Background: Gut microbiome composition may influence the risk of intracranial aneurysm rupture. Methods: This study analyzed the gut microbiota of 48 patients—24 with ruptured aneurysms (RA) and 24 with unruptured intracranial aneurysms (UIA)—using next-generation sequencing. Results: While alpha diversity was similar between groups, beta diversity revealed significant taxonomic differences (Bray–Curtis: p = 0.02; unweighted UniFrac: p = 0.0291). Both groups were dominated by the phyla Bacillota, Bacteroidota, and Proteobacteria, but genus- and family-level differences were observed. RA patients showed higher abundances of Anaerotruncus, Coprobacillus, Sellimonas, Hungatella, and Ruthenibacterium, whereas UIA patients exhibited greater levels of Faecalibacterium, Brotolimicola, Clostridiaceae, Roseburia, and Agathobaculum. Linear discriminant analysis identified one class, 10 genera, and 17 species that differed significantly between groups. Notably, Faecalibacterium prausnitzii and Agathobaculum butyriciproducens—bacteria known for their anti-inflammatory and neuroprotective properties—were enriched in UIA patients. Conclusions: These findings suggest that gut microbiota, particularly short-chain fatty acid–producing bacteria, may contribute to vascular protection and aneurysm pathophysiology. Microbiome-based therapeutic strategies could offer new avenues for the prevention of cerebrovascular disease.

We aimed to investigate the characteristics of serum metabolomics in aneurysmal subarachnoid hemorrhage patients (aSAH) with different 3-month outcomes (good = modified Rankin score: 0–3 vs. poor = mRS 4–6). We collected serum samples from 46 aSAH patients at 24 (D1) and 168 (D7) hours after injury for analysis by liquid chromatography-mass spectrometry. Ninety-six different metabolites were identified. Groups were compared using multivariate (orthogonal partial least squares discriminant analysis), univariate, and receiving operator characteristic (ROC) methods. We observed a marked decrease in serum homocysteine levels at the late phase (D7) compared to the early phase (D1). At both D1 and D7, mannose and sorbose levels were notably higher, alongside elevated levels of kynurenine (D1) and increased 2-hydroxybutyrate, methyl-galactoside, creatine, xanthosine, p-hydroxyphenylacetate, N-acetylalanine, and N-acetylmethionine (all D7) in the poor outcome group. Conversely, levels of guanidinoacetate (D7) and several amino acids (both D1 and D7) were significantly lower in patients with poor outcomes. Our results indicate significant changes in energy metabolism, shifting towards ketosis and alternative energy sources, both in the early and late phases, even with adequate enteral nutrition, particularly in patients with poor outcomes. The early activation of the kynurenine pathway may also play a role in this process.

Aneurysmal subarachnoid hemorrhage (aSAH) is a serious condition complicated by delayed cerebral ischemia (DCI), where inflammation plays a key role. Although altered gut permeability is noted in other conditions, its significance in aSAH remains unclear. Fatty acid-binding protein (FABP-I), lipopolysaccharide-binding protein (LBP), and soluble CD-14 (sCD-14) are established markers of barrier dysfunction. This study investigates gut permeability marker changes in early and late aSAH phases. The study included 177 aSAH patients and 100 controls. Serum samples were collected on days 1 (D1) and 9 (D9) after ictus. FABP-I, LBP, and sCD-14 levels were measured via ELISA, and clinical data were recorded. Outcomes were assessed using the 90-day modified Rankin scale (mRS 0–3 = favorable outcome). Serum FABP-I was significantly lower in aSAH patients (p < 0.05), while LBP and sCD-14 were higher (p < 0.001) compared to controls. FABP-I did not differ between outcome groups, but LBP and sCD-14 were significantly elevated in unfavorable outcomes (p < 0.001). These markers differed in patients without in-hospital infection, with higher levels noted in DCI patients during the later phase (p < 0.05). In aSAH patients without infection, differences in LBP and sCD-14 levels between outcome groups suggest potential endotoxin release from microbial systems, contributing to neuroinflammation and influencing outcomes.