Etoricoxib for arthritis and pain Key pharmacologic features Rapidly and completely absorbed via oral route Suitable for once-daily dosing, without dose adjustment (except hepatic insufficiency) Greater COX-2 selectivity than rofecoxib, valdecoxib, or celecoxib Less interference with aspirin antiplatelet activity compared with other NSAIDs ETORICOXIB Efficacy* Osteoarthritis Comparable with diclofenac Comparable with naproxen Comparable with ibuprofen Rheumatoid arthritis Comparable with diclofenac Comparable with or greater than naproxen Acute gouty arthritis Comparable with indomethacin Ankylosing spondylitis Greater than naproxen Chronic lower back pain Greater than placebo† Postoperative pain Comparable with naproxen Greater than opioid/acetaminophen Primary dysmenorrhea Comparable with naproxen Tolerability Overall Generally well tolerated No new findings during long-term treatment Gastrointestinal Superior to nonselective NSAIDs Renal Similar to naproxen or ibuprofen Significant increase in hypertension-related adverse events and significantly higher percentage of patients discontinuing therapy in the etoricoxib 90 mg/day group compared with diclofenac 150 mg/day in the EDGE study Serious hypertension-related adverse events were rare in EDGE Cardiovascular Thrombotic event risk similar to non-naproxen NSAIDs COX-2 inhibitor class effect for increased cardiovascular risk in product labeling Ongoing evaluation in MEDAL program Hepatic Adjust etoricoxib dose in patients with hepatic insufficiency Figure 4 Clinical summary of etoricoxib in arthritis and pain management. *Greater efficacy defined here as a statistically significant benefit with etoricoxib versus active comparator in an efficacy study. †An active comparator study has not been performed. Abbreviations: EDGE, Etoricoxib versus diclofenac sodium gastrointestinal tolerability and effectiveness study; MEDAL, Multinational etoricoxib and diclofenac arthritis long-term study; NSAIDs, nonsteroidal antiinflammatory drug. patients at risk of peptic ulceration (ACRRAG 2002). Alternatively, low-dose prednisone therapy, a nonacetylated salicylate, or a nonselective NSAID with concomitant gastroprotective therapy to reduce gastroduodenal ulceration (eg, proton pump inhibitor, high-dose H2 blocker, or oral prostaglandin analog) may be used in high risk patients (ACRRAG 2002). However, routine use of H2 blockers for dyspepsia is not recommended due to the potential risk of other gastrointestinal complications (ACRRAG 2002). Moreover, patients receiving gastroprotective therapy may still be at risk of lower gastrointestinal tract events. ACR guidelines recommend that pharmacologic therapy for OA Therapeutics and Clinical Risk Management 2006:2(1) 53