Lumiracoxib Does Not Affect the Ex Vivo Antiplatelet Aggregation Activity of Low‐Dose Aspirin in Healthy Subjects

Jermany, J.; Branson, Janice; Schmouder, Robert; Guillaume, M.; Rordorf, Christiane

doi:10.1177/0091270005280377

Cited by 11 publications

(3 citation statements)

References 37 publications

(39 reference statements)

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“…Jermany and colleagues conducted a study in 28 healthy volunteers that were randomly assigned to receive either lumiracoxib 400 mg once daily or placebo for 11 days, with concomitant ASA 75 mg daily for days 5-11 [35]. This study was designed to investigate the effect of selective COX-2 inhibitors on ASA's antiplatelet activity.…”

Section: Fig 1 Cyclooxygenase Inhibition With Both Aspirin and Ibuprmentioning

confidence: 99%

Possible mechanisms of drug-induced aspirin and clopidogrel resistance

Schroeder

Ghobrial²,

Gandhi

2006

J Thromb Thrombolysis

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Aspirin (ASA) and clopidogrel have been identified as standard of care in the prevention of major cardiovascular events. Aspirin irreversibly inhibits the cyclooxygenase-1 (COX-1) enzyme, whereas non-steroidal anti-inflammatory drugs (NSAIDs) reversibly inhibit the COX-1 enzyme. An analysis of the literature revealed a statistically significant decrease in clinical benefit of ASA with concomitant administration of ibuprofen. Another NSAID, diclofenac, showed minimal effect on the inhibition of platelet aggregation when administered with ASA. Furthermore, the selective COX-2 inhibitor, rofecoxib, was not shown to influence the effect of ASA. Clopidogrel is metabolized to an active thiol metabolite by the CYP 3A4 enzyme. Some HMG CoA reductase inhibitors have the ability to inhibit the CYP 3A4 enzyme, which can result in a possible interaction if administered concomitantly with clopidogrel. Studies have demonstrated clopidogrel's platelet inhibition being significantly attenuated by atorvastatin. However in a post-hoc analysis, it was demonstrated that there was no difference in clinical outcomes between patients taking clopidogrel and HMG-CoA reductase inhibitors metabolized by and not metabolized by CYP 3A4. Data suggest that the interaction observed involving clopidogrel and HMG-CoA reductase inhibitors appears to be significant in-vitro. Therefore, practitioners should advise patients receiving chronic aspirin therapy to limit the use of ibuprofen and may consider concomitant administration of clopidogrel with HMG-CoA reductase inhibitors without regard for the drug interaction. The intent of this paper is to review the literature discussing possible mechanisms of drug-induced aspirin and clopidogrel resistance and discuss whether the interactions translate into clinical effects.

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Section: Fig 1 Cyclooxygenase Inhibition With Both Aspirin and Ibuprmentioning

confidence: 99%

Possible mechanisms of drug-induced aspirin and clopidogrel resistance

Schroeder

Ghobrial²,

Gandhi

2006

J Thromb Thrombolysis

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“…Etoricoxib has no effects on bleeding time, or platelet aggregation and does not interfere with the antiplatelet effect of low-dose aspirin. Similarly, lumiracoxib did not affect the ex vivo antiplatelet aggregation activity of low dose-aspirin in healthy volunteers; lumiracoxib 400mg once daily showed no inhibition of arachidonic acid and collagen-induced platelet aggregation; serum TXB 2 levels and urinary excretion of TXB 2 were not affected [69]. Thus, etoricoxib is associated with less GI mucosal damage and spares gastric mucosal COX-1, the predominant source of PGs.…”

Section: Discussionmentioning

confidence: 90%

Global Gastrointestinal Safety Profile of Etoricoxib and Lumiracoxib

Yuan¹,

Hunt

2007

CPD

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Cyclo-oxygenase (COX)-2 selective inhibitors (coxibs) were designed to reduce the incidence of gastrointestinal (GI) adverse events (AEs) which occur with non-selective NSAIDs (ns-NSAIDs). Etoricoxib and lumiracoxib are regarded as second generation coxibs because of their higher COX-2 selectivity. There are three published pooled analyses relating to the GI tolerability of etoricoxib (60-120 mg/day) and lumiracoxib (200-400 mg/day) which used individual patient's data from studies sponsored by the manufacturers. We also reviewed new clinical trials published after the pooled analyses, to determine the global GI safety profiles of etoricoxib and lumiracoxib. We included discontinuations due to GI events, endoscopic ulcers, symptomatic ulcers, and ulcer complications. Current evidence suggests that etoricoxib and lumiracoxib have significantly more favorable GI profiles than ns-NSAIDs, and are similar to first generation coxibs with respect to GI safety. The most clinically important benefit of the coxibs is seen in the reduced rate of symptomatic ulcer and ulcer complications, which are still common in chronic NSAIDs users especially in high risk patients. In the largest GI outcome study of any coxib, TARGET, involving more than 18,000 patients, lumiracoxib was associated with a 79% reduction in ulcer complications in patients not taking aspirin. The differences between etoricoxib or lumiracoxib and ns-NSAIDs in relation to ulcer complications are apparent early during treatment and remain constant over time during the course of treatment; therefore, benefit of etoricoxib and lumiracoxib can be seen in patients with high GI ulcer complication risk who require NSAIDs from the beginning of use to throughout the prescription duration.

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“…In healthy subjects, lumiracoxib does not affect the ex-vivo antiplatelet aggregation activity of low-dose aspirin (Jermany et al 2005). In contrast, naproxen inhibits platelet aggregation and has been suggested to have an antithrombotic effect, suppressing thromboxane production to a similar level as lowdose aspirin (Capone et al 2004).…”

Section: Cardiovascular Safetymentioning

confidence: 97%

Lumiracoxib: the evidence of its clinical impact on the treatment of osteoarthritis

Journal¹

2007

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Core evidence clinical impact summary for lumiracoxib in osteoarthritisLumiracoxib has a similar CV risk profile as ibuprofen, and a similar CV profile as naproxen in patients taking aspirin. Lumiracoxib has an increased risk of CV events compared with naproxen in patients not taking aspirin continued overleaf... AbstractIntroduction: The symptoms of osteoarthritis (OA) include joint pain, stiffness, and a reduced ability to perform normal daily activities, which result in decreased quality of life. There is currently no known cure or means of preventing the progression of joint damage due to OA. Therefore, treatment focuses on the control of symptoms, including the use of various agents [including nonselective and selective nonsteroidal antiinflammatory drugs (NSAIDs)] to provide pain relief and reduce inflammation. Lumiracoxib is a selective cyclooxygenase-2 (COX-2) inhibitor for the treatment of OA.

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Lumiracoxib Does Not Affect the Ex Vivo Antiplatelet Aggregation Activity of Low‐Dose Aspirin in Healthy Subjects

Cited by 11 publications

References 37 publications

Possible mechanisms of drug-induced aspirin and clopidogrel resistance

Possible mechanisms of drug-induced aspirin and clopidogrel resistance

Global Gastrointestinal Safety Profile of Etoricoxib and Lumiracoxib

Lumiracoxib: the evidence of its clinical impact on the treatment of osteoarthritis

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