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Gout is a chronic, progressive disease. A key to managing chronic gout is to lower sUA to <6 mg/dL to reduce flares and tophi
Although gout is best known for the flare, or the acute phase, it is a chronic, progressive disease defined in 4 stages It is important to recognize the distinction between hyperuricemia, a biochemical aberration, and gout, a disease state. Currently asymptomatic hyperuricemia is not treated even though sUA is elevated The diagnosis of gout cannot occur until the initial symptom of an acute flare occurs. It is in this stage where urate crystals initiate acute inflammation because they stimulate the release of numerous inflammatory mediators such as cytokines In advanced gout, symptoms become more chronic and persistent
At 6.8 mg/dL, urate crystals begin to form and precipitate into joints and soft tissues The urate solubility of 6.8 mg/dL is based on in vitro studies at 37 °C. The predilection of gouty arthritis and tophi for the peripheral parts of the body such as extremities and ears may be partly attributed to the fact that these areas are subjected to sustained mean temperatures considerably below 37 °C. Notably, urate solubility drops to 6 mg/dL at 35°C Overall, there is a higher risk of crystals depositing in joints with increasing levels of sUA. The Normative Aging Study showed that 22% of men (n=2046) with sUA >9.0 mg/dL developed gout over 5 years In time, these urate crystals form deposits known as tophi around joints and elsewhere
First resolve the flare with anti-inflammatory agents, then provide anti-inflammatory prophylaxis when initiating urate-lowering therapy. Prevent future flares by adherence to chronic urate-lowering therapy, which will maintain sUA <6 mg/dL Patients should consider lifestyle and dietary changes to reduce their sUA, such as losing weight and reducing the intake of alcohol (especially beer), red meat, and seafood; however, pharmacologic therapy is usually needed in patients with recurrent gout flares to achieve a target serum urate level of <6 mg/dL The goals of therapy are to terminate the acute painful attack, prevent recurrences, and prevent or reverse the complications of urate deposition in joints, kidneys, or other involved sites Reduction of sUA concentrations to ≤ 6 mg/dL may eventually decrease the number of gouty attacks or may prevent future occurrences Initiation of urate-lowering therapy may result in a “mobilization” flare, which occurs when urate moves from tissue deposits Anti-inflammatory prophylaxis during initiation of urate-lowering therapy, which is recommended for up to 6 months, reduces the frequency and severity of acute flares and reduces the likelihood of recurrent flares
There was a clear relationship between average sUA concentration and the percentage of patients who experienced at least 1 recurrent gout attack during the observation period in a study by Shoji et al This retrospective analysis of 267 patients in Tokyo, Japan, demonstrated the correlation between sUA levels and the incidence of a gout flare. Recurrence of acute gouty attacks was associated with average sUA concentration during the whole investigation period (1-3 years) with an odds ratio of .42 ( P <.001) Inclusion criteria were ≥1 gouty attack before the initial visit and treatment at the clinic for >1 year after the first visit. No patients received antihyperuricemic medication before their first visit 232 patients (medication group) received allopurinol (n=95), benzbromarone (n=136), or both (n=1; some patients were later switched from allopurinol to benzbromarone [n=2] or from benzbromarone to allopurinol [n=10] or sulfinpyrazone [n=1] because of adverse reactions); 35 patients continued not to receive antihyperuricemic medication for ≥1 year after the initial visit (no-medication group) 98% received allopurinol 300 mg daily or up to 50 mg of benzbromarone daily Data were collected for up to 3 years, and statistical analysis was performed on data from >1 year after study entry 91 of the patients analyzed experienced at least 1 recurrence of acute gouty arthritis a year or more after the initial visit (attack subgroup: average sUA 7.2 mg/dL [SE 0.09 mg/dL]) 99% were men, and the mean age was 45.5 years 176 patients had no recurrences a year or more after the initial visit (no-attack subgroup: average sUA 6.46 mg/dL [SE 0.07 mg/dL]) 98% were men, and mean age was 50 Mean baseline sUA and percentage of patients experiencing ≥4 attacks before the initial visit were 7.79 mg/dL and 35% in the attack subgroup and 7.45 mg/dL and 23% in the no-attack subgroup, respectively
sUA should be maintained at <6 mg/dL to reduce the risk of recurrent gout attacks; monitoring sUA levels can ensure the target level of <6 mg/dL is achieved and maintained sUA measurements are often normal during a flare, so measurements should be made at least 2 weeks post-flare Once a patient is treated with urate-lowering therapy, treatment should be chronic
Recurrent Flares In a 2009 study, Lee et al enrolled gout patients from arthritis clinics, primary care centers, and healthcare systems in 3 major cities (n=371) to assess health-related quality of life using Short Form-36 Of the patients who reported a gout diagnosis (n=298), nearly half of the patients (n=147) reported at least 3 gout flares during the past year About two-thirds (n=195) reported taking anti-gout medication (allopurinol, colchicine, or both). Of those on anti-gout medication, >80% (n=159) were taking allopurinol alone or with colchicine High sUA Levels In a claims database study of elderly, chronic gout patients (n=2237), logistic regression analysis revealed an association of flare incidence and sUA level when sUA surpassed 6 mg/dL. With each 1-unit increase in sUA above 6 mg/dL, there was a ~12% increase in the average number of gout flares per year Renal Insufficiency Renal impairment is a typical comorbidity in chronic gout patients. In a retrospective claims analysis of a managed care database (n=5942), 13% of the subjects with gout had renal impairment (n=771) In the Lee et al 2009 study, 278 chronic gout patients who completed SF-36 reported demographic information, and 35% indicated they had kidney disease Tophi More than a quarter of chronic gout patients may have tophi, which can lead to joint erosion and damage. Tophi are more common in longstanding disease and with sUA levels exceeding 9 mg/dL
The long-term management of gout involves maintaining sUA <6 mg/dL to help reduce the risk of recurrent gout attacks. It is important to remember that gout is a chronic disease and its management involves treating the underlying condition of hyperuricemia in addition to addressing the acute attack
Core Slides Understanding Gout As A Chronic Disease