Related Experiment Video
Updated: Oct 25, 2025

A Mouse Model of Hemorrhagic Transformation Induced by Acute Hyperglycemia Combined with Transient Focal Ischemia
Published on: November 15, 2024
Association between aspirin-induced hemoglobin decline and outcome after acute ischemic stroke in G6PD-deficient
Yicong Chen1, Jianle Li1, Zilin Ou1
1Department of Neurology, The First Affiliated Hospital, Sun Yat-sen University, Guangdong Provincial Key Laboratory for Diagnosis and Treatment of Major Neurological Diseases, National Key Clinical Department and Key Discipline of Neurology, Guangzhou, China.
Insights
Glucose-6-phosphate dehydrogenase (G6PD) deficiency increases hemoglobin decline risk during aspirin treatment for ischemic stroke. This decline is linked to poorer stroke outcomes, necessitating careful monitoring in G6PD-deficient patients.
Area of Science:
- Neurology
- Hematology
- Pharmacology
Background:
- Low-dose aspirin is commonly used for secondary stroke prevention.
- Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a genetic disorder affecting red blood cells.
- The impact of G6PD deficiency on aspirin's effects and stroke outcomes is not well understood.
Purpose of the Study:
- To investigate the effect of G6PD deficiency on hemoglobin levels during aspirin therapy.
- To assess the association between G6PD deficiency, hemoglobin decline, and outcomes in acute ischemic stroke patients.
Main Methods:
- A cohort study of 279 acute ischemic stroke patients treated with aspirin 100 mg/day.
- Comparison of hemoglobin decline (≥25 g/L or 25%) and anemia rates between G6PD-deficient and G6PD-normal groups.
- Modified Rankin Scale (mRS) at 3 months used to define poor functional outcomes.
Main Results:
- G6PD-deficient patients showed significantly higher rates of hemoglobin decline (15.0% vs. 3.3%) and anemia (30.0% vs. 14.6%) after aspirin treatment.
- Higher bilirubin increase observed in the G6PD-deficient group, suggesting hemolysis.
- G6PD-deficient patients had a higher rate of poor functional outcomes (RR = 1.31) at 3 months.
Conclusions:
- Aspirin treatment in G6PD-deficient patients with ischemic stroke can lead to significant hemoglobin decrease and hemolysis.
- Lower hemoglobin levels post-aspirin are associated with increased risk of poor functional outcomes.
- Close monitoring of hemoglobin is crucial for G6PD-deficient patients with ischemic stroke receiving aspirin.
Aims:
The risk of hemoglobin decline induced by low-dose aspirin in glucose-6-phosphate dehydrogenase (G6PD) deficiency remains unknown, and its influence on stroke outcome remains to be investigated. This study aimed to evaluate the effect of G6PD deficiency on hemoglobin level during aspirin treatment and its association with outcome after acute ischemic stroke.
Methods:
In total, 279 patients (40 G6PD-deficient and 239 G6PD-normal) with acute ischemic stroke treated with aspirin 100 mg/day from a cohort study were examined. The primary safety endpoint was a hemoglobin decline ≥25 g/L or 25% from baseline within 14 days after aspirin treatment. Poor outcomes were defined as a modified Rankin Scale score ≥2 at 3 months. The χ2 test was used to compare stroke outcomes, and multivariate logistic regression analyses were performed to analyze the association between hemoglobin level and outcomes.
Results:
The G6PD-deficient group had lower baseline hemoglobin and tended to develop comorbid pulmonary infection more frequently (p < 0.05). The proportion of patients with hemoglobin decline ≥25 g/L or 25% from baseline (15.0% vs. 3.3%; p = 0.006) and anemia (30.0% vs. 14.6%; p = 0.016) after aspirin treatment was higher in the G6PD-deficient group, which was accompanied by a more significant bilirubin increase. The rate of poor functional outcomes at 3 months after acute ischemic stroke was higher in the G6PD-deficient group (Risk ratio = 1.31 [95% confidence interval (CI) = 1.10-1.56]; p = 0.017). Confounder-adjusted analysis showed that lower hemoglobin levels (odds ratio = 0.98 [95% CI = 0.96-0.99]; adjusted p = 0.009) increased the risk of poor functional outcomes.
Conclusion:
Hemoglobin decrease with bilirubin increase after aspirin treatment in patients with G6PD deficiency suggests hemolysis, which may influence stroke prognosis. The risk of hemoglobin decline should be carefully monitored in G6PD-deficient patients with ischemic stroke taking aspirin.
More Related Videos
Related Concept Videos
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
Pharmacodynamics in Geriatric Patients: Effects of Age
Disorders of Hemostasis
Thromboembolic Disorders
Two factors primarily cause thromboembolic conditions.
Effect of Hepatic Disease on Pharmacokinetics: Dose Adjustments Due to Hepatic Impairment
Anticoagulant Drugs: Low-Molecular-Weight Heparins
Genome-wide Association Studies-GWAS
GWAS does not require the identification of the target gene involved in...

