Key result
ASA treatment augmented pro-inflammatory cytokines during endotoxaemia, while adding P2Y12 antagonists did not affect circulating cytokines except for ticagrelor attenuating TNFα increases.
Why the study?
Does antiplatelet therapy (ASA alone or combined with P2Y12 inhibitors) modulate the systemic inflammatory response in healthy subjects undergoing experimental endotoxaemia?
Population
n=40 healthy subjects undergoing experimental endotoxaemia via intravenous administration of Escherichia…
Comparison
Seven days of placebo with acetylsalicylic acid… vs Seven days of placebo
Design
RCT, randomised
Follow-up
7 days
Authors
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ASA may worsen inflammation in endotoxaemia; challenges anti-inflammatory assumptions and extends differential P2Y12 effects to patient trials.
RCT (n=40)
randomised
No
Does antiplatelet therapy (ASA alone or combined with P2Y12 inhibitors) modulate the systemic inflammatory response in healthy subjects undergoing experimental endotoxaemia?
In a human experimental endotoxaemia model, ASA augments pro-inflammatory cytokine responses, an effect largely unmodified by the addition of P2Y12 inhibitors except for a reduction in TNFα by ticagrelor.
Kiers et al. (2017) conducted an RCT in Healthy subjects (experimental endotoxaemia) (n=40). Antiplatelet therapy (ASA, ticagrelor + ASA, or clopidogrel + ASA) vs. Placebo was evaluated on Systemic inflammatory response (plasma concentration of cytokines). ASA treatment augmented pro-inflammatory cytokines during endotoxaemia, while adding P2Y12 antagonists did not affect circulating cytokines except for ticagrelor attenuating TNFα increases.
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