Key result
Acute administration of either selective or non-selective NSAIDs combined with long-term low-dose aspirin induced significant gastric damage in rats (p < 0.05), without affecting kidney function.
Why the study?
Does acute administration of selective or non-selective NSAIDs induce gastric or renal damage in rats receiving chronic low-dose aspirin therapy?
Does acute administration of selective or non-selective NSAIDs induce gastric or renal damage in rats receiving chronic low-dose aspirin therapy?
Acute use of either selective or non-selective NSAIDs exacerbates gastric damage in an animal model of chronic low-dose aspirin therapy, highlighting the need for clinical caution when prescribing NSAIDs to patients on aspirin.
May increase gastric risk when adding acute NSAIDs to chronic aspirin; rat data are hypothesis-generating and require clinical confirmation.
The consumption of low-dose aspirin (LDA) to prevent cardiovascular disease continues to increase worldwide. Consequently, the number of chronic LDA users seeking dental procedures that require complementary acute anti-inflammatory medication has also grown. Considering the lack of literature evaluating this interaction, we analyzed the gastric and renal effects caused by a selective COX-2 inhibitor (etoricoxib) and a non-selective COX-2 inhibitor (ibuprofen) nonsteroidal anti-inflammatory drug (NSAID) in rats receiving chronic LDA therapy. Male Wistar rats were divided into six experimental groups (carboxymethylcellulose (CMC) - vehicle; LDA; LDA + ibuprofen; ibuprofen; LDA + etoricoxib; and etoricoxib) and submitted to long-term LDA therapy with a subsequent NSAID administration for three days by gavage. After the experimental period, we analyzed gastric and renal tissues and quantified serum creatinine levels. The concomitant use of LDA with either NSAID induced the highest levels of gastric damage when compared to the CMC group (F = 20.26, p < 0.05). Treatment with either LDA or etoricoxib alone was not associated with gastric damage. No significant damage was observed on kidney morphology and function (F = 0.5418, p > 0.05). These results suggest that even the acute use of an NSAID (regardless of COX-2 selectivity) can induce gastric damage when combined with the long-term use of low-dose aspirin in an animal model. Additional studies, including clinical assessments, are thus needed to clarify this interaction, and clinicians should be careful of prescribing NSAIDs to patients using LDA.
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Moro et al. (2016) studied chronic low-dose aspirin therapy. NSAID (etoricoxib or ibuprofen) vs. carboxymethylcellulose (CMC) vehicle was evaluated on gastric damage (p=< 0.05). Acute administration of either selective or non-selective NSAIDs combined with long-term low-dose aspirin induced significant gastric damage in rats (p < 0.05), without affecting kidney function.
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