- Low-dose (75 mg/day) aspirin irreversibly acetylates Ser529 of cyclo-oxygenase (COX)-1 (while higher and repeated doses are required to acetylate COX-2).
- This results in the complete inhibition of the ability of platelets and mature megakaryocytes to synthesize thromboxane (Tx) A2.
- This effect is reached 1 h after ingestion, while the plasma concentration peaks 30–40 min after aspirin ingestion and the half-life of aspirin is 15–20 min in plasma.
- It takes 5–6 days to recover 50% of normal platelet function.
- It is important to understand that, depending on the agonist used, aspirin is a potent or a weak inhibitor of platelet aggregation.
Monitoring
- Salicylate testing
- may be ordered when it is suspected that someone has ingested a large amount of aspirin or other drugs containing salicylate.
- Usually, blood is drawn and tested at least 4 hours after last known ingestion.
- Results from tests done earlier than this are difficult to interpret.
- Light transmission aggregometry (LTA)
- using arachidonic acid as the agonist or the VerifyNow ASA cartridge.
- Concerning aspirin, since <5% of patients are poor responders, of which a proportion are non-compliant, it does not seem reasonable to propose the monitoring of every patient on aspirin therapy.
- Rather, in case of any doubt, increasing the dosage may be sufficient to ensure that the drug is not responsible for the treatment failure
- Measures 11-dehydrothromboxane B2 in urine.
- High levels of 11-dehydrothromboxane B2 (a metabolic breakdown product of thromboxane A2) in the urine may indicate a lack of response to aspirin.
References:
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