Secondary traumatic brain injury (TBI) consequences continue multiple cascades of biochemical reactions caused by initial neurotrauma and one of the important pathogenetic processes is mitochondrial dysfunction partly characterized by elevation of lactate/pyruvate ratio in brain following metabolic failure.
To identify lactate, pyruvate, lactate dehydrogenase, tau protein, ceruloplasmin blood levels in the post-injury period following TBI in relation to its different forms.
Ninety-six patients (mean age ± SD 38.8 ± 10.39 years) at 12 months post-injury follow-ups TBI (post-TBI) were investigated; plasma lactate and pyruvate levels were measured by the spectrophotometric method according to the manufacturer protocols; tau protein, ceruloplasmin and lactate dehydrogenase (LDH) were measured in sera by enzyme-linked immunosorbent assays. Group 1 was comprised of 54 participants who had a history of mild TBI, group 2 was comprised of 42 patients who had a history of moderate TBI.
In this work, we found the highest plasma lactate levels in the patients with the post-injury period following moderate TBI as compared to controls (p = 0.0047, t = 2.924, 95 % CI -0.2154 to -0.04071) where the median lactate level was 0.832 ± 0.033 and 0704 ± 0.021 mmol/L in controls. No significant differences were seen between mild and moderate post-TBI (p = 0.079; t = 1.772); significant difference was also seen between general post-TBI group versus controls (p = 0.0181; t = 2.396; 95 % CI -0.1627 to -0.01551) with the median total lactate level of 0.793 ± 0.019 mmol/L. Lactate data did not distinguish with the respect to gender or age. The results showed no significant differences in tau protein, pyruvate, LDH and ceruloplasmin levels.
This study shows higher lactate levels in the post-injury period following TBI that reflect post-injury oxidative dysmetabolism and are more expressed in the post-injury period following moderate TBI.
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