Hyperuricaemia and gout

Abstract

Gout is a painful, inflammatory disease that affects more men than women. The incidence of gout has increased substantially over the past few decades, as evidenced by information from the Rochester project. Some of the risk factors for the development of gout include: increased ethanol intake, high dietary purine consumption, obesity and the use of certain drugs, such as diuretics. Another important risk factor for the development of gout is hyperuricaemia. Hyperuricaemia results from an imbalance between the rate of production and excretion of uric acid in the body. An excess of uric acid thus builds up in the body, supersaturating body fluids and leading to the formation of monosodium urate crystals. These crystals accumulate in tissue and around joints, leading to an acute gout attack. Gout can be divided into four phases, namely symptomatic hyperuricaemia, acute gout attacks or recurrent gout, intercritical gout and chronic tophaceous gout. Various treatment options are available for gout, and the treatment for each gout patient is determined by the stage of the disease. Non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids, corticotropin and colchicine are used for the treatment of acute gout attacks. Allopurinol and probenecid are used for long-term hypouricaemic therapy, while NSAIDs and colchicine are prescribed for the prophylaxis of future gout attacks. All of these treatments have side effects, ranging from mild to life-threatening in nature. There is a need for novel gout therapies that have fewer side effects but are still as effective.