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Background. The secondary traumatic brain injury (TBI) consequences are associated with multiple cascades of biochemical reactions caused by initial neurotrauma. We assessed changes in radical oxidation and marker membrane-associated enzymes involved into various redox reactions reflecting basic metabolic processes by measuring creatine phosphokinase (CPK), CPK-BB, adenosine triphosphate (ATP), adenosine diphosphate (ADP), aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase, lactate dehydrogenase (LDH) in the patients with long-term consequences after TBI. Materials and methods. Eighty-two patients (mean age (±SD) 39.04 ± 14.62 years), thirty controls (29.60 ± 4.73 years) were tested for serum CPK, CPK-BB, ATP, ADP measured using spectrophotometry methods according to standard manufacturer’s protocols. Serum AST, ALT, alkaline phosphatase, LDH levels were detected on gas-liquid chromatograph, by calorimetric methods. Results. We found elevated serum CPK level in patients with long-term consequences after TBI compared to controls (P < 0.001, t = 5.073, 95% CI –188.6 to –92.16) with the medians of total CPK of 163.5 ± 14.1 versus 92.6 ± 11.4 pg/ml in the basic and control groups, respectively. We found abnormal high serum CPK-BB level in the basic group with medians of total CPK-BB level of 24.7 ± 2.7 versus 16.14 ± 1.83 IU/L in controls (p < 0.05; t = 4.9). Metabolic changes in our patients were associated with higher LDH content being in direct proportion with disease duration (p < 0.05; r = +0.42); the median of total LDH level was 694.1 ± 16.3 and 381.9 IU/l in basic and control groups (p < 0.05), respectively. The patients investigated were detected with deficiency of macroergic compounds: ATP and ADP being in direct proportion with disease duration over 15 years (p < 0.05; r = +0.67); the medians of total ATP level were 627.60 ± 12.38 and 735.48 ± 14.57 μmol/l (p < 0.05) in the basic and control groups; for ADP: 256.20 ± ± 14.21 versus 273.88 ± 11.42 (p < 0.05), respectively. Conclusions. Patients with long-term consequences after TBI showed higher serum CPK level associated with increased LDH level reflecting bioenergy dyshomeostasis and severity of secondary brain injuries. keywords: creatine phosphokinase; long-term consequences after traumatic brain injury; bioenergy dyshomeostasis Introduction The secondary and delayed traumatic brain injury (TBI) consequences are associated with multiple and interacting cascades of different biochemical reactions caused by the initial neurotrauma [6, 7, 16, 18] whereas the pathogenetic mechanisms maintaining the long-term consequences after TBI are still unclear. The previous experimental data have reported that in white or grey matter brain injuries, calcium influx is a key initiating element in molecular cascades resulting in both delayed cell death and/or their dysfunction, and delayed axonal disconnections [2, 4, 17, 18]. Many studies have demonstrated that in neurons calcium influx through NMDA channels results in excitotoxicity, generation of free radicals with the development of oxidative stress, mitochondrial dysfunction and postsynaptic receptor modifications [5, 6]. Other foreign reports have shown the presence of astrocytes proliferation that

Повышенный уровень креатинфосфокиназы у больных с отдаленными последствиями после перенесенной закрытой черепно-мозговой травмы