MARKERS OF SYSTEMIC INFLAMMATION AND ENERGY BALANCE IN THE BLOOD OF COMBATANTS FOLLOWING COMBAT MUSCULOSKELETAL TRAUMA
DOI:
https://doi.org/10.17721/1728.2748.2026.105.16-20Keywords:
combat trauma, musculoskeletal system, blood, inflammation, hypoxia, gene expressionAbstract
Background. Modern combat musculoskeletal trauma, caused by the use of high-tech weaponry, is characterized by the multi-component nature of injuries and a high risk of developing severe systemic complications. A key pathogenetic factor in the post-traumatic period is the combination of a systemic inflammatory response and pronounced metabolic imbalance resulting from ischemia-reperfusion tissue injury. The recovery rate of combatants depends on the coordination efficiency of the immune response and the body's ability to maintain energy homeostasis under hypoxic conditions. The aim of the work was to determine a range of indicators of inflammation and energy balance in the blood of combatants following combat musculoskeletal trauma.
Methods. The study was conducted with the participation of two groups. The first group (n = 10) consisted of apparently healthy individuals (control). The second group (n = 14) included patients with combat musculoskeletal trauma. The concentrations of C-reactive protein, lactate, glucose, and the activity of lactate dehydrogenase in blood plasma were determined using standard biochemical methods. The expression levels of NFKB1 and PTGS2 genes were assessed using quantitative real-time PCR. Statistical processing of the results was performed using methods of variational statistics.
Results. Analysis of the blood plasma of patients with combat trauma revealed the development of an acute phase of inflammation, as confirmed by an increase in C-reactive protein concentration. Significant disturbances in energy metabolism were established: an increase in lactate dehydrogenase activity and lactate accumulation against the background of a decrease in glucose concentration, indicating an intensification of anaerobic glycolysis. At the molecular genetic level, a substantial increase in the expression of regulatory genes was recorded – NFKB1, which encodes the central transcriptional factor of inflammation, and the effector gene PTGS2 (cyclooxygenase-2). The synchronous activation of these genetic markers against the backdrop of metabolic deficit indicates the formation of a persistent pro-inflammatory status.
Conclusions. The study results demonstrate the coupling of systemic inflammation processes and metabolic decompensation, leading to a progressive depletion of energy reserves in combatants with gunshot wounds.
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