Key result
Mild acute ischemic stroke linked to lower clopidogrel active metabolite Cmax versus healthy controls.
Why the study?
Inflammatory states like acute ischaemic stroke may cause CYP2C19 phenoconversion, temporarily reducing enzyme activity and impairing clopidogrel activation.
Does mild acute ischaemic stroke reduce CYP2C19 activity and clopidogrel activation compared to healthy controls?
Comparison
Acute phase vs post-acute phase (21 days after acute ischaemic stroke)
Design
Pharmacokinetic study
Follow-up
21 days
Authors
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May reduce clopidogrel activation in mild stroke regardless of genotype; leaves open whether phenoconversion warrants adjusted monitoring or dosing.
Observational (n=33)
Does mild acute ischaemic stroke reduce CYP2C19 activity and clopidogrel activation compared to healthy controls?
p-value: p=<0.05
Acute ischaemic stroke induces CYP2C19 phenoconversion, reducing clopidogrel activation regardless of genotype, suggesting genotyping alone may be insufficient to identify poor metabolizers.
Alaei et al. (2026) conducted an observational in Mild acute ischaemic stroke (n=33). Mild acute ischaemic stroke vs. Healthy controls was evaluated on H4-clopi maximum plasma concentration (Cmax) (p=<0.05). Mild acute ischaemic stroke was associated with significantly lower clopidogrel active metabolite Cmax compared to healthy controls in both acute and post-acute phases (p < 0.05).
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