What question did this study set out to answer?

The aim is to identify early metabolic changes that predict delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage.

March 30, 2026Open Access

Systemic metabolic reprogramming within 24 h predicts delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage

Key Points

The aim is to identify early metabolic changes that predict delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage.
Analyzed serum samples from 44 aSAH patients within 24 hours of admission.
Used untargeted metabolomics via liquid chromatography–tandem mass spectrometry.
Performed supervised multivariate modeling and pathway enrichment analysis.
Assessed clinical predictors with multivariate logistic regression.
Identified 110 differential metabolites associated with DCI, with specific metabolites upregulated or downregulated.
Found clear separation in metabolic profiles between DCI and non-DCI groups.
Vasospasm and age emerged as independent predictors of DCI.

Abstract

Background Delayed cerebral ischemia (DCI) remains a major determinant of poor outcomes after aneurysmal subarachnoid hemorrhage (aSAH), yet early risk stratification is challenging. Methods A retrospective cohort of 44 aSAH patients was analyzed (DCI, n = 22; non-DCI, n = 22). Serum collected within 24 h of admission underwent untargeted liquid chromatography–tandem mass spectrometry metabolomics. Between-group separation was evaluated using supervised multivariate modeling with permutation testing. Differential metabolites were identified using a combined multivariate and univariate strategy (two-sided P 0.05), followed by pathway enrichment analysis. Independent clinical predictors were assessed using multivariate logistic regression, and aneurysm morphology was quantified on admission CT angiography using radiomics-derived parameters. Results The DCI group was older, had a higher proportion of females, worse admission neurological status, higher vasospasm incidence, and lower hemoglobin. Vasospasm and age were independent predictors. Aneurysm morphological parameters showed no between-group differences. Metabolic profiles showed clear separation, supported by permutation testing ( R 2 = 0.6485; Q 2 intercept = −0.4173). A total of 110 differential metabolites were identified (39 upregulated and 71 downregulated in DCI). Representative changes included increased sphinganine, 2-octenoylcarnitine, guanidoacetic acid, and 5-aminopentanoic acid, with decreased lysophosphatidylcholine 16:0, lysophosphatidylethanolamine 16:0, xanthine, and dehydroepiandrosterone sulfate. Enrichment highlighted coordinated alterations in energy-related, amino-acid, and nucleotide-related pathways. Conclusion Early serum metabolomics within 24 h after aSAH revealed a DCI-associated systemic metabolic signature, supporting the identification of exploratory serum metabolic features associated with DCI in a Chinese cohort, which may inform future biomarker development following targeted validation.

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