Key result
Ibuprofen suppressed the antiplatelet effects of aspirin regardless of concentration, whereas a 6-hour interval between loxoprofen and aspirin avoided this interaction in vitro.
Why the study?
Does the timing of NSAID (ibuprofen or loxoprofen) administration relative to aspirin affect aspirin's antiplatelet effects in vitro?
Does the timing of NSAID (ibuprofen or loxoprofen) administration relative to aspirin affect aspirin's antiplatelet effects in vitro?
Absolute Event Rate: 4.1% vs 5.9%
p-value: p=<0.05
In vitro findings suggest that a 6-hour interval between loxoprofen and aspirin administration can prevent loxoprofen from inhibiting aspirin's antiplatelet effects, whereas ibuprofen co-administration should be avoided entirely.
These in vitro findings warrant caution with ibuprofen-aspirin co-use; clinical studies needed to confirm loxoprofen timing relevance in patients.
Low-dose aspirin irreversibly inhibits platelet cyclooxygenase-1 (COX-1) and suppresses platelet aggregation. It is effective for secondary prevention of cardiovascular events. Because nonsteroidal anti-inflammatory drugs (NSAIDs) reversibly bind with COX-1, the antiplatelet effects of aspirin may be suppressed when NSAIDs are co-administered. This interaction could be avoided by avoiding simultaneous administration; however, the minimum interval that should separate the administration of aspirin and loxoprofen is not well known. In this study, we investigated how to avoid the influence of NSAIDs on the antiplatelet effects of aspirin. An in vitro experiment was performed to investigate the influence of ibuprofen and loxoprofen at various concentrations on aspirin’s antiplatelet action. Platelet aggregation and thromboxane B2 (TXB2) levels were measured after addition of aspirin only and NSAIDs plus aspirin to platelet-rich plasma. NSAIDs were used at their maximum plasma concentrations, the assumed concentration after 6 h (for loxoprofen only), and the assumed concentration after 12 h of taking one clinical dose. Platelet aggregation threshold index (PATI), defined as the putative stimulus concentration giving 50% aggregation, was calculated as an index of aggregation activity. PATI decreased in ibuprofen plus aspirin group compared to that in the aspirin only group, regardless of ibuprofen concentration. Furthermore, PATI significantly decreased when aspirin was added after loxoprofen-trans-OH addition at the maximum concentration (4.1 ± 0.1 μg/mL), compared to that in aspirin only group (5.9 ± 0.1 μg/mL). PATI showed no significant difference after addition of loxoprofen at the assumed concentration after 6 h (aspirin only group, 5.0 ± 0.5 μg/mL; loxoprofen-trans-OH plus aspirin group, 4.9 ± 0.4 μg/mL).In addition, TXB2 concentration tended to decrease with increasing PATI. It is desirable to avoid ibuprofen co-administration with the usual once-daily low-dose aspirin therapy; however, a 6-h interval between loxoprofen and aspirin could avoid this potential interaction when loxoprofen is taken before aspirin.
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Shibata et al. (2017) studied Healthy volunteers (in vitro platelet aggregation) (n=6). Loxoprofen-trans-OH plus aspirin vs. Aspirin only was evaluated on Platelet aggregation threshold index (PATI) in μg/mL (p=<0.05). Ibuprofen suppressed the antiplatelet effects of aspirin regardless of concentration, whereas a 6-hour interval between loxoprofen and aspirin avoided this interaction in vitro.
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