Marjory Toussaint Case

The development and expression of gout depends on three key steps: (1) chronic hyperuricemia, (2) the growth of monosodium urate (MSU) crystals, and (3) interaction between MSU crystals and the inflammatory system. Epidemiological studies have continued to improve our understanding of the environmental and genetic factors which influence chronic hyperuricemia and gout. The influence of obesity, alcohol, race, sex, age, and specific dietary components will be discussed below. The primary mechanism of hyperuricemia is insufficient renal clearance of uric acid which in turn is dependent on transport of uric acid in the proximal renal tubule. Knowledge of the transport mechanisms has improved understanding of the genetic influences on gout and is relevant to understanding of the effects of drugs which can increase or decrease renal uric acid clearance. The application of established principles of management including diagnosis through crystal identification, the gradual introduction of hypouricemic therapy with the use of prophylaxis to reduce the risk of flares, identification of a suitably low target of plasma urate, a progressive increase in therapy to achieve the target and taking steps to encourage good compliance, has the potential to improve outcomes for patients with this very common affliction. The potential role for new therapies will also be discussed.

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