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高迁移率族蛋白 B1 作为急性缺血性卒中患者机械取栓术后恶性脑水肿的预测因子
Authors Chen X, E Y, Wang W, Huang Y, Xin X, Chen G
Received 20 March 2025
Accepted for publication 18 June 2025
Published 25 June 2025 Volume 2025:18 Pages 3393—3400
DOI https://doi.org/10.2147/IJGM.S529326
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Professor Kenneth Adler
Xiao Chen,1,* Yan E,2,* Wei Wang,2 Yong Huang,1 Xueting Xin,1 Gang Chen1
1Department of Neurology, Haimen People’s Hospital, Nantong, Jiangsu, 226100, People’s Republic of China; 2Department of Neurology, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, 210000, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Gang Chen, Department of Neurology, Haimen People’s Hospital, No. 1201 Beijing Road, Nantong, Jiangsu Province, 226100, People’s Republic of China, Tel/Fax +86 051382263512, Email 15206283321@163.com
Background and Purpose: Emerging experimental evidence has established that high-mobility group box 1 (HMGB-1) plays a pivotal role in cerebral ischemia pathogenesis, primarily through mediating neuroinflammatory cascades following ischemic injury. This study sought to investigate the potential association between circulating HMGB-1 levels and the risk of malignant brain edema (MBE) in patients undergoing mechanical thrombectomy (MT).
Methods: This study prospectively recruited patients presenting with large vessel occlusive stroke in the anterior circulation and receiving MT treatment. Serum HMGB-1 levels were quantitatively assessed for all participants upon hospital admission. MBE was defined as defined as a midline shift of ≥ 5 mm observed on follow-up neuroimaging after MT. Multivariate logistic regression analyses were conducted to investigate the potential correlation between serum HMGB-1 concentrations and MBE development.
Results: Among the cohort of 261 eligible patients (mean age: 69.7 years; male: 166 [63.6%]), 59 individuals (22.6%; 95% confidence interval [CI]: 17.6%-28.3%) developed MBE. After adjusted for demographic characteristics and other potential confounders, multivariate logistic regression demonstrated that higher serum HMGB-1 levels were associated with an increased risk of MBE (odds ratios [OR], highest vs lowest quartile: 3.130; 95% CI, 1.077– 9.098; P = 0.036). In addition, restricted cubic spline analysis revealed a dose-response relationship between elevated serum HMGB-1 levels and MBE risk (P for non-linearity=0.764).
Conclusion: This study confirmed that elevated circulating HMGB-1 levels were significantly associated with MBE after MT. These findings suggested that HMGB-1 could serve as a predictive biomarker for post-MT MBE risk, potentially enabling early identification of high-risk patients who may benefit from intensified monitoring or targeted therapeutic interventions.
Keywords: HMGB-1, brain edema, endovascular treatment, ischemic stroke