Etoricoxib is primarily metabolised by CYP3A4. It is an inhibitor of CYP3A4, but no data indicates mechanism-based inhibition. Risk for gastrointestinal adverse events in the form of diarrhoea, nausea and vomiting motivates vigilance against insufficient intake of food, especially of carbohydrate.

The sulphonamide function of these drugs is devoid of molecular characteristics indicative of porphyrogenicity.

Etoricoxib is indicated for the symptomatic relief of osteoarthritis (OA), rheumatoid arthritis (RA), ankylosing spondylitis, and the pain and signs of inflammation associated with acute gouty arthritis. It is also indicated for the short-term treatment of moderate pain associated with dental surgery. Very common side effects that can be potentially porphyrinogenic through reduction in carbohydrate intake and that also can be confused with an acute porphyria attack are abdominal pain, diarrhoea, nausea and vomiting. Other common side effects are obstipation and headache.

Etoricoxib is primarily metabolised by CYP3A4 in vivo. In vitro studies indicate that CYP2D6, CYP2C9, CYP1A2 and CYP2C19 are also involved in the metabolism (SPC and Takemoto 2008). Half-life elimination is around 22 hours. Etoricoxib has been shown to be a weak CYP2C19 inhibitor (Takemoto 2008) In vitro data indicates that it has limited inhibitory effect on CYP3A4 (Takemoto 2008 and SPC), but co-administration of 120 mg etoricoxib with oral contraceptive increased the steady-state AUC(0-24h) of ethinyl estradiol (CYP3A4 substrate) by 50-60% (Schwartz 2009 and SPC). This indicates that etoricoxib inhibits CYP3A4, but no data indicates mechanism-based inhibition.

Uneventful use reported in 4 patients with acute porphyria.