SOURCE: Ruoff G, Edwards NL. Overview of serum uric acid treatment targets in gout: Why less than 6 mg/dL? Postgrad Med 2016;128:706-715.
In addition to the burden caused by painful acute gout flares, inadequately managed gout can lead to substantial long-term disability and deformity. Not everyone presenting with hyperuricemia develops gout or requires treatment. Indeed, ≤ 10% of patients demonstrating marked elevation in serum uric acid (> 9.0 mg/dL) go on to develop gout annually. Once patients experience diathesis to deposit inflammatory urate crystals in joints (or other tissues) during a single attack of gout, ≥ 90% will suffer another attack within 10 years, suggesting that most sufferers will not be so lucky as to experience a one-time event.
In vitro, crystals tend to form when uric acid levels exceed about 6.8 mg/dL, reflecting saturation at that point. Various guidelines suggest clinicians treating gout should aim for a lowering to a minimum of 6.0 mg/dL, noting that sustained uric acid lowering ultimately is associated with a disappearance of flares as well as a dissolution of tissue deposits of uric acid (e.g., tophi). Indeed, the rate of tophus dissolution has been shown to be proportional to the degree of lowering of serum uric acid levels.
Although clinicians might be tempted to aim for a goal just below 6.8 mg/dL, it is probably unwise to do so. Dietary and physiologic changes may cause fluctuation substantially above 6.8 mg/dL unless a wide margin of safety is created. Tissue deposition of uric acid can cause chronic silent joint destruction at elevated levels of uric acid. Consistent abolition of acute flares has been confirmed only when uric acid levels < 6.0 mg/dL are maintained over the long term.
Consistent abolition of acute flares has been confirmed only when uric acid levels < 6.0 mg/dL are maintained over the long term.
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