OUCH!!! My Toe is Killing Me

4% of Americans at some point in their lives will be diagnosed with gout (over 8 million people). This prevalence is increasing in developed countries over the last decade, exacerbated by increasing rates of co-morbidities that mediate elevated uric acid levels including obesity, metabolic syndrome, alcohol intake, use of diuretics, diets high in proteins such as meat, chronic kidney disease and hypertension.

Acute gout is characterized by joint swelling and pain. In some individuals, these acute attacks increase in frequency and severity leading to chronic gout. Chronic, intermittent gout, affects quality of life, and metabolic function including cardiac function.

Managing Acute Gout

The American College of Physicians released a new guideline on managing acute, recurrent gout[1] which provides recommendations for both non-pharmacologic and pharmacologic strategies for improved management and avoidance of chronic gout. These guidelines released in January 2017 re-examined evidence relating to specific therapeutic interventions, and concluded four major recommendations for the management of acute gouty attacks.

#1: Acute attacks should be managed by NSAIDS, steroids, or colchicine. One placebo controlled trial demonstrated that NSAIDs were superior in managing pain but provided no additional benefit in reducing swelling. There are no placebo controlled trials of oral steroids but six randomized controlled trials demonstrated similar pain outcomes with NSAIDS. There have been five randomized controlled trials of colchicine that have all demonstrated that it reduces pain in acute gout. Moderate quality evidence suggests that low dose colchicine (1.2mg followed by 0.6 mg after 1 hour) are as effective as higher dose regimens with fewer gastrointestinal side effects.

#2: When using colchicine in managing acute gout, the recommendation is to use the low dose regimen as described above.

#3: Urate lowering therapy should not be used following first episode or in patients who have infrequent episodes (<= 2 per year). For patients with more severe episodes, recurrent attacks (>=2 per year), and tophi, chronic renal disease or uric acid renal stones), shared decision making is warranted. Continuation of colchicine or NSAIDs are useful for up to 8 weeks after the acute flare. There is no compelling evidence that monitoring uric acid levels is useful, although levels of 6.8 mg/dl are often used as a trigger for initiating urate lowering therapy.

#4: Shared decision making between clinician and patient should occur to discuss benefits, harms, costs and preferences before initiating urate lowering therapy including concomitant prophylaxis in patients with recurrent gout.

The 2012 American College of Rheumatology guidelines for prophylaxis support the use of colchicine (low dose) or NSAIDS as first line prophylaxis, with low dose steroids as second line. These guidelines recommend starting prophylaxis prior to or at the time of starting urate lowering therapy.  Prophylaxis should be continued for at least 8 weeks though regimens longer than 12 months have not been studied in randomized trials and there is no evidence of optimal duration of urate lowering therapy. It should be noted that in several studies when prophylaxis was discontinued after 8 weeks, rates of acute flares doubled, and that when continued for at least six months resulted in a significant decline in acute flares.

[1] http://annals.org/aim/article/2578528/management-acute-recurrent-gout-clinical-practice-guideline-from-american-college

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