Update on Gout and its Therapy

Update on Gout and its Therapy

See Medscape for more info…

Amplify’d from www.medscape.org

From Medscape Education Clinical Briefs

Diagnosis and Treatment of Gout Reviewed CME/CE

News Author: Laurie Barclay, MD
CME Author: Désirée Lie, MD, MSEd

CME/CE Released: 02/07/2011; Valid for credit through 02/07/2012



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CME/CE Information

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This article is intended for primary care clinicians, rheumatologists, and other specialists who care for patients with gout.


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Laurie Barclay, MD
Freelance writer and reviewer, Medscape, LLC
Disclosure: Laurie Barclay, MD, has disclosed no relevant financial relationships.

Brande Nicole Martin
CME Clinical Editor, Medscape, LLC
Disclosure: Brande Nicole Martin has disclosed no relevant financial relationships.

Désirée Lie, MD, MSEd
Clinical Professor; Director of Research and Faculty Development, Department of Family Medicine, University of California, Irvine at Orange
Disclosure: Désirée Lie, MD, MSEd, has disclosed the following relevant financial relationship:
Served as a nonproduct speaker for: “Topics in Health” for Merck Speaker Services

Sarah Fleischman
CME Program Manager, Medscape, LLC
Disclosure: Sarah Fleischman has disclosed no relevant financial relationships.

Laurie E. Scudder, DNP, NP
Nurse Planner, Continuing Professional Education Department, Medscape, LLC; Clinical Assistant Professor, School of Nursing and Allied Health, George Washington University, Washington, DC
Disclosure: Laurie E. Scudder, DNP, NP, has disclosed no relevant financial relationships.

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February 7, 2011 — The diagnosis and treatment of gout are reviewed in an article published in the February 3 issue of the New England
of Medicine.

“Gout is a type of inflammatory arthritis induced by the deposition of monosodium urate crystals in synovial fluid and other tissues,” writes Tuhina Neogi, MD, PhD, from the Section of Clinical Epidemiology Research and Training Unit, Boston University School of Medicine; and the Department of Epidemiology, Boston University School of Public Health, in Massachusetts. “It is associated with hyperuricemia, which is defined as a serum urate level of 6.8 mg per deciliter (404 μmol per liter) or more, the limit of urate solubility at physiologic temperature and pH. Humans lack uricase and thus cannot convert urate to soluble allantoin as the end product of purine metabolism. Hyperuricemia that is caused by the overproduction of urate or, more commonly, by renal urate underexcretion is necessary but not sufficient to cause gout.”

Definitive diagnosis of gout requires synovial fluid or tophus aspiration to identify negatively birefringent monosodium urate crystals under polarizing microscopy, but crystal evaluation is not routinely performed in clinical practice. Hyperuricemia may not be present during acute gout attacks and therefore may not be useful for diagnosis.

Diagnosis of acute gout is largely clinical based on a characteristic presentation with rapid (within 24 hours) development of severe pain, erythema, and swelling in the first metatarsophalangeal joint (podagra) or other typical distribution. Differential diagnosis of acute gout includes calcium pyrophosphate dehydrate or other crystal-induced arthritides and a septic joint. If a septic joint is suspected, joint aspiration with Gram staining and culture must be performed.

“The main aim of therapy for acute gout is rapid relief of pain and disability caused by intense inflammation,” Dr. Neogi writes. “Options for managing acute attacks include the use of nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, glucocorticoids, and possibly corticotropin. The choice of agent, dose, and duration of therapy is guided by consideration of coexisting illnesses that preclude the safe use of a particular regimen, as well as the severity of the gout.”

First-line agents for acute attacks are NSAIDs and colchicines, and adjunctive measures include applying ice to and resting the affected joint. NSAIDs should be avoided in patients with renal or hepatic impairment, bleeding disorder, congestive heart failure, or allergy and may increase the risk for adverse thrombotic and gastrointestinal tract events.

Naproxen may be used at a dose of 375 to 500 mg orally twice daily for 3 days, then 250 to 375 mg orally twice daily for 4 to 7 days or until the attack resolves. Indomethacin may be given 50 mg orally 3 times daily for 3 days, then 25 mg orally 3 times daily for 4 to 7 days or until the attack resolves.

Oral colchicine has a long history of use but was only approved in 2009 by the Food and Drug Administration (FDA) for use in patients with acute gout. Based on a randomized trial, colchicine 1.2 mg at the onset of a flare, followed by 0.6 mg 1 hour later, was significantly more likely than placebo to be associated with pain reduction of 50% or more 24 hours later (rates, 37.8% vs 15.5%, respectively). Colchicine should be avoided in older adults and in patients with renal or hepatic impairment or known gastrointestinal tract symptoms, and there are numerous drug-drug interactions.

When the use of NSAIDs or colchicine is poorly tolerated or contraindicated, glucocorticoids such as prednisolone or prednisone or corticotropin may be prescribed for acute gout, although evidence from randomized controlled trials is lacking for the use of intraarticular and intramuscular glucocorticoids and corticotropin.

To help prevent acute flares and development of tophi in the patient with gout, urate-lowering therapy may be helpful, but not without risk. Urate-lowering therapy should be considered in patients with hyperuricemia who have 2 or more gout attacks per year or tophi, as determined either clinically or radiographically. Additional considerations are the severity and frequency of flares, the presence of kidney stones and other coexisting illnesses, and patient preference.

Xanthine oxidase inhibitors, uricosuric agents, and uricase agents are 3 classes of drugs approved for lowering urate levels. Allopurinol is the most commonly prescribed xanthine oxidase inhibitor, with an acceptable adverse effect profile in most patients. Approximately 2% of patients experience a mild rash, with potentially life-threatening severe hypersensitivity to allopurinol much less common. Most patients receive 300 mg of allopurinol daily, but this dose may not achieve target urate levels, and daily doses up to 800 mg may be used in patients with normal renal function. Patients with renal impairment are typically given a lower dose.

Febuxostat, another xanthine oxidase inhibitor approved by the FDA in 2009 for treatment of hyperuricemia in patients with gout, is second-line therapy. Starting dose is 40 mg orally daily, increasing to 80 mg daily after 2 to 4 weeks if needed to achieve a target serum urate level. It is contraindicated for use with theophylline. No dose adjustments are needed for patients with mild to moderate renal or hepatic impairment, but data are insufficient regarding patients with severe impairment.

Probenecid, sulfinpyrazone, benzbromarone, and other uricosuric drugs block renal tubular urate reabsorption, but they are contraindicated in patients with a history of nephrolithiasis.

“Because rapid lowering of urate levels is associated with gout flares, with an increased risk associated with therapies that more effectively lower urate levels, prophylaxis against acute flares is advised during the initiation of urate-lowering therapy,” Dr. Neogi concludes. “…[T]he general recommendation for flare prophylaxis is to use colchicine at a dose of 0.6 mg once or twice daily, with dose adjustments as needed for renal impairment, potential drug interactions, or intolerance. Although NSAIDs are also used for prophylaxis, there are few studies that support their use.”

Dr. Neogi has served as a core expert panel leader for the American College of Rheumatology Gout Treatment Guidelines and has disclosed no other relevant financial relationships.

N Engl J Med. 2011;364:443-452. Abstract

Read more at www.medscape.org


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