Managing gout: There’s more we can do
Acute and chronic gout arthritis are increasingly prevalent, but often poorly managed. This review, based largely on the American College of Rheumatology’s gout guidelines, details the components of high-quality care.
› Prescribe an anti-inflammatory drug whenever you initiate urate-lowering therapy (ULT). A
› Do not initiate ULT during an acute gout attack; if a patient on an established ULT regimen has an acute attack, however, therapy should not be stopped. C
› Increase the dosage of ULT to achieve a lower target if gout symptoms persist despite a serum urate level <6 mg/dL. B
Strength of recommendation (SOR)
A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series
From the 1960s to the ’90s, the prevalence of gout more than doubled among US residents.1 In the years since,1-5 gout has become increasingly prevalent worldwide. The key causes—an aging population, poor diet, widespread use of diuretics to treat cardiovascular disease, and comorbidities that promote hyperuricemia—have made the presentation of gout more complex and harder to manage, as well.4-6
In fact, gout is frequently poorly managed. Initiation and maintenance of urate-lowering therapy (ULT)—as well as monitoring of serum urate—is not done often enough, and there is significant variation in medications used to treat gout. As a result, recommended serum urate targets commonly remain unattained.7-9
We can do better. Enhanced understanding of risk factors for gout, augmented by recent research and the approval of 2 new pharmacologic agents (febuxostat in 200910 and pegloticase in 201011), led to the American College of Rheumatology (ACR)’s first edition of gout guidelines, published in 2012.12,13 The key components of gout management—patient education, lifestyle modifications, and pharmacologic therapy—are detailed in the text and tables that follow.
Understanding gout
Gout is actually a heterogeneous spectrum of diseases. It is characterized by an elevated serum urate concentration, with recurrent attacks of acute arthritis associated with monosodium urate crystals in synovial fluid leukocytes, but may also include tophi— typically painless nodular deposits of monosodium urate crystals in tissues in and around the joints—interstitial renal disease, and uric acid nephrolithiasis.14 Symptoms occur when the excess uric acid, the result of inefficient excretion rather than overproduction,2,12,14,15 is deposited in restricted joint spaces.
Who’s at risk?
Risk factors include numerous cardiovascular and metabolic conditions, such as increased adiposity, hypertension, dyslipidemia, heart failure, insulin resistance, hyperglycemia, and renal disease.3,6,12 Older age, genetics, poor diet, alcohol consumption, and medications associated with hyperuricemia, such as loop and thiazide diuretics and low-dose acetylsalicylic acid, are risk factors, as well.
Defined as a serum urate level ≥6.8 mg/dL—the point at which urate becomes insoluble in extracellular fluids12,16,17—hyperuricemia is the most important modifiable risk factor for the development of gout. It can precipitate painful episodic attacks and complications such as chronic arthritis, urolithiasis, and tophi.12
What you’ll see
Patients often present with acute onset of pain and inflammation of a single joint, usually the first metatarsophalangeal. Other joints and soft tissues that may be involved to a lesser extent include (in order of frequency) the insteps, ankles, heels, knees, fingers, and elbows.14 Polyarticular attacks are an atypical manifestation and are sometimes confused with rheumatoid arthritis or osteoarthritis, particularly in the elderly.
Clinical evaluation should include a history of symptom severity, disease burden, and comorbidities, and a thorough physical examination focused on findings such as tophi and acute and chronic synovitis.12 Imaging studies are not recommended for the evaluation of gout because therapy is guided by symptoms.14
Asymptomatic hyperuricemia alone does not establish a diagnosis of gout, and there is no evidence to support ULT for isolated hyperuricemia. However, advice regarding lifestyle modifications and treatment of associated comorbidities may be warranted for such patients.18
How best to manage gout
Optimal gout management encompasses nonpharmacologic therapy, symptom management of acute attacks, and combination anti-inflammatory and ULT prophylaxis for patients with chronic gout.12,13 It is important to work with patients to track and document both the number and the severity of acute attacks occurring over a 12-month period so that those who qualify for ULT can begin it without delay.12 It is important to discuss treatment objectives and management of comorbidities, as well.
Review the medications the patient is taking, and consider eliminating prescription drugs associated with hyperuricemia if the risks outweigh the benefits.19-21 In many cases, however, lifestyle modification—ie, eating a heart-healthy diet, exercising regularly, and losing weight—may do more to prevent gout attacks and manage complications than stopping medications that provide cardioprotection.6 The ACR divides food and beverages into 3 simple categories—avoid, limit, or encourage (TABLE 1.)12
