Key result
Acute ingestion of a large dose of alcohol (1.5 g/kg) transiently enhanced thromboxane-mediated platelet activation (P<0.05) and increased plasminogen activator inhibitor 1 activity 7-fold.
Why the study?
Does acute ingestion of a large dose of alcohol alter hemostatic markers and their circadian variation in healthy men?
Population
12 healthy, nonsmoking men
Comparison
Acute intake of a large dose of alcohol vs Fruit juice alone
Design
RCT, Treatments were randomized
Follow-up
12 to 24 hours
Authors
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Acute binge drinking transiently promotes thrombosis; extends mechanistic evidence linking alcohol to cardiovascular events.
RCT (n=12)
randomized
Does acute ingestion of a large dose of alcohol alter hemostatic markers and their circadian variation in healthy men?
p-value: p=<0.05
Acute ingestion of a large dose of alcohol transiently enhances thromboxane-mediated platelet activation and alters the circadian periodicity of the hemostatic system, providing a potential mechanism for binge drinking-triggered cardiovascular events.
Numminen et al. (2000) conducted an RCT in Healthy, nonsmoking men (n=12). Alcohol (ethanol in fruit juice) vs. Fruit juice alone was evaluated on Urinary excretion of the platelet thromboxane A(2) metabolite 2, 3-dinor-thromboxane B(2) (p=<0.05). Acute ingestion of a large dose of alcohol (1.5 g/kg) transiently enhanced thromboxane-mediated platelet activation (P<0.05) and increased plasminogen activator inhibitor 1 activity 7-fold.
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