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What is Gout? 
Gout is characterized by deposition of monosodium urate (MSU) monohydrate crystals in synovial fluid and other tissues, resulting in painful recurrent flares and tissue damage When urate levels exceed the limit of solubility under normal physiologic conditions (400 μmol/L), MSU monohydrate crystals can form. The primary method to prevent and reduce gout flares, tophi, and chronic inflammatory arthritis is to reduce serum urate levels to well below this saturation threshold. The pathophysiology of gout is well-understood and effective therapies are available; however, it remains poorly managed.
Risk factors for gout include:  
- Hyperuricemia,
- male sex,
- older age,
- obesity,
- a diet high in animal sources of purines (e.g., red meat, shellfish),
- consumption of alcohol and high-fructose corn syrup- sweetened drinks (e.g., soda),
- medications (e.g., thiazide or loop diuretics, cyclosporine),
- renal insufficiency,
- organ transplantation,
- genetic risk factors.
Serum uric acid level was the strongest predictor of gout although only 22% of the participants with serum urate levels (>9 mg/dL) developed gout over a 5-year period. Gout patients with serum urate levels 6 to 9 mg/dL were twice as likely to have a flare in 12 months than those whose levels were <6 mg/dL, and those with levels >9 mg/dL were 3 times more likely. A loss of >10 lb was associated with a 39% reduction in risk for incident gout. Consumption of purine-rich vegetables was not associated with an increased risk for incident gout. Diet soft drinks were not associated with increased risk for gout in the study.
Asymptomatic hyperuricemia (i.e., in the absence of clinical gout) is not an indication for therapy in the United States or Europe because hyperuricemia has not been proven to have adverse consequences, and long-term urate-lowering treatment (ULT) may carry long-term risks. However, evidence that hyperuricemia may confer increased risk for renal disease progression and possibly cardiovascular disease is increasing, although data are presently insufficient to change clinical treatment guidelines.
Tests that are useful in diagnosing gout - Examination of synovial fluid or tophus aspirate (polarized microscopy, cell count, culture), serum urate level measurement, complete blood count with differential (if considering septic arthritis), radiography (to rule out other causes primarily, and/or to look for gouty erosions in patient with long-standing symptoms). Although not used routinely in clinical practice, ultrasound and dual-energy computed tomography can identify findings specific for gout.
Indications for urate-lowering therapy - the acute flare of gout, tophus on clinical examination or imaging study, chronic kidney disease stage 2 or worse, past urolithiasis (of any type).
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