Inflammatory Biomarkers in Stroke: A Comprehensive Review

Stroke remains a leading cause of disability and death globally, with accumulating evidence suggesting that inflammation plays a key role in its pathogenesis. This review has summarized current evidence regarding prominent inflammatory biomarkers high-sensitivity C-reactive protein (hsCRP), interleukin-6(IL-6), interleukin-18(IL-18), tumor necrosis factor-alpha (TNF-α), and serine proteinase inhibitor A3(SERPINA3) and their involvement in stroke severity, progression, and recurrence. hsCRP was associated with larger infarct volume and predicted cardiovascular events in 8,420 patients. IL-6, detectable within 2.5hours of stroke onset, has been linked with 8% rise in recurrence risk for each 1pg/mL increment. IL-18 was associated with neuroinflammation and post-stroke depression with reduced levels reducing risk of cardioembolic stroke, though its role in acute environment remains uncertain. TNF-α levels dropped from 7.39 to 5.12pg/mL within seven days, in relation to poor functional outcome and enhanced atherosclerotic risk. Elevated levels of SERPINA3 (>78.90ng/mL) have been linked with increased cerebral small vessel disease burden. These biomarkers have been promising for clinical application in risk stratification and pathway-targeting interventions, e.g., IL-6 or TNF-α pathway targeting. There are, however, limitations, including the non-causal role of hsCRP in atherosclerosis, controversial data on IL-18, and lack of standard assays for SERPINA3. This review has emphasized the need for further validation in representative cohorts, the development of composite biomarker panels, and the incorporation of these markers into predictive models to enable enhanced clinical decision-making. In summary, the findings confirm the central role of inflammation in stroke and validate biomarker-guided strategies to optimize patient outcomes.