.affiliation: Institute of Biochemistry, Medical Faculty, University of Pristina, Kosovska Mitrovica, Serbia.
authors.forename: D
authors.initials: D
authors.lastname: Miric
authors.forename: R
authors.initials: R
authors.lastname: Katanic
authors.forename: B
authors.initials: B
authors.lastname: Miric
authors.forename: B
authors.initials: B
authors.lastname: Kisic
authors.forename: N
authors.initials: N
authors.lastname: Popovic-Katanic
authors.forename: V
authors.initials: V
authors.lastname: Nestorovic
mesh_terms: D000995:Antitubercular Agents / Q000627:therapeutic use*; D001205:Ascorbic Acid / Q000097:blood* / Q000134:cerebrospinal fluid*; D001206:Ascorbic Acid Deficiency / Q000097:blood / Q000134:cerebrospinal fluid; D015415:Biomarkers / Q000097:blood / Q000134:cerebrospinal fluid; D016022:Case-Control Studies; D002648:Child; D002675:Child, Preschool; D005260:Female; D006801:Humans; D007223:Infant; D008297:Male; D008315:Malondialdehyde / Q000097:blood / Q000134:cerebrospinal fluid; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000187:drug effects*; D013053:Spectrophotometry; D013997:Time Factors; D016896:Treatment Outcome; D014390:Tuberculosis, Meningeal / Q000097:blood / Q000134:cerebrospinal fluid / Q000175:diagnosis / Q000188:drug therapy*
chemical_list: D000995:Antitubercular Agents; D015415:Biomarkers; D008315:Malondialdehyde; D001205:Ascorbic Acid