Diagnostic value of cellular inflammatory markers in CNS tumor patients undergoing glucocorticoid therapy

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.

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.

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.

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.