Increasing evidence suggests that stroke is a systemic disease affecting multiple organs. Systemic inflammatory response and immune dysregulation associated with hemorrhagic stroke, may play an important role in brain injury, its recovery, and stroke outcomes. However, it is worth of note that, from our point of view, the classical concepts about inflammation in pathophysiology and general pathology do not entirely meet the needs of modern medical practice. The existence of this problem is also typical for assessing pathogenesis, as well as for optimizing pathogenetic therapy of severe strokes. Therefore, within the framework of this work, a dynamic observation and assessment of pathogenesis in severe intracerebral hemorrhage was carried out using the criteria of a systemic inflammation scale. The study included patients with intracerebral hemorrhage and effective cerebral blood flow. Blood sampling was carried out on days 1-3 and 5-7 after clinical manifestation of intracerebral hemorrhage. To determine markers of systemic inflammation in the blood plasma of patients, the levels of IL-6, IL-8, IL-10, TNFá, procalcitonin, cortisol, myoglobin, troponin I and D-dimers were examined using an enzyme-linked immunosorbent assay. The Kolmogorov–Smirnov test was used to confirm the normal data distribution. Further comparison of quantitative data was carried out using the nonparametric Wilcoxon test for paired comparisons. All results were considered statistically significant at p 0.05. In patients on days 1-3 and 5-7, statistically significant differences were not observed in almost all studied markers of systemic inflammation, except for IL-8 and tumor necrosis factor-á. Such increased contents of pro-inflammatory cytokines may indicate increased systemic inflammation over time in the patients with intracerebral hemorrhage and effective cerebral blood flow. Hence, the condition of such patients may worsen on days 5-7 after manifestations of intracerebral hemorrhage, thus requiring more careful monitoring of patients’ blood counts and therapy aimed at suppression of increasing inflammation.
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