Homocysteine, vitamin B6, vitamin B12 and folate profiles in acute ischemic stroke: a hospital-based case-control study

Homocysteine and its vitamin cofactors are associated with vascular biology, but post-stroke measurements are vulnerable to confounding and reverse causation. This study compared serum homocysteine, vitamin B6, vitamin B12 and folate between adults with acute ischemic stroke and non-stroke clinic controls. This single-centre hospital-based case-control study was conducted from January to December 2026 and included 75 adults with imaging-confirmed acute ischemic stroke and 86 non-stroke controls. Clinical and biochemical data were summarised descriptively. Pooled correlations and binary logistic regression were treated as exploratory because controls were unmatched and several important confounders and laboratory-process details were not reported. Cases were older and differed markedly in haemodynamic and metabolic characteristics. They had higher homocysteine (51.3 ± 28.0 vs. 14.7 ± 18.1 µmol/L) and vitamin B6 (4.8 ± 1.5 vs. 1.7 ± 0.9 µg/L), and lower vitamin B12 (180.3 ± 55.7 vs. 356.3 ± 133.3 pg/mL) and folate (3.3 ± 2.7 vs. 7.1 ± 4.5 ng/mL); all p < 0.001. Pooled correlations may reflect case-control separation. In an exploratory adjusted model, vitamin B6 and vitamin B12 were associated with acute ischemic stroke status, but the vitamin B6 estimate was imprecise (adjusted OR, 19.60; 95% CI, 1.69–227.95). The cohort showed a distinct between-group biomarker pattern, including an unexpected elevation of vitamin B6. Marked baseline imbalance, incomplete confounder and assay details, pooled analyses and post-event sampling preclude causal, predictive or clinical-utility claims. Prospective studies with matched controls and standardised measurements are required.