Key result
CYP2C19 poor metaboliser phenotype linked to ~131% higher risk of ischemic cerebrovascular disease.
Why the study?
The role of CYP2C19 gene polymorphisms and dyslipidaemic metabolism in ischemic cerebrovascular disease among Mongolian patients and their interaction with conventional risk factors was unclear.
Does the CYP2C19 poor metaboliser phenotype increase the risk of ischemic cerebrovascular disease and does genotype-guided therapy improve outcomes in Mongolian patients?
Case-Control (n=300)
No
Does the CYP2C19 poor metaboliser phenotype increase the risk of ischemic cerebrovascular disease and does genotype-guided therapy improve outcomes in Mongolian patients?
Odds Ratio: 2.31 (95% CI 1.25–4.26)
p-value: p=0.008
CYP2C19 poor metaboliser phenotype is a significant risk factor for ischemic cerebrovascular disease in the Mongolian population, and genotype-guided antiplatelet therapy improves neurological and lipid outcomes.
CYP2C19 poor metabolizer phenotype was associated with higher ischemic cerebrovascular disease risk in Mongolians; leaves open whether genotype-guided therapy improves outcomes.
This study investigates the role of cytochrome P450 2C19 (CYP2C19) gene polymorphisms and dyslipidaemic metabolism in ischemic cerebrovascular disease among Mongolian patients, analyzing their interaction with conventional risk factors. This case-control study enrolled 300 patients with ischemic cerebrovascular disease: 150 Mongolian patients (observation group) receiving CYP2C19 genotype-guided treatment and 150 Han Chinese patients (control group) undergoing standard care. Baseline characteristics, lipid profiles, CYP2C19 genotypes, NIHSS, and activities of daily living scores were analyzed. Baseline characteristics and CYP2C19 genotype distributions showed no significant differences between groups ( P > .05). Multivariate logistic regression revealed that the poor metaboliser phenotype significantly increased the risk of ischemic cerebrovascular disease odds ratio (OR) = 2.31, 95% confidence interval: 1.25–4.26, P = .008), alongside hypertension (OR = 1.87, P = .043) and diabetes mellitus (OR = 2.12, P = .024). Dyslipidaemia prevalence was marginally but not significantly higher across genotypes in the Mongolian group. After 3 months of treatment, the genotype-guided observation group exhibited significantly greater reductions in total cholesterol and low-density lipoprotein cholesterol, and a slight increase in high-density lipoprotein cholesterol ( P < .05). Furthermore, the observation group demonstrated significantly superior neurological recovery National Institutes of Health Stroke Scale and improved daily functioning (ADL) compared to the control group ( P < .001). CYP2C19 poor-metaboliser status is associated with an increased risk of ischemic cerebrovascular disease in the Mongolian population and may contribute to dyslipidaemia and treatment response heterogeneity. Individualised intervention guided by CYP2C19 genotyping offers potential benefits in improving lipid profiles, neurological function, and short-term outcomes, serving as a valuable tool for precision medicine in this population.
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Hu et al. (2026) conducted a case-control in Ischemic cerebrovascular disease (n=300). CYP2C19 poor metaboliser phenotype vs. Non-poor metaboliser phenotypes was evaluated on Risk of ischemic cerebrovascular disease (OR 2.31, 95% CI 1.25-4.26, p=0.008). The CYP2C19 poor metaboliser phenotype significantly increased the risk of ischemic cerebrovascular disease (OR 2.31, 95% CI 1.25-4.26, p=0.008) in the Mongolian population.
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