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.

在伤后12个月随访中，对96名TBI（创伤性脑损伤）患者进行了研究；根据制造商协议，采用分光光度法测量了血浆乳酸和丙酮酸水平。这些检测采用标准试剂盒（乳酸酸Abris，REF320.1.50和丙酮酸Abris，REF333.1.50；Abrisplus，俄罗斯）进行。通过酶联免疫吸附测定法在血清中测量了铜蓝蛋白和乳酸脱氢酶，使用商用ELISA试剂盒（Sigma，美国）在Stat Fax分析仪上测定；光密度值在450 nm下由微孔板阅读器确定。通过浑浊度法（Olympus AU680，日本）在340 nm下使用检测试剂盒（Spinreact，N1102062，西班牙）测定铜蓝蛋白水平。通过ELISA方法使用人Tau ELISA试剂盒（Sigma，美国）在Stat Fax分析仪（临床生物化学系；哈尔科夫国立医学院）上测定Tau浓度。第1组由54名参与者组成（平均年龄±标准差39.92±10.5岁），他们有轻度TBI病史；第2组（平均年龄±标准差37.36±10.2岁）由42名患者组成，他们有中度TBI病史。研究发现，与对照者相比，在经历了中度TBI后伤后期的患者中，血浆乳酸水平最高（p=0.0047，t=2.924，95%置信区间-0.2154至-0.04071），其中对照组的乳酸中位数为0.832±0.033和0.704±0.021 mmol/L。在轻度与中度伤后TBI之间没有观察到显著差异（p=0.079；t=1.772）；与对照者相比，一般伤后TBI组也显示出显著的差异（p=0.0181；t=2.396；95%置信区间-0.1627至-0.01551），总乳酸中位数为0.793±0.019 mmol/L。乳酸数据在性别和年龄方面没有区分。结果显示，在tau蛋白、丙酮酸、乳酸脱氢酶和铜蓝蛋白水平方面没有显著差异。与对照者相比，在一般临床组的患者血清样本中没有发现tau蛋白水平的升高（p=0.0897，t=1.710；95%置信区间-1.27至18.19），在此患者组中，总tau蛋白的中位数为79.57±24.41 pg/ml，对照者为71.14±20.56 pg/ml。结论：本研究揭示了创伤性脑损伤后伤后期间乳酸水平升高的数据，这反映了伤后氧化代谢紊乱，且在伤后中度TBI期间更为显著。