Key result
Ibuprofen interfered with the antiplatelet effect of aspirin by lowering the platelet aggregation threshold index (1.15 µg/mL vs 1.43 µg/mL for aspirin alone), whereas five other NSAIDs did not.
Why the study?
Does the addition of NSAIDs interfere with the antiplatelet effect of aspirin in human platelet rich plasma?
Does the addition of NSAIDs interfere with the antiplatelet effect of aspirin in human platelet rich plasma?
Absolute Event Rate: 1.15% vs 1.43%
In vitro experiments demonstrate that ibuprofen interferes with the antiplatelet effect of aspirin, an interaction that correlates with the NSAID's level of platelet COX-1 inhibition.
Ibuprofen may blunt aspirin's antiplatelet effect in vitro; leaves open clinical relevance and effects of other NSAIDs.
Low dose aspirin acts as an antiplatelet agent through irreversible acetylation of platelet cyclooxygenase (COX)-1,which inhibits platelet aggregation.Nonsteroidal anti-inflammatory drugs (NSAIDs) have a similar mechanism of action to aspirin,and may interact pharmacodynamically with it.In view of this,we performed an in vitro experimental study in which 6 NSAIDs with various COX-1 activities were added to human blank blood to investigate the influence of each one on the antiplatelet action of aspirin.Platelet rich plasma (PRP) was obtained from 8 healthy volunteers (23.3±3.2 years old).After adding aspirin (plasma concn.: 16μg/mL) and NSAIDs (plasma concn.: maximal concentration in clinical use) to the PRP,aggregation was measured using collagen as the stimulus.We used the platelet-aggregation threshold index (PATI) as the index of aggregation activity for this study.The PATI of a group in which aspirin was added after ibuprofen (Ibu→Asp) and that of a group in which both drugs were added at the same time (Asp+Ibu) were 3.54±0.80 and 3.53±1.01μg/mL,respectively.These were lower than the PATI for aspirin alone (5.17±1.18μg/mL),indicating interference with the antiplatelet effect by the NSAID.For the other 5 NSAIDs,the PATI obtained was similar to that for aspirin,regardless of the order of addition.The logarithmic value of the unbound drug concentration of each NSAID (Df) divided by platelet COX-1 IC50[log (Df/COX-1 IC50)]was correlated with its PATI (R=0.817,p<0.001),suggesting that the interaction between low dose aspirin and NSAIDs may be inferred from the level of inhibition of platelet COX-1 at clinical drug concentrations.
No takes yet. Share an insight, caveat, or question.
Akagi et al. (2010) studied Healthy (n=10). Ibuprofen and other NSAIDs vs. Aspirin alone was evaluated on Platelet aggregation threshold index (PATI). Ibuprofen interfered with the antiplatelet effect of aspirin by lowering the platelet aggregation threshold index (1.15 µg/mL vs 1.43 µg/mL for aspirin alone), whereas five other NSAIDs did not.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: