Lumiracoxib

Oral
Osteoarthritis of the knee

Moderate to severe (CrCl <50 mL/min): Contraindicated.

Contraindicated.

May be taken with or without food.

Patient w/ ischaemic heart disease, cerebrovascular disease, or peripheral arterial disease. Patient w/ history of drug-induced increases in transaminase values >3 times the upper limit of normal (ULN) or in those taking other drugs known to cause clinically significant hepatotoxicity. Patient w/ inflammatory bowel disease, moderate to severe heart failure (NYHA class II-IV). Concomitant use w/ drugs known to cause hepatotoxicity. Hepatic impairment. Moderate to severe renal impairment (CrCl <50 mL/min).

Dehydrated patient; patient w/ significant risk factors for CV disease e.g. HTN, hyperlipidaemia, and DM.

Anorexia, nausea, vomiting, abdominal pain, fatigue, dark urine and jaundice.
Potentially Fatal: Severe hepatotoxicity, upper GI ulceration and bleeding.

PO: Z (NSAIDs caused foetal ductus arteriosus premature closure, foetal renal impairment and persistent pulmonary hypertension. Avoid near term, else use lowest dose for shortest time.)

LFTs should be monitored mthly. Monitor renal function at the beginning and during treatment.

May decrease the clearance of CYP2C9 substrates (e.g. phenytoin, warfarin). May increase anticoagulant effect of warfarin, acenocoumarol, anisindione and dicoumarol. Concomitant use w/ telmisartan may increase the risk of acute renal failure and hyperkalaemia. Tolbutamide may decrease the metabolism and clearance of lumiracoxib. May antagonise the antihypertensive effect of timolol. May increase lithium serum levels. May decrease antihypertensive effect of trandolapril.
Potentially Fatal: Increased risk of hepatotoxicity w/ drugs known to cause hepatotoxicity.

Description:
Mechanism of Action: Lumiracoxib is an NSAID and a selective inhibitor of cyclo-oxygenase-2 (COX-2). Its action is due to inhibition of prostaglandin synthesis via inhibition of COX-2.
Pharmacokinetics:
Absorption: Rapidly absorbed. Absolute bioavailability: 74%. Time to peak plasma concentration: Approx 2 hr.
Distribution: Plasma protein binding: ≥98%.
Metabolism: Undergoes extensive hepatic metabolism via glucurosyltransferase and CYP450 isoenzymes. Major metabolites include 4'-hydroxy-lumiracoxib (active as COX-2 inhibitor), 5-carboxy-lumiracoxib, and 4'-hydroxy-5-carboxy-lumiracoxib.
Excretion: Via urine (54%) and faeces (approx 43%); approx 5% as unchanged drug. Plasma half-life: Approx 4 hr.

Thuốc kháng viêm không steroid

Buckingham R (ed). Lumiracoxib. Martindale: The Complete Drug Reference [online]. London. Pharmaceutical Press. https://www.medicinescomplete.com. Accessed 10/03/2014.

Lumiracoxib (Prexige): Suspension of Marketing Authorisations. Medicines & Healthcare products Regulatory Agency. https://www.gov.uk/government/organisations/medicines-and-healthcare-products-regulatory-agency. Accessed 10/03/2014.