SLR - July 2016 - Timmy Truong

Oral Prednisolone in Treatment of Acute Gout: A Pragmatic, Multicenter, Double-Blind, Randomized Trial

Reference: Rainer TH, Cheng CH, Janssens HJ, Man CY, Tam LS, Choi YF, Yau WH, Lee KH, Graham CA. Oral Prednisolone in the Treatment of Acute Gout: A Pragmatic, Multicenter, Double-Blind, Randomized Trial. Ann Intern Med. 2016 Apr 5; 164(7): 464–471.

Scientific Literature Review

Reviewed By: Timmy Truong, DPM
Residency Program: James A. Haley Veterans Hospital

Podiatric Relevance: Acute gouty attacks are an intensely painful and disabling inflammatory arthritis that affects up to 3 percent of the adult population in America.  We, as podiatric physicians, see acute gouty attacks frequently as they present in the emergency departments or in our clinic. The current goal of therapy is symptomatic relief of pain and disability with use of NSAIDS, colchicine or glucocorticoids. However, not every patient is a candidate is the use of NSAIDs due to renal insufficiency or history of GI ulcer. Colchicine is another alternative to NSAIDs. However, patients with mild renal or hepatic impairment are not good candidates as colchicine is metabolized in the kidneys and liver. The purpose of this study was to determine if prednisolone was equivalent to indomethacin for reducing pain in acute gout attacks.

Methods: This study was a double blind, randomized control trial that was based in 4 emergency departments in Hong Kong. A total of 416 adults were included in this study. The inclusion criteria consisted of: symptoms of gout (rapid onset of severe pain, swelling, tenderness and erythema of a joint) within 3 days of onset, one or more joints involved with gouty tophi, past aspiration confirming gout, hyperuricemia and one or more clinical gouty attacks in the past. Patients were excluded if they had the following: use of corticosteroids or indomethacin in past 24 hours, past bleeding disorder or anticoagulant use, suspected septic arthritis, absence of monosodium urate crystals on joint aspiration, unstable cardiac conditions, allergy to drug or estimated glomerular filtration rate < 30 mL/min/1.73m. The oral prednisolone group (n=208) received 30mg/d for 5 days plus a placebo for indomethacin. The Indomethacin group (n=208) received 50mg of indomethacin 3 times a day for 3 days plus a placebo for prednisolone. Patients rated joint pain using 100-mm visual analogue scale at 2 hours in ED (at rest and with activity) and 1–14 days (at rest and with activity). Clinically important change in pain was described as greater than 13mm in 100mm VAS.

Results: A total of 376 patients completed the study. Both prednisolone and indomethacin group achieved equivalent and clinical significant reductions in mean pain score at 2 hours in the ED and days 1–14. The indomethacin group at 2 hours after treatment had pain reduction of 13.08 mm with rest, 23.38 mm with activity. At 14 days, the indomethacin group had pain reduction of 25.2mm at rest and 41.44 mm with activity. The prednisolone group at 2 hours after treatment in ED, had pain reduction of 10.1mm at rest and 22.76mm with activity. At 14 days, the prednisolone group had pain reduction of 23.52 mm at rest and 44.66 mm with activity. Both groups did not have any major adverse events.

Conclusions: Oral prednisolone was just as effective as indomethacin for pain reduction in acute gout attacks. Comorbidities like renal insufficiency, GI ulcers or hepatic impairment make oral prednisolone a safer treatment option than NSAIDs or colchicine. 

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