RESUMEN
OBJECTIVE: Histone deacetylase 4 (HDAC4) is engaged in the pathophysiology of acute ischemic stroke (AIS) through modulating atherosclerosis, inflammation and neurocyte death. This study aimed to investigate the clinical role of HDAC4 in AIS. METHODS: Serum samples were collected from 176 AIS patients and 80 controls for HDAC4 detection by enzyme-linked immunosorbent assay (ELISA). In AIS patients, disease severity was assessed by National Institute of Health Stroke Scale (NIHSS) score and their recurrence-free survival (RFS) and overall survival (OS) were calculated, inflammatory cytokines and adhesion molecules were detected by ELISA. RESULTS: HDAC4 was declined in AIS patients vs. controls (p < 0.001), it also had certain ability of distinguishing AIS patients from controls with an area under curve of 0.748 (95% confidence interval: 0.689-0.806). Among AIS patients, HDAC4 was negatively linked with NIHSS score (p < 0.001) but no other clinical features (all p > 0.05). Moreover, HDAC4 was negatively related to interleukin (IL)-17 (p = 0.010) and tumor necrosis factor alpha (p = 0.001), while it was not correlated with IL-1ß (p = 0.081) or IL-6 (p = 0.074). Furthermore, HDAC4 was negatively associated with intercellular cell adhesion molecule-1 (p < 0.001) and vascular cell adhesion molecule-1 (p = 0.003). During a median follow-up of 19.0 months, 17 (9.7%) patients had recurrence and 10 (5.7%) patients died. Additionally, high HDAC4 was linked with prolonged RFS (p = 0.044) but not OS (p = 0.079). CONCLUSION: HDAC4 possesses the potential to monitor disease risk, inflammation and estimate recurrence of AIS, while further study with larger scale is needed to verify our findings.