OralAcute pain, Dysmenorrhoea, Osteoarthritis, Postoperative painAdult: 100 mg bid. Use in the European Union (EU) is limited to a max of 15 days.
RectalAcute pain, Osteoarthritis, Primary dysmenorrhoeaAdult: 200 mg bid
Topical/CutaneousAcute traumatic tendinitis, SprainsAdult: 3% gel/cream: Apply thin layer to affected area bid-tid. Duration: 7-15 days.
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Should be taken with food.
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Hypersensitivity; GI bleeding, active peptic ulcer disease; severe renal and heart failure; hepatic impairment or known liver disease; coagulation disorders; pregnancy; children <12 yr.
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History of GI tract disease, infections, oedema, hypertension, elderly, lactation.
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Epigastric discomfort, heartburn or abdominal cramps, nausea, vomiting and diarrhoea; skin rash, pruritus, oedema, headache, dizziness, drowsiness; hypersensitivity reactions (e.g. bronchospasm, rhinitis, angioedema urticaria); GI haemorrhage/perforation; bullous/erosive stomatitis, purpura, thrombocytopenia, toxic epidermal necrolysis, haematuria, oliguria, and renal failure; increases in liver enzymes. Potentially Fatal: Fatal hepatitis, Stevens Johnson syndrome.
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Epigastric pain, nausea, vomiting, drowsiness, lethargy, GI haemorrhage, seizures, hypertension, apnoea, coma, anaphylactic reactions and renal failure. Treatment is supportive.
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Additive hepatotoxic effects with known hepatotoxins: anti-convulsants (e.g. valproic acid), anti-fungals (e.g. ketoconazole), anti-tuberculous drugs (e.g. isoniazid), tacrine, pemoline, amiodarone, methotrexate, methyldopa, amoxicillin/clavulanic acid. May decrease the oral bioavailability of furosemide and the natriuretic and diuretic response to furosemide. Increased risks of GI and hepatic adverse effects with other NSAIDs, including aspirin. May increase anti-coagulant effect of warfarin. Potentiates the action of phenytoin. May be displaced from binding sites with fenofibrate, salicylic acid, and tolbutamide. Interactions between NSAIDs and lithium, probenecid and ciclosporin, have been documented.
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Alcohol increases the risk of hepatic reactions.
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Description: Mechanism of Action: Nimesulide is a nonsteroidal anti-inflammatory drug (NSAID) with anti-inflammatory, anti-pyretic, and analgesic properties. It inhibits prostaglandin synthetase/cyclooxygenase, which limits prostaglandin production. Its cyclooxygenase inhibiting potency is intermediate, but is relatively selective for the cyclo-oxygenase-2 (COX-2) thus the potential for gastric injury and intolerance is less. It is also a free radical scavenger, and helps protect against the tissue damage that occurs during inflammation. Pharmacokinetics: Absorption: Well absorbed from GI tract following oral admin. Peak plasma levels:1-3 hr. With bid admin of 100 mg, steady-state is achieved within 24-36 hr. Distribution: 99% bound to plasma protein. Metabolism: Hepatic biotransformation; principal metabolite is 4-hydroxy-nimesulide. Excretion: Elimination half-life: 2-5 hr. Metabolites in urine: 80%, feces: 20% of the administered dose.9% bound to plasma protein.
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Oral: Protect from heat and humidity; store at <25°C.
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