Gout ( GOWT) is a form of inflammatory arthritis characterized by recurrent attacks of a red, tender, hot and swollen joint, caused by deposition of monosodium urate monohydrate crystals. Pain typically comes on rapidly, reaching maximal intensity in less than 12 hours. The joint at the base of the big toe is affected in about half of cases. It may also result in tophi, kidney stones, or kidney damage.Gout is due to persistently elevated levels of uric acid in the blood. This occurs from a combination of diet, other health problems, and genetic factors. At high levels, uric acid crystallizes and the crystals deposit in joints, tendons, and surrounding tissues, resulting in an attack of gout. Gout occurs more commonly in those who regularly drink beer or sugar-sweetened beverages or who eat foods that are high in purines such as liver, shellfish, or anchovies, or are overweight. Diagnosis of gout may be confirmed by the presence of crystals in the joint fluid or in a deposit outside the joint. Blood uric acid levels may be normal during an attack.Treatment with nonsteroidal anti-inflammatory drugs (NSAIDs), glucocorticoids, or colchicine improves symptoms. Once the acute attack subsides, levels of uric acid can be lowered via lifestyle changes and in those with frequent attacks, allopurinol or probenecid provides long-term prevention. Taking vitamin C and eating a diet high in low-fat dairy products may be preventive.Gout affects about 1 to 2% of adults in the developed world at some point in their lives.
They are often used in combination with either an NSAID or colchicine for the first three to six months.While it has been recommended that urate-lowering measures should be increased until serum uric acid levels are below 300–360 µmol/L (5.0–6.0 mg/dl), there is little evidence to support this practice over simple putting people on a standard dose of allopurinol. If these medications are in chronic use at the time of an attack, it is recommended that they be continued. Levels that cannot be brought below 6.0 mg/dl while attacks continue indicates refractory gout.While historically it is not recommended to start allopurinol during an acute attack of gout, this practice appears acceptable. Allopurinol blocks uric acid production, and is the most commonly used agent. Long term therapy is safe and well-tolerated and can be used in people with renal impairment or urate stones, although hypersensitivity occurs in a small number of individuals. The HLA-B*58:01 allele of the human leukocyte antigen B (HLA-B) is strongly associated with severe cutaneous adverse reactions during treatment with allopurinol and is most common among Asian subpopulations, notably those of Korean, Han-Chinese, or Thai descent.Febuxostat is only recommended in those who cannot tolerate allopurinol. There are concerns about more deaths with febuxostat compared to allopurinol. Febuxostat may also increase the rate of gout flares during early treatment. However, there is tentative evidence that febuxostat may bring down urate levels more than allopurinol.Probenecid appears to be less effective than allopurinol and is a second line agent.