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Prednisolone was equivalent to indomethacin for pain reduction in acute gout

Question In patients who present to the emergency department (ED) with acute gout, is prednisolone equivalent to indomethacin for reducing pain? Methods Design Randomized controlled trial (RCT). Current Controlled Trials ISRCTN 45724113. Allocation {Concealed}*. Blinding Blinded {patients, clinicians, data collectors, and outcome assessors}*. Follow-up period 14 days. Setting 4 EDs in Hong Kong. Patients 416 adults 18 years of age (mean age 65 y, 74% men) who presented to the ED within 3 days of onset of gout symptoms (rapid onset of severe pain, swelling, tenderness, and erythema of a joint, which reached a maximum within 6 to 12 h). Patients had to have 1 of metatarsophalangeal joint involvement; or knee, ankle, wrist, or elbow joint involvement with gouty tophi, past joint aspiration confirming gout, hyperuricemia, or 1 previous clinical gouty arthritis attack. Exclusion criteria included use of corticosteroids or indomethacin in the past 24 hours, past bleeding disorder or anticoagulant use, suspected septic arthritis or other joint disease, absence of monosodium urate crystals on joint aspiration, unstable cardiac conditions, comorbidities that could interfere with assessment, allergy to study drug, or estimated glomerular filtration rate <30 mL/min/1.73 m2. Intervention Oral prednisolone (n =208) or indomethacin (n =208). Patients in the prednisolone group received 30 mg/d for 5 days plus placebo for indomethacin. Patients in the indomethacin group received 50 mg of indomethacin 3 times/d for 2 days, then 25 mg 3 times/d for 3 days, plus placebo for prednisolone. Outcomes Joint pain (100-mm visual analogue scale [VAS]) at rest and with activity. Secondary outcomes included adverse events and study drug discontinuation. 318 patients were needed to detect noninferiority of oral prednisolone compared with indomethacin for joint pain (expected success rate 85%, noninferiority margin for treatment difference 13 mm, 2-sided =0.025, 80% power). Patient follow-up 90% (intention-to-treat analysis). Main results Groups did not differ for change in pain score or for achieving a clinically important change in pain (13 mm on the VAS) during the first 2 hours in hospital or at day 14 (Table). Fewer patients in the prednisolone group had adverse events in the first 2 hours (6.3% vs 19%, P <0.001); groups did not differ for adverse events during days 1 to 14. 1 patient from the prednisolone group and 7 in the indomethacin group discontinued treatment at the physicians' request due to suspected serious clinical signs or symptoms. Conclusions In patients who present to the emergency department with acute gout, prednisolone was equivalent to indomethacin for pain reduction. Prednisolone vs indomethacin in patients who present to the emergency department with acute gout Reduction in pain Mean reduction from baseline Difference in reduction from baseline(95% CI) Prednisolone Indomethacin At rest at 2 h (mm/h) 5.05 6.54 1.49 (0.64 to 3.61) With activity at 2 h (mm/h) 11.38 11.69 0.31 (1.8 to 2.42) At rest at 1 to 14 d (mm/d) 1.68 1.80 0.12 (0.32 to 0.55) With activity at 1 to 14 d (mm/d) 3.19 2.96 0.22 (0.70 to 0.25) CI defined in Glossary. Pain measured on a visual analogue scale (VAS), range 0 mm (no pain) to 100 mm (worst pain ever). Groups were equivalent (minimal clinically important difference of 13 mm on the VAS was not achieved). Commentary Treatment of acute gout is based mainly on anecdotal clinical experience rather than scientific evidence. It is reasonable to expect that a short course of prednisolone will probably be at least as effective as, and safer than, nonsteroidal antiinflammatory drugs (NSAIDs), but this has not been adequately tested. The RCT by Rainer and colleagues found that prednisolone was as effective as, and safer than, indomethacin. Given the high incidence of concomitant medical problems and the relatively high average age of patients, the findings will be welcomed by prescribing doctors and patients. Prednisolone is indeed a better choice than indomethacin. As Rainer and colleagues point out, there are grounds for caution. The diagnosis of gout was not rigorously proven in study patients. The pattern of medical supervision in the treated community means that there was no long-term follow-up to establish the accuracy of the gout diagnosis or the cumulative morbidity of prednisolone or indomethacin in this cohort of patients with a high incidence of other medical problems. The relatively high incidence of tophi also indicates that other measures to prevent recurrent gout had usually not been taken. Moreover, the trial could not establish the long-term efficacy and safety of prednisolone. In this trial, prednisolone was superior to indomethacin. However, indomethacin was not compared with other NSAIDs, which might prove to be at least as safe and effective as prednisolone. Rheumatologists who have found that a particular NSAID is as effective as prednisolone in some patients will continue to prescribe those drugs in preference to prednisolone. The situation may change if other NSAIDs are tested in RCTs as rigorous as this one and prednisolone is consistently shown to be the best choice. The choice of prednisolone or other drugs to treat gout will also depend on the clinical circumstances of individual patients.