Data for: TARGETING HIGHER LEVELS OF LACTATE IN THE POST-INJURY PERIOD FOLLOWING TRAUMATIC BRAIN INJURY
Ninety-six patients 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. These assays were performed using standard kits (Lactate acid Abris, REF320.1.50 and Pyruvate Abris, REF333.1.50; Abrisplus, Russia). Ceruloplasmin and lactate dehydrogenase were measured in sera by enzyme-linked immunosorbent assays according to the manufacturer’s protocol using the commercially available ELISA kit (Sigma, USA) on the USA Stat Fax analyzer; the optical density was determined with a microplate reader set to 450 nm. The ceruloplasmin levels were determined by turbidimetry (Olympus AU680, Japan) at 340 nm using the assay kit (Spinreact, N1102062, Spain). Tau concentrations were measured by ELISA method using Human Tau ELISA kit (Sigma, USA) on the USA Stat Fax analyzer (Department of Clinical Biochemistry; Kharkiv National Medical University). Group 1 was comprised of 54 participants (mean age±SD 39.92±10.5 years) who had a history of mild TBI, group 2 (mean age±SD 37.36±10.2 years) was comprised of 42 patients who had a history of moderate TBI. 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 0,704±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 of total lactate level 0.793±0.019 mmol/L. Lactate data did not distinguish with the respect to gender and age. The results showed no significant differences in tau protein, pyruvate, lactate dehydrogenase and ceruloplasmin levels. We didn’t find elevated tau protein levels in the serum samples of the patients from the general clinical group as compared to controls (p=0.0897, t=1.710; 95% CI -1.27 to 18.19) and in this patient group the median of total tau level was 79.57±24.41 pg/ml and 71.14±20.56 pg/ml, in controls. Conclusion: The study shows data, revealing 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.