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Introduction: While inflammation is recognized as a key driver of solid tumor progression, the diagnostic and pathophysiological relevance of cellular inflammatory biomarkers in central nervous system (CNS) neoplasms remains incompletely defined. Materials and methods: Clinical and hematological data were analyzed from 44 patients with glioblastoma, 32 with brain metastases, and 33 patients with meningioma who underwent primary surgical treatment between 2024 and 2025. A control group of healthy age-matched volunteers (n = 20) was included for comparison. The diagnostic performance of cellular inflammatory markers was evaluated across tumor entities, with additional stratification according to glucocorticosteroid exposure. Results: Patients with intracerebral tumors exhibited higher neutrophil and monocyte counts, as well as elevated neutrophil-to-lymphocyte ratio (NLR) and pan-immune inflammation value (PIV), along with a lower lymphocyte-to-monocyte ratio (LMR) compared to both the meningioma group and healthy volunteers (p<0.05). In glioblastoma patients, dexamethasone administration significantly affected neutrophil and monocyte counts, NLR and PIV (p<0.05). In the group with metastatic brain lesions, glucocorticoid therapy led to an increase in neutrophil count and NLR (p<0.05). The LMR level was not influenced by dexamethasone. Conclusion: For patients with glioblastoma, the LMR serves as a diagnostically significant inflammatory biomarker independent of glucocorticoid administration. In patients with metastatic brain lesions, the most significant diagnostic value was demonstrated by monocyte counts, PIV and LMR.
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Sklyar et al. (2026) studied this question.
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