Plasma levels of oxidative stress biomarkers and hospital mortality in severe head injury: A multivariate analysis

Abstract

IntroductionThe association between biomarkers of oxidative stress and the prognosis of patients with traumatic brain injury (TBI) remains inconclusive. ObjectiveThe objective was to investigate the association between plasma levels of lipid peroxidation (thiobarbituric acid reactive species [TBARS]) and protein oxidation (carbonyl) biomarkers and the hospital mortality of patients with severe TBI. MethodsPlasma levels of TBARS and carbonyl were determined in 79 consecutive patients with severe TBI (Glasgow Coma Scale [GCS] ≤8) at a median of 12 hours (interquartile range [IQ] 25-75, 6.5-19.0), 30 hours (IQ 25-75, 24.7-37.0), and 70 (IQ 25-75, 55.0-78.5) hours after TBI and were compared with age- and sex-matched controls. The association between the TBARS and carbonyl levels and the hospital mortality was analyzed by multiple logistic regression analysis. ResultsThe mean age of patients was 34.8 years. Eighty-six percent were male. The TBARS and carbonyl levels were significantly higher in patients than in controls. There was a trend (P = .09) for higher plasma levels of TBARS and carbonyl proteins at 12 hours, but not at 30 or 70 hours, after trauma in nonsurvivors than in survivors. These findings were not confirmed after the adjustments by multiple logistic regression analysis. The final model showed a higher adjusted odds ratio for death for patients with admission GCS lower than 5 (odds ratio [OR] = 4.04; 95% confidence interval [CI], 1.33-12.13; P = .01) than those with higher GCS scores. Abnormal pupils were also associated with higher mortality (OR = 3.97; 95% CI, 1.22-12.13; P = .02). There was a nonsignificant trend for association between glucose greater than or equal to 150 mm/dL in the first 12 hours and death than levels between 70 and 149 mg/dL (OR = 2.92; 95% CI, 0.96-9.02; P = .06). ConclusionsPlasma levels of TBARS and carbonyl increase significantly in the first 70 hours after severe TBI but are not independently associated with the hospital mortality.