Lumiracoxib inhibits cyclo-oxygenase 2 completely at the 50 mg dose: is liver toxicity avoidable by adequate dosing?
1 Institute of Toxicology and Pharmacology, University of Rostock, Rostock, Germany
2 Institute of Experimental and Clinical Pharmacology and Toxicology, Friedrich Alexander University Erlangen-Nuremberg, Erlangen, Germany
Correspondence to:
Dr B Hinz, Institute of Toxicology and Pharmacology, University of Rostock, Schillingallee 70, D-18057 Rostock, Germany; burkhard.hinz@med.uni-rostock.de
Accepted 30 March 2008
| The first 150 words of the full text of this article appear below. |
Lumiracoxib is a selective cyclo-oxygenase 2 (COX-2) inhibitor used for symptomatic treatment of osteoarthritis and acute pain. Among the available COX-2 inhibitors, lumiracoxib is the only compound with gastrointestinal benefit in patients with osteoarthritis that has been demonstrated in a large outcome study.1
Several countries have approved lumiracoxib at doses of 200 mg (for osteoarthritis) and 400 mg (for acute pain), both of them exceeding the dose necessary to inhibit COX-2 at the time of maximal plasma concentration.2 In line with this notion, one clinical trial reported that patients with knee or hip osteoarthritis randomised to receive lumiracoxib at 50, 100 or 200 mg twice daily or at 400 mg once daily experienced a comparable pain relief.3 Regrettably, a systematical analysis of dose-dependent therapeutic effects of lumiracoxib is lacking.
The interest in administering lower doses of lumiracoxib gains new importance in view of recent reports on its dose-dependent1 liver toxicity,
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