Zhurnal voprosy neirokhirurgii imeni N. N. Burdenko · 2026
[Clinical and prognostic value of IL-6 and IL-2 monitoring in patients with severe traumatic brain injury].
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Sychev A A, Savin I A, Danilov G V, Baranich A I, Kakurin K O, Strunina Yu V, Oshorov A V, Kravchuk A D
Аннотация
UNLABELLED: Traumatic brain injury (TBI) is characterized by high mortality and severe disability worldwide representing a major social, economic, and medical problem. Pathogenesis of secondary brain damage is underpinned by a cascade of neuroinflammatory reactions triggered by cytokine release. Key mediators include interleukin-6 (IL-6) and interleukin-2 (sIL-2R) system. However, their daily dynamics in acute period of severe trauma and relationship with intracranial hypertension remain poorly understood.
MATERIAL AND METHODS: The study was conducted at the Burdenko Neurosurgical Center. Inclusion criteria: acute TBI, admission within 24 hours, age 18-75 years. Exclusion criteria: atonic coma, decompensation of chronic diseases. IL-6, sIL-2R, C-reactive protein, and procalcitonin were assessed.
RESULTS: There were 74 patients with severe TBI (19 women, mean age 34.0±12.5 years). The mortality rate was 14.9% (11 patients). Biphasic cytokine dynamics was revealed. Early increase in IL-6 on day 1 reflected extent of primary injury. On the 2nd day, IL-6 levels remained significantly higher in patients with fatal outcome (median 40.2 vs. 22.4 pg/ml, p<0.05). Secondary increase was recorded after 3 days and coincided with manifestation of infectious complications peaking on day 5. On day 5, sIL-2R levels were found to be more than 2.5-fold higher in patients with fatal outcome (1660.0 vs. 649.0 pg/ml, p<0.05). In fatal patients, we found strong direct correlation between IL-6 and intracranial pressure (rho=0.71), as well as inverse correlation with cerebral perfusion pressure.
CONCLUSION: Biphasic cytokine response develops in acute phase of severe traumatic brain injury. Early phase (2 days) is characterized by increased IL-6 according to extent of primary cerebral injury. The second phase (days 3-14) is associated with infectious complications and characterized by increased sIL-2R and IL-6. It is not their absolute value, but temporal dynamics is prognostically significant. No IL-6 reduction by 48 hours after injury indicates uncontrollable neuroinflammation and potentially unfavorable outcomes. Peak (more than 2.5 times) increase in sIL-2R on day 5 is a marker of transformation of protective inflammation into systemic hyperinflammatory syndrome. Direct correlation between IL-6 and intracranial hypertension in fatal patients confirms pathogenetic role of this cytokine in secondary brain injury. IL-6 and sIL-2R monitoring may enable timely identification of patients with high risk of fatal intracranial hypertension and ensure a personalized approach to intensive care.
MATERIAL AND METHODS: The study was conducted at the Burdenko Neurosurgical Center. Inclusion criteria: acute TBI, admission within 24 hours, age 18-75 years. Exclusion criteria: atonic coma, decompensation of chronic diseases. IL-6, sIL-2R, C-reactive protein, and procalcitonin were assessed.
RESULTS: There were 74 patients with severe TBI (19 women, mean age 34.0±12.5 years). The mortality rate was 14.9% (11 patients). Biphasic cytokine dynamics was revealed. Early increase in IL-6 on day 1 reflected extent of primary injury. On the 2nd day, IL-6 levels remained significantly higher in patients with fatal outcome (median 40.2 vs. 22.4 pg/ml, p<0.05). Secondary increase was recorded after 3 days and coincided with manifestation of infectious complications peaking on day 5. On day 5, sIL-2R levels were found to be more than 2.5-fold higher in patients with fatal outcome (1660.0 vs. 649.0 pg/ml, p<0.05). In fatal patients, we found strong direct correlation between IL-6 and intracranial pressure (rho=0.71), as well as inverse correlation with cerebral perfusion pressure.
CONCLUSION: Biphasic cytokine response develops in acute phase of severe traumatic brain injury. Early phase (2 days) is characterized by increased IL-6 according to extent of primary cerebral injury. The second phase (days 3-14) is associated with infectious complications and characterized by increased sIL-2R and IL-6. It is not their absolute value, but temporal dynamics is prognostically significant. No IL-6 reduction by 48 hours after injury indicates uncontrollable neuroinflammation and potentially unfavorable outcomes. Peak (more than 2.5 times) increase in sIL-2R on day 5 is a marker of transformation of protective inflammation into systemic hyperinflammatory syndrome. Direct correlation between IL-6 and intracranial hypertension in fatal patients confirms pathogenetic role of this cytokine in secondary brain injury. IL-6 and sIL-2R monitoring may enable timely identification of patients with high risk of fatal intracranial hypertension and ensure a personalized approach to intensive care.