Treating acute gouty arthritis with selective COX 2 inhibitorsBMJ 2002; 325 doi: https://doi.org/10.1136/bmj.325.7371.980 (Published 02 November 2002) Cite this as: BMJ 2002;325:980
Preliminary evidence supports their relative efficacy and safety
- Adel G Fam, professor of medicine (firstname.lastname@example.org)
- Division of Rheumatology, Sunnybrook and Women's College Health Sciences Centre, University of Toronto, Toronto, ON, Canada M4N 3M5
Few arthritides are as painful, incapacitating, and stressful as a severe attack of acute gout, pseudogout, or calcific periarthritis. Successful treatment of these acute microcrystalline events depends on early use of an effective and safe anti-inflammatory drug in full dosage. The sooner such treatment is started the more rapid and complete the response. Treatment options include colchicine, non-steroidal anti-inflammatory drugs (NSAIDs), and corticosteroids including adrenocorticotrophic hormone.1 Although colchicine is traditionally rooted in the treatment of acute gout, in recent years its use has declined steadily.1 Its drawbacks include slow onset of action, narrow ratio of benefit to toxicity, and reduced efficacy when used more than 24 hours after the an attack begins. Colchicine (0.6 mg orally every 2 hours, up to 4-6 mg/day) is now reserved for patients without renal, hepatic, or bone marrow disease, in whom the more effective NSAIDs are contraindicated or poorly tolerated. Intravenous colchicine is best avoided given its potential for serious toxicity, which potentially can result in myelosuppression, hepatic necrosis, renal failure, hypotension, seizures, and death.
Intra-articular corticosteroids (for example, methylprednisolone acetate 5-25 mg per joint), systemic corticosteroids (oral prednisone 20 mg/day tapered off over 4-10 days, or intramuscular triamcinolone hexacetonide 60 mg/day, repeated …
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