Options for prevention include allopurinol, febuxostat, and probenecid. Lowering uric acid levels can cure the disease. Treatment of associated health problems is also important. Lifestyle interventions have been poorly studied. It is unclear whether dietary supplements have an effect in people with gout. NSAIDs
NSAIDs are the usual first-line treatment for gout. No specific agent is significantly more or less effective than any other. Improvement may be seen within four hours and treatment is recommended for one to two weeks. They are not recommended for those with certain other health problems, such as gastrointestinal bleeding, kidney failure, or heart failure. While indometacin has historically been the most commonly used NSAID, an alternative, such as ibuprofen, may be preferred due to its better side effect profile in the absence of superior effectiveness. For those at risk of gastric side effects from NSAIDs, an additional proton pump inhibitor may be given. There is some evidence that COX-2 inhibitors may work as well as nonselective NSAIDs for acute gout attack with fewer side effects. Colchicine
Colchicine is an alternative for those unable to tolerate NSAIDs. At high doses, side effects (primarily gastrointestinal upset) limit its usage. At lower doses, which are still effective, it is well tolerated. Colchicine may interact with other commonly prescribed drugs, such as atorvastatin and erythromycin, among others. Glucocorticoids
Glucocorticoids have been found to be as effective as NSAIDs and may be used if contraindications exist for NSAIDs. They also lead to improvement when injected into the joint.
When they break through the tophi, they trigger a local immune-mediated inflammatory reaction in macrophages, which is initiated by the NLRP3 inflammasome protein complex. Activation of the NLRP3 inflammasome recruits the enzyme caspase 1, which converts pro-interleukin 1β into active interleukin 1β, one of the key proteins in the inflammatory cascade. An evolutionary loss of urate oxidase (uricase), which breaks down uric acid, in humans and higher primates has made this condition common.The triggers for precipitation of uric acid are not well understood. While it may crystallize at normal levels, it is more likely to do so as levels increase. Other triggers believed to be important in acute episodes of arthritis include cool temperatures, rapid changes in uric acid levels, acidosis, articular hydration and extracellular matrix proteins. The increased precipitation at low temperatures partly explains why the joints in the feet are most commonly affected. Rapid changes in uric acid may occur due to factors including trauma, surgery, chemotherapy and diuretics. The starting or increasing of urate-lowering medications can lead to an acute attack of gout with febuxostat of a particularly high risk. Calcium channel blockers and losartan are associated with a lower risk of gout compared to other medications for hypertension. Diagnosis
Gout may be diagnosed and treated without further investigations in someone with hyperuricemia and the classic acute arthritis of the base of the great toe (known as podagra). Synovial fluid analysis should be done if the diagnosis is in doubt.