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Updated: Mar 7, 2026
Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model
Published on: June 18, 2021
Impact of High-Mobility Group Box 1 Polymorphism on Delayed Cerebral Ischemia After Aneurysmal Subarachnoid
Philipp Hendrix1, Paul M Foreman2, Mark R Harrigan2
1Department of Neurosurgery, Saarland University Medical Center and Saarland University Faculty of Medicine, Homburg/Saar, Germany.
Background And Objective:
The high-mobility group box 1 (HMGB1) protein is a eukaryotic, ubiquitously expressed protein that serves as a biomarker for various diseases and is involved in the promotion of a proinflammatory response to cell injury. In aneurysmal subarachnoid hemorrhage (aSAH), increased HMGB1 levels have been linked to poor outcome and an increased risk for cerebral vasospasm. The role of HMGB1 polymorphisms in aSAH has not been previously investigated.
Methods:
Patients with aSAH and controls enrolled in the prospective, 2-center CARAS (Cerebral Aneurysm Renin Angiotensin System) study were evaluated. The 3814 C/G HMGB1 single nucleotide polymorphism (SNP) rs2249825 was detected using 5'exonuclease (Taqman) genotyping assays from blood samples from patients with aSAH and controls. Associations between aSAH and its clinical sequelae with the HMGB1 SNP were assessed.
Results:
Samples from 149 patients with aSAH and 50 controls were available for analysis. No increased risk for aSAH associated with the SNP was found compared with the control group. Delayed cerebral ischemia (DCI) was defined as a cerebral infarction at the time of discharge from the intensive care unit and identified in 21.2% of patients with aSAH. In multivariable logistic regression analysis, the G allele of rs2249825 was independently associated with DCI (odds ratio, 5.695; 95% confidence interval, 1.804-17.975; P = 0.003).
Conclusions:
The minor allele G of rs2249825 was associated with an increased risk for DCI, or cerebral infarction, after aSAH. This finding may be attributable to an increased HMGB1 protein expression in these patients.
