Gout guidelines highlight risk factor analysis.
The guidelines are similar to quality care indicators for gout published in 2004 that are used mostly for quality of care research (Arthritis Rheum. 2004:50:937-43), said Dr. Kenneth Saag, director of the University of Alabama's Center for Education and Research on Therapeutics of Musculoskeletal Disorders, Birmingham.
With more people using long-term thiazide diuretics and people with chronic illness generally living longer, the incidence of gout is increasing, Dr. Saag noted.
EULAR commissioned a 20-member panel that included 11 rheumatologists and 1 expert in evidence-based medicine to develop the guidelines. It drew its management recommendations from a review of 181 studies published from 1945 to 2005. The recommendations are graded according to a formula that includes risk/benefit tradeoffs. Expert commentary accompanies those recommendations that reflect standard clinical practice but lack significant supporting research (Ann. Rheum. Dis. 2006:65:1312-24).
Treatment in all stages of gout should be tailored to specific risk factors (serum urate level, radiographic evidence), clinical phase (acute, intercritical, or chronic), and general risk factors (gender, age, obesity, alcohol use, urate elevating drugs, and other comorbidities), according to the guidelines. Nonpharmacologic treatments are also important, because they can potentiate drugs' effectiveness, are inexpensive, and do not cause harmful or distressing side effects.
The EULAR panel's recommendations for managing gout include these points:
* Patients should reduce alcohol and purine-rich food consumption and lose weight if they are obese.
* Hyperlipidemia, hypertension, hyperglycemia, obesity, and smoking should also be addressed. The link between metabolic syndrome and elevated serum uric acid has been proved in clinical studies. Smoking has not been linked directly to gout, but smoking has been associated with increased alcohol consumption, thereby having an association with gout.
* During acute gout, oral colchicine and/or nonsteroidal anti-inflammatory drugs should be the first-line treatment. Patients who cannot tolerate the GI effects of colchicine, however, can be treated with NSAIDs which provide gastroprotection.
* A 1-mg loading dose of colchicine followed by 0.5 mg every 2-3 hours relieves symptoms in acute attacks, but even this level may cause serious GI side effects. A lower dose (0.6 mg three times per day) may be appropriate and effective, but there are no studies addressing this.
* Neither intra-articular aspiration nor injection of long-acting steroids has been studied in controlled trials. But case reports and uncontrolled trials indicate the treatments are well tolerated and reduce pain. They may be especially suited for patients who cannot tolerate pharmacotherapy.
* Only patients with recurrent acute attacks, arthropathy, tophi, or radiographic changes should receive urate-lowering drugs. There is little agreement on whether less severe patients should have long-term urate-lowering therapy. However, all gout patients should lower urates through diet change.
* A uric acid level of less than 6 mg/dL--below the saturation point for monosodium urate--should be the target serum level. Many patients with serum uric acid in the normal range can still have joint damage. Maintaining the lower level keeps crystals from precipitating.
* "Start low, go slow" with allopurinol for long-term therapy. To avoid the rare but life-threatening allopurinol hypersensitivity syndrome, begin with 100 mg/day and increase by 100 mg/day every 2-4 weeks.
* Patients who have normal renal function and cannot tolerate allopurinol may do well with a uricosuric drug such as probenecid or sulphinpyrazone. For renal patients, benzbromarone can be tried, but liver function should be carefully monitored.
* Low-dose colchicine (0.5-1.0 mg daily) and/or NSAIDs may have a place in preventing additional attacks. One placebo-controlled trial suggested that colchicine could prevent half of acute attacks, although all colchicine-treated patients experienced diarrhea. Evidence suggests that NSAIDs are not as effective.
* If possible, stop diuretic therapy in gout patients. Replace the diuretic with another antihypertensive; losartan and fenofibrate are effective and have modest uricosuric effects.
BY MICHELE G. SULLIVAN
RELATED ARTICLE: Guidelines Offer Diagnostic Criteria
The presence of monosodium urate monohydrate crystals in synovial fluid remains the gold standard for gout diagnosis, with a sensitivity of 84% and a specificity of 100%, according to new gout diagnostic guidelines issued by the European League Against Rheumatism.
But the crystals may be present only during an acute attack, and their identification requires a clinician who is both well trained and experienced, the document notes. Additionally, the cost-effectiveness of the test has not been fully demonstrated (Ann. Rheum. Dis. 2006:65:1301-11).
The guidelines analyze 10 diagnostic criteria for gout, ranked not only upon extant research but also on benefit and risk, cost, and the clinical expertise required to effectively use the criteria.
"This seems a better system, reflecting both research evidence and expert opinion, than the traditional semiautomatic estimation based on category of research data alone," wrote Dr. Weiya Zhang of the University of Nottingham (England), who led a 20-person panel in developing the document.
The recommendations, which address clinical, biochemical, and radiographic diagnostic techniques, were drawn from the same 181 studies, published from 1945 to 2005, from which the EULAR panel drew its 12 recommendations on gout management.
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|Author:||Sullivan, Michele G.|
|Publication:||Internal Medicine News|
|Date:||Dec 1, 2006|
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