Gouty arthritis is the most common inflammatory arthritis in adults and is characterized by very painful flares. Gouty arthritis results from an elevated body uric acid pool, which leads to deposition of monosodium urate crystals, mainly in the joints. These crystals trigger the release of proinflammatory cytokines, in particular interleukin (IL)-1β, which stimulates inflammation. Gouty arthritis can progress to a chronic, deforming and physically disabling disease through the development of disfiguring tophi, joint destruction and persistent pain. Standard treatments are effective in most patients. Acutely, anti-inflammatory therapies provide rapid pain relief and resolution of flares. Chronically, urate-lowering therapies reduce serum urate levels and, in combination with anti-inflammatory prophylaxis, reduce the risk of flares. However, for a growing number of patients, current standard treatments are ineffective or are contraindicated, largely due to the presence of co-morbidities. Indeed, metabolic syndrome, hypertension, dyslipidaemia, cardiovascular disease, diabetes mellitus and renal impairment are all highly prevalent in individuals with gouty arthritis, and may lead to standard treatments being ineffective or inappropriate. Such patients with difficult-to-treat disease require alternative therapies.