We report a 74-year-old man with acute on chronic tophaceous gout in whom conventional treatments failed but who responded to treatment with the interleukin-1 receptor antagonist, anakinra. The patient presented in February 2004 with a severe flare of gout. Multiple joints were swollen, including the right fifth proximal interphalangeal (PIP), the left fourth PIP, and the first metatarsophalangeal (MTP) joints bilaterally. Apart from chronic tophaceous gout, he also had a history of membranous glomerulonephritis (for which he was on prednisolone 5 mg/day), hypertension, and ischaemic heart disease. Allopurinol had previously induced a severe anaphylactic reaction and his renal impairment was exacerbated by non-steroidal antiinflammatory drugs.

On examination, the above mentioned joints were swollen with associated tenderness and erythema, and there were multiple tophi. Investigations revealed a raised Creactive protein (CRP) of 72 mg/l (normal, 10 mg/l), a raised urate of 0.6 mmol/l (0.20–0.42 mmol/l), urea of 13.9 mmol/l, and creatinine of 155 mmol/l, with creatinine clearance reduced to 54 ml/min. The patient could only tolerate colchicine 0.5 mg daily and probenicid 1 g daily, both of which were continued throughout anakinra therapy. A prednisolone dose of up to 40 mg daily was used but his symptoms worsened whenever steroids were tapered. This inadequate control resulted in foot deformities with dropping of the right metatarsal arch, associated with radiographic osteopenia and erosions of the left first interphalangeal joint. Febuxostat, benzbromarone, and uricase inhibition were considered but were not used because of lack of availability or concerns about toxicity. 1–3 However,