According to the panel, physicians are often worse at gout management than patients. "[A} recent cross-sectional study showed that the prevalence of predefined mismanagement of gout (no medicine, analgesic alone, or urate-lowering therapy without prophylaxis) was over two times greater with physician management than with patient self-management,"3 Zhang et al write.
Gout diagnosis recommendations
The Gout Task Force, a part of EULAR's Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT), issued 10 key recommendations for the diagnosis of gout, which were developed using a combination of research-based evidence and expert consensus. They are:
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"In acute attacks the rapid development of severe pain, swelling, and tenderness that reaches its maximum within just 6–12 hours, especially with overlying erythema, is highly suggestive of crystal inflammation, though not specific for gout."
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"For typical presentations of gout (such as recurrent podagra with hyperuricemia) a clinical diagnosis alone is reasonably accurate but not definitive without crystal confirmation"
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"Demonstration of monosodium urate (MSU) crystals in synovial fluid or tophus aspirates permits a definitive diagnosis of gout."
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"A routine search for MSU crystals is recommended in all synovial fluid samples obtained from undiagnosed inflamed joints."
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"Identification of MSU crystals from asymptomatic joints may allow definite diagnosis in intercritical periods."
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"Gout and sepsis may coexist, so when septic arthritis is suspected, gram stain and culture of synovial fluid should still be performed even if MSU crystals are identified."
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"Although the most important risk factor for gout, serum uric acid levels do not confirm or exclude gout, since many people with hyperuricaemia do not develop gout, and during acute attacks serum levels may be normal."
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"Renal uric acid excretion should be determined in selected gout patients, especially those with a family history of young-onset gout, onset of gout under age 25, or with renal calculi."
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"Although radiographs may be useful for differential diagnosis and may show typical features in chronic gout, they are not useful in confirming the diagnosis of early or acute gout."
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"Risk factors for gout and associated comorbidity should be assessed, including features of the metabolic syndrome (obesity, hyperglycemia, hyperlipidemia, hypertension)."
The Gout Task Force also developed a series of high-priority proposals for future gout research, including establishing an optimal protocol (including training) for the identification of MSU crystals, determining the validity of diagnosis based on MSU crystal identification from asymptomatic joints in between acute attacks, and determining the value of magnetic resonance imaging (MRI) and ultrasound in gout diagnosis and monitoring.
Gout treatment recommendations
The Gout Task Force issued 12 recommendations on gout management. The panel first notes that optimal treatment requires both pharmacological and nonpharmacological approaches tailored to specific risk factors, clinical phase, and general risk factors such as age, gender, obesity, alcohol consumption, urate-elevating drugs, drug interactions, and comorbidity. They recommend that educating patients on weight loss, diet, and reduced alcohol (especially beer) should be core parts of the treatment plan. Risk factors (hyperlipidemia, hypertension, hyperglycemia, obesity, smoking) should be addressed as part of the management plan.
The EULAR panel recommends that first-line agents for acute attacks should be oral colchicine and/or NSAIDs. "In the absence of contraindications, an NSAID is a convenient and well-accepted option," the panel writes. Out of a concern over the toxicity of high-dose colchicine, they note that low-dose colchicine (0.5 mg tid) may be sufficient in acute gout and is preferred to possibly toxic higher doses. The panel concluded that acute attacks also can be effectively treated with intraarticular aspiration and injection of a long-acting steroid.
Gout patients with recurrent acute attacks, arthropathy, tophi, or radiographic changes of gout are candidates for urate-lowering therapy, which should aim at maintaining serum uric acid below the saturation point for monosodium urate (<e;360 μmol/L), Zhang et al write.
They recommend long-term allopurinol as an appropriate urate-lowering therapy and advise starting at a low dose (100 mg/day) and escalating by 100 mg every 2–4 weeks, with adjustments for patients with renal impairment. Alternatives in cases of allopurinol toxicity are other xanthine oxidase inhibitors, a uricosuric agent, or allopurinol desensitization. Probenecid and sulphinpyrazone are alternatives to allopurinol in patients with normal renal function.
Since rapid reductions in serum uric acid levels can trigger acute attacks, colchicine (0.5–1mg/day) and/or an NSAID (with gastroprotection if indicated) are recommended as prophylaxis against acute attacks during the first months of urate-lowering therapy.
The authors note, "The optimal drug (colchicine or NSAID), dose, and duration for prophylaxis of acute attacks when commencing urate-lowering therapy, and whether this should vary in different clinical settings (eg, presence of tophi) needs to be determined."
Finally, the panel recommends stopping diuretics if possible, or switching to losartan or fenofibrate for gout patients with hypertension or hyperlipidemia.
References
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Zhang W, Doherty M, Pascual E, et al. EULAR evidence-based recommendations for gout. Part I. Diagnosis: Report of a task force of the Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT). Ann Rheum Dis [serial online]; 17 May 2006. Available at www.bmjjournals.com.
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Zhang W, Doherty M, Bardin T, et al. EULAR evidence-based recommendations for gout. Part II. Management: Report of a task force of the EULAR Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT). Ann Rheum Dis [serial online]; 17 May 2006. Available at www.bmjjournals.com
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Neugi T, Hunter DJ, Chasson CE, Cunningham JA, Zhang YQ. Frequency of inappropriate management of acute gout attacks. J Rheumatol. 2006;33:104-109.