Managing Gout: FAAFP; Brianna Smith, Pharmd Research Family Medicine There’S More We Can Do Residency Program (Drs

Tatum Mead, PharmD; Kavitha Arabindoo, MD, Managing gout: FAAFP; Brianna Smith, PharmD Research Family Medicine There’s more we can do Residency Program (Drs. Mead and Arabindoo); School of Pharmacy (Drs. Acute and chronic gout arthritis are increasingly prevalent, Mead and Smith), University of Missouri- but often poorly managed. This review, based largely Kansas City on the American College of Rheumatology’s gout [email protected] guidelines, details the components of high-quality care. The authors reported no potential conflict of interest relevant to this article. rom the 1960s to the ’90s, the prevalence of gout more PrAcTice 1 recommendationS than doubled among US residents. In the years since, gout has become increasingly prevalent worldwide.1-5 › Prescribe an anti- F The key causes—an aging population, poor diet, widespread inflammatory drug whenever use of diuretics to treat cardiovascular disease, and comorbidi- you initiate urate-lowering ties that promote hyperuricemia—have made the presentation therapy (ULT). A of gout more complex and harder to manage, as well.4-6 › Do not initiate ULT during In fact, gout is frequently poorly managed. Initiation and an acute gout attack; if a maintenance of urate-lowering therapy (ULT)—as well as patient on an established monitoring of serum urate—is not done often enough, and ULT regimen has an acute there is significant variation in medications used to treat gout. attack, however, therapy should not be stopped. C As a result, recommended serum urate targets commonly re- main unattained.7-9 › Increase the dosage of We can do better. Enhanced understanding of risk factors ULT to achieve a lower for gout, augmented by recent research and the approval of target if gout symptoms 10 persist despite a serum 2 new pharmacologic agents (febuxostat in 2009 and pegloti- 11 urate level <6 mg/dL. B case in 2010 ), led to the American College of Rheumatology 12,13 (ACR)’s first edition of gout guidelines, published in 2012. Strength of recommendation (SOR) The key components of gout management—patient education, A Good-quality patient-oriented lifestyle modifications, and pharmacologic therapy—are de- evidence tailed in the text and tables that follow. B Inconsistent or limited-quality patient-oriented evidence C Consensus, usual practice, opinion, disease-oriented evidence, case series Understanding gout Gout is actually a heterogeneous spectrum of diseases. It is char- acterized by an elevated serum urate concentration, with recur- rent 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 overpro- duction,2,12,14,15 is deposited in restricted joint spaces. conTinueD jfponline.com Vol 63, no 12 | DECemBeR 2014 | The jouRnal of family PracTice 707 TABLe 1 Dietary recommendations for patients with gout: What the guidelines call for12 avoid limit encourage organ meats high in purine content Serving sizes of purine-rich meats (beef, lamb, low-fat or nonfat dairy (sweetbreads, liver, kidney) pork) and seafood (sardines, shellfish) products high fructose corn syrup-sweetened sodas Serving sizes of fruit juice, table sugar, Vegetables and other beverages and foods sweetened beverages and desserts, and table salt, including salt in sauces and gravies alcohol overuse (>2 drinks/d for men and alcohol (particularly beer, but also wine and >1 drink/d for women). Refrain from all spirits) alcohol during periods of frequent gout attacks or advanced, poorly controlled gout Who’s at risk? aging studies are not recommended for the Risk factors include numerous cardiovascular evaluation of gout because therapy is guided Asymptomatic and metabolic conditions, such as increased by symptoms.14 hyperuricemia adiposity, hypertension, dyslipidemia, heart z Asymptomatic hyperuricemia alone alone does not failure, insulin resistance, hyperglycemia, does not establish a diagnosis of gout, and establish and renal disease.3,6,12 Older age, genetics, there is no evidence to support ULT for isolat- a diagnosis of poor diet, alcohol consumption, and medica- ed hyperuricemia. However, advice regarding gout and there tions associated with hyperuricemia, such as lifestyle modifications and treatment of asso- is no evidence loop and thiazide diuretics and low-dose ace- ciated comorbidities may be warranted for to support tylsalicylic acid, are risk factors, as well. such patients.18 urate-lowering Defined as a serum urate level ≥6.8 mg/dL therapy —the point at which urate becomes insoluble for isolated in extracellular fluids12,16,17—hyperuricemia is How best to manage gout hyperuricemia. the most important modifiable risk factor for Optimal gout management encompasses the development of gout. It can precipitate nonpharmacologic therapy, symptom man- painful episodic attacks and complications agement of acute attacks, and combination such as chronic arthritis, urolithiasis, and anti-inflammatory and ULT prophylaxis for tophi.12 patients with chronic gout.12,13 It is important to work with patients to track and document What you’ll see both the number and the severity of acute Patients often present with acute onset of attacks occurring over a 12-month period pain and inflammation of a single joint, usu- so that those who qualify for ULT can begin ally the first metatarsophalangeal. Other it without delay.12 It is important to discuss joints and soft tissues that may be involved to treatment objectives and management of co- a lesser extent include (in order of frequency) morbidities, as well. the insteps, ankles, heels, knees, fingers, and Review the medications the patient is elbows.14 Polyarticular attacks are an atypical taking, and consider eliminating prescription manifestation and are sometimes confused drugs associated with hyperuricemia if the with rheumatoid arthritis or osteoarthritis, risks outweigh the benefits.19-21 In many cas- particularly in the elderly. es, however, lifestyle modification—ie, eating Clinical evaluation should include a his- a heart-healthy diet, exercising regularly, and tory of symptom severity, disease burden, losing weight—may do more to prevent gout and comorbidities, and a thorough physi- attacks and manage complications than stop- cal examination focused on findings such as ping medications that provide cardioprotec- tophi and acute and chronic synovitis.12 Im- tion.6 The ACR divides food and beverages 708 The jouRnal of family PracTice | DECemBeR 2014 | Vol 63, no 12 mAnAging gOUT TABLe 2 Pharmacologic agents for acute gout attacks8,13,14 Type of agent Drugs Dosing common adverse considerations effects* nSaiDs • indomethacin use fDa-approved headache, Gi (pain, caution required for patients (first-line) anti-inflammatory or dyspepsia, heartburn, with puD, active bleeding, • naproxen analgesic doses nausea) anticoagulation or antiplatelet • Sulindac therapy, renal dysfunction, cKD, hTn, fluid retention, chf, or hepatic disease anti-gout agent colchicine 1.2 mg loading dose Gi (cramping, Do not initiate >36 hrs after (first-line) and 0.6 mg 1 hr later, abdominal pain, symptom onset then 0.6 mg after nausea, vomiting, if patient has received colchicine 12 hrs, as needed, diarrhea) therapy within 14 days, use an 1-2 times/d until nSaiD or corticosteroid instead symptoms resolve caution required for patients with renal dysfunction, cKD, or hepatic disease contraindicated with concurrent use of p-glycoprotein or cyp3a4 inhibitors Systemic • prednisone 0.5 mg/kg/d for Gi (abdominal caution required for patients corticosteroids 5-10 days distension, ulcers), with Dm, fluid retention, (first-line) hypertension, ongoing infection or increased oR headache, insomnia infection risk, or puD 2-5 days at full dose, ia, iV, or im administration then taper for possible for patients who are 7-10 days npo • Methyl- methylprednisolone prednisolone dose pack: Taper according to package instructions hormone (stimulates acTh 25-40 iu Sc musculoskeletal, option for patients who are npo corticosteroid endocrine, metabolic, Gi, less effective in patients on production) cardiovascular, nervous long-term oral corticosteroid system, dermatological therapy effects, hypersensitivity reactions Short duration of action acTh, adrenocorticotropic hormone; chf, congestive heart failure; cKD, chronic kidney disease; Dm, diabetes mellitus; fDa, uS food and Drug administration; Gi, gastrointestinal; hTn, hypertension; ia, intra-articular; im, intramuscular; iu, international unit; iV, intravenous; npo, nothing by mouth; nSaiD, nonsteroidal anti- inflammatory drug; puD, peptic ulcer disease; Sc, subcutaneous. * partial listing. into 3 simple categories—avoid, limit, or en- mined by both a pain score on a visual analog courage (TABLe 1.)12 scale (VAS) and the number of affected joints; patient preference, prior response, and asso- responding to an acute attack ciated comorbidities are also important con- Whenever possible, initiate pharmacologic siderations (TABLe 28,13,14). When medications therapy within 24 hours of symptom on- are prescribed for acute attacks or chronic set, because this has been associated with gout, a discussion of adverse effects, drug decreased pain and shorter duration of an interactions, contraindications, cost, and the acute attack.8,13 The choice of drug should be importance

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