Gout and Pseudogout Medication

  • Author: Bruce M Rothschild, MD; Chief Editor: Herbert S Diamond, MD   more...
 
Updated: Mar 26, 2012
 

Medication Summary

Acute inflammation due to gout can be treated with NSAIDs, corticosteroids, or colchicine. NSAIDs are generally the drugs of choice unless the patient has a risk factor that contraindicates these agents. Ultimately, gout is treated by decreasing tissue stores of uric acid with allopurinol or probenecid. Because agents that lower uric acid can precipitate attacks of gout, low-dose colchicine is used as prophylaxis when such therapy is initiated.

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Nonsteroidal anti-inflammatory drugs

Class Summary

These agents as a class are the drugs of choice to treat acute inflammation of gout in patients who can safely take these medications. They are most commonly used for the relief of mild to moderate pain. Although the effects of NSAIDs in the treatment of pain tend to be patient specific, indomethacin has been superseded as the drug of choice for initial therapy. Other options include naproxen, oxaprozin, and ketoprofen (or celecoxib [Celebrex] or diclofenac and misoprostol [Arthrotec]) or use of gastroprotection for individuals older than 51 years or with other risk factors for toxicity.

Nevertheless, the choice of NSAID is more habit than science. Use of concomitant misoprostol gastric protection or consideration of a cyclooxygenase 2 (COX-2)–specific NSAID might be considered if the patient has gastrointestinal risk or is older than 51 years. To control the attack as quickly and safely as possible (recalling that it takes 5 half-lives to reach steady state), consider using an NSAID with a short half-life. Use the maximum dose of NSAID and taper over approximately 2 weeks, depending on patient's response.

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Naproxen (Anaprox, Naprelan, Naprosyn)

 

Naproxen is used for relief of mild to moderate pain. It inhibits inflammatory reactions and pain by decreasing activity of the enzyme cyclooxygenase, resulting in prostaglandin synthesis.

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Ketoprofen

 

Ketoprofen is used for the relief of mild-to-moderate pain and inflammation. Small doses are initially indicated in small and elderly patients and in those with renal or liver disease. Individual doses >75 mg do not increase therapeutic effects. Administer high doses with caution, and closely observe patient for response.

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Tolmetin (Tolectin)

 

This agent is used for relief of mild to moderate pain and inflammation. Small doses are initially indicated in small and elderly patients and in those with renal or liver disease. Administer high doses with caution, and closely observe the patient for response.

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Diclofenac (Voltaren XR, Cataflam, Arthrotec)

 

Diclofenac inhibits prostaglandin synthesis by decreasing activity of enzyme cyclo-oxygenase, which in turn decreases formation of prostaglandin precursors.

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Indomethacin (Indocin)

 

Indomethacin have been the traditional NSAID used to treat acute inflammation in gout, although other NSAIDs are effect. Like all NSAIDs, indomethacin blocks cyclooxygenase and, thereby, the generation of prostaglandins.

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Anti-inflammatory agents

Class Summary

Colchicine reduces the formation of uric acid crystals in affected joints, thereby reducing acute inflammation and pain; it also decreases uric acid levels in blood. Colchicine is now considered a second-line agent in the treatment of acute gout flares because of its narrow therapeutic window. More often, it is used at a lower dose as a prophylactic agent to prevent flares of gout when adding agents that lower uric acid.

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Colchicine (Colcrys)

 

This agent inhibits microtubules and thereby may inhibit phagocytosis, neutrophil mobility, and chemotaxis. It also may inhibit generation of prostaglandins.

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Corticosteroids

Class Summary

These agents are potent and effective anti-inflammatory drugs that can be used to treat acute gout in patients who cannot tolerate NSAIDs or colchicine. Steroids can be given PO, IM, IV, intra-articularly or, preferably, indirectly via adrenocorticotropic hormone (ACTH). No intrinsic advantage to treating with IV corticosteroids exists unless the patient cannot take oral medications.

The short-burst corticosteroid regimen used to treat an acute flare of gout is generally well tolerated, but is associated with the adverse effects seen with long-term steroid use.

In patients with only 1 or 2 involved joints, intra-articular corticosteroids are a safe and effective treatment option if infection is excluded. Water-soluble steroids (eg, Decadron) are teleologically inappropriate for use as a depot steroid treatment. Although case reports of adrenal crisis related to multiple intra-articular injections of steroids for gout have been documented, this has not been clearly proven.

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Prednisone

 

Oral prednisone can be given to abort an attack of gout. By reversing increased capillary permeability and suppressing polymorphonuclear (PMN) activity, this agent may decrease inflammation. Steroid dose packs that clearly label the dose to be taken each day can be convenient for some patients.]'

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Triamcinolone (Aristocort)

 

Intra-articular use is considered by some as the treatment of choice for pseudogout and for acute gouty attacks in patients with renal transplant and others who cannot be given NSAIDs or colchicine.

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Corticotropin (H.P. Acthar)

 

Corticotropin stimulates endogenous production of corticosteroids. It decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.

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Uricosuric agents

Class Summary

Uricosuric agents lower uric acid levels by inhibiting the renal tubular reabsorption of uric acid, thereby increasing net renal excretion of uric acid. They are better tolerated than allopurinol but are less effective and cannot be used in all circumstances. These agents increase the risk of renal stones. These agents should not be started during an attack of acute gouty arthritis. The goal of therapy is to lower serum uric acid to approximately 5-6 mg/dL without causing renal stones.

These agents increase renal clearance of uric acid by inhibiting the renal tubular reabsorption of uric acid.

Reduce uric acid load by blocking metabolism of the purine metabolite xanthine to uric acid.

Note that febuxostat (a thiazolecarboxylic acid derivative, but not a purine base analog) is a potential alternative to allopurinol. It was approved by the US Food and Drug Administration in February 2009. Common adverse events include upper respiratory tract infections, arthralgias, diarrhea, headache, and liver function abnormalities. Atrioventricular block or atrial fibrillation in 5% and cholecystitis in 2% have also been reported.[114] Febuxostat physically blocks the channel to the molybdenum-pterin active site of xanthine oxidase and is metabolized by liver oxidation and glucuronidation.[28] Cardiovascular safety issues have yet to be determined. As with other uricosuric agents, it may precipitate gouty attacks when inititated.[28, 114]

Losartan (angiotensin II receptor antagonist) is uricosuric at 50 mg/d. Fenofibrate (anti-hyperlipidemic) at 200 mg/d reduces serum urate 19% and increases clearance by 36%. Vitamin C reduces uric acid by 0.5 mg/dL (but should be avoided with nephrolithiasis or urate nephropathy, cystinuria, penicillamine.)

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Probenecid

 

Probenecid lowers tissue stores of uric acid by increasing net renal excretion of uric acid by inhibiting tubular reabsorption. Some authorities recommend alkalizing the urine when starting probenecid to reduce the risk for renal stone formation. Probenecid is indicated for long-term management of hyperuricemia associated with gout.

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Colchicine

 

Colchicine reduces the formation of uric acid crystals in affected joints, thereby reducing the amount of acute inflammation and pain. It also decreases levels of uric acid in the blood.

Colchicine can be used either in combination with probenecid on a long-term basis to prevent gout or by itself to treat pain and inflammation of acute gout attacks.

Colchicine has a very narrow window between toxic and therapeutic effects and should be used with caution for acute attacks. Generally other treatment options are available with less potential for toxic side effects. The traditional approach of giving colchicine until vomiting and/or diarrhea appear is to be discouraged as these are signs of toxicity.

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Xanthine oxidase inhibitors

Class Summary

Inhibition of xanthine oxidase, the enzyme that synthesizes uric acid from hypoxanthine, reduces the synthesis of uric acid without disrupting the biosynthesis of vital purines. This result in the reduction of the tissue stores of uric acid.

Allopurinol is more likely to be effective than uricosuric agents but carries an increased risk for significant adverse effects. Allopurinol should not be started during an attack of acute gouty arthritis. The goal of therapy is to lower the serum uric acid level to approximately 5-6 mg/dL.

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Allopurinol (Zyloprim, Aloprim)

 

Allopurinol reduces production of uric acid, thereby allowing the body to dispose of excess uric acid stores. It is the most effective therapy to lower serum uric acid. Most patients achieve the target uric acid level of 5 mg/dL at 300-400 mg/d. A lower dose is used if renal insufficiency is present.

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Febuxostat (Uloric)

 

Febuxostat is a potential alternative to allopurinol.[115] It was approved by the US Food and Drug Administration in February 2009.

Like allopurinol, febuxostat is a xanthine oxidase inhibitor that prevents uric acid production and lowers elevated serum uric acid levels. Unlike allopurinol, it is a thiazolecarboxylic acid derivative, not a purine base analog. Febuxostat physically blocks the channel to the molybdenum-pterin active site of xanthine oxidase and is metabolized by liver oxidation and glucuronidation.[28]

Common adverse events include upper respiratory tract infections, arthralgias, diarrhea, headache, and liver function abnormalities. Atrioventricular block or atrial fibrillation in 5% and cholecystitis in 2% have also been reported.[114] As with other uricosuric agents, it may precipitate gouty attacks when initiated.[28, 114]

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Uric acid oxidizers

Class Summary

These agents facilitate conversion of urate to a more soluble product, allantoin, thus preventing acute renal failure. Estrogens reduce serum uric acid levels 20% in postmenopausal women.[28]

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Pegloticase (Krystexxa)

 

This agent is a pegylated uric acid–specific enzyme that is a polyethylene glycol conjugate of recombinant uricase. It achieves its therapeutic effect by catalyzing oxidation of uric acid to allantoin, thereby lowering serum uric acid levels. Pegloticase is indicated for gout in adults refractory to conventional therapy (ie, serum uric acid levels have failed to normalize and signs and symptoms are inadequately controlled with xanthine oxidase inhibitors at maximum appropriate dose or xanthine oxidase inhibitors are contraindicated).

The dosage is 8 mg IV every 2 weeks. Complications include flare of gout attacks in 63-86% of patients and nephrolithiasis in 13-14%, along with arthralgias, nausea, dyspepsia, muscles spasms, pyrexia, back pain, diarrhea, and rash.[116]

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Rasburicase (Elitek)

 

Rasburicase is a recombinant form (derived from Saccharomyces cerevisiae-synthesized, Aspergillus flavus) of the enzyme urate oxidase, which oxidizes uric acid to allantoin. It is indicated for treatment and prophylaxis of severe hyperuricemia associated with the treatment of malignancy. Hyperuricemia causes a precipitant in the kidneys, which leads to acute renal failure. Unlike uric acid, allantoin is soluble and easily excreted by the kidneys. Elimination half-life is 18 h.

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Corticotropic Hormones

Class Summary

These agents stimulate synthesis and release of corticosteroid hormones. They are principally used in diagnostic tests to differentiate primary adrenal insufficiency from secondary adrenal insufficiency. They have limited therapeutic value in conditions responsive to corticosteroid therapy where a corticosteroid should be the drug of choice.

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Cosyntropin (Cortrosyn)

 

This agent is an adrenocorticotropic hormone (corticotropin) that stimulates the production and release of endogenous steroids. It is an effective treatment of acute crystal-induced arthritis in postoperative patients and others who cannot take oral medications.

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COX-2 Inhibitors

Class Summary

Unlike most NSAIDs, which inhibit both cyclooxygenase-1 (COX-1) and COX-2, selective COX-2 inhibitors offer the possibility of relieving inflammation and pain but with a lower risk of gastrointestinal side effects. COX-2 expression in monocytes has been suggested to be induced in response to urate crystals. However, several drugs in this class are currently under investigation because of a suspected increase in the risk of cardiac disease. One of these drugs, rofecoxib (Vioxx), has already been removed from the market.

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Celecoxib (Celebrex)

 

Several studies have found that selective COX-2 inhibitors are more effective than NSAIDs for treating acute gouty arthritis. Unfortunately, celecoxib was not one of the COX-2 inhibitors studied. Given its drug class, it may be assumed to be helpful in the treatment of acute gout, but no clear evidence supports this. Celecoxib is currently under investigation for associated risk of accelerated cardiac disease.

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Contributor Information and Disclosures
Author

Bruce M Rothschild, MD  Professor of Medicine, Northeastern Ohio Universities Colleges of Medicine and Pharmacy; Adjunct Professor, Department of Biomedical Engineering, University of Akron; Research Associate, University of Kansas Museum of Natural History; Research Associate, Carnegie Museum

Bruce M Rothschild, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Rheumatology, International Skeletal Society, New York Academy of Sciences, Sigma Xi, and Society of Skeletal Radiology

Disclosure: Nothing to disclose.

Coauthor(s)

Anne V Miller, MD  Assistant Professor of Medicine, Division of Rheumatology, Southern Illinois University School of Medicine

Anne V Miller, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology, and International Society for Clinical Densitometry

Disclosure: Nothing to disclose.

Sriya K M Ranatunga, MD, MPH  Associate Professor, Department of Clinical Medicine, Southern Illinois University School of Medicine

Disclosure: Nothing to disclose.

Mark L Francis, MD  Consulting Staff, Arthritis and Osteoporosis Associates of New Mexico

Mark L Francis, MD is a member of the following medical societies: American College of Rheumatology, Illinois State Medical Society, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Chief Editor

Herbert S Diamond, MD  Adjunct Professor of Medicine, Division of Rheumatology, University of Pittsburgh School of Medicine; Chairman Emeritus, Department of Internal Medicine, Western Pennsylvania Hospital

Herbert S Diamond, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology, American Medical Association, and Phi Beta Kappa

Disclosure: Merck Ownership interest Other; Smith Kline Ownership interest Other; Zimmer Ownership interest Other

Additional Contributors

Richard W Allinson, MD Associate Professor, Department of Ophthalmology, Texas A&M University Health Science Center; Senior Staff Ophthalmologist, Scott and White Clinic

Richard W Allinson, MD, is a member of the following medical societies: American Academy of Ophthalmology, American Medical Association, and Texas Medical Association

Disclosure: Nothing to disclose.

Lawrence H Brent, MD Associate Professor of Medicine, Jefferson Medical College of Thomas Jefferson University; Chair, Program Director, Department of Medicine, Division of Rheumatology, Albert Einstein Medical Center

Lawrence H Brent, MD is a member of the following medical societies: American Association for the Advancement of Science, American Association of Immunologists, American College of Physicians, and American College of Rheumatology

Disclosure: Abbott Honoraria Speaking and teaching; Centocor Consulting fee Consulting; Genentech Grant/research funds Other; HGS/GSK Honoraria Speaking and teaching; Omnicare Consulting fee Consulting; Pfizer Honoraria Speaking and teaching; Roche Speaking and teaching; Savient Honoraria Speaking and teaching; UCB Honoraria Speaking and teaching

Andrew A Dahl, MD Director of Ophthalmology Teaching, Mid-Hudson Family Practice Institute, The Institute for Family Health; Assistant Professor of Surgery (Ophthalmology), New York College of Medicine

Andrew A Dahl, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Ophthalmology, American College of Surgeons, American Medical Association, American Society of Cataract and Refractive Surgery, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Paul E Di Cesare, MD, FACS Professor and Chair, Department of Orthopedic Sugery, University of California, Davis, School of Medicine

Paul E Di Cesare, MD, FACS is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American College of Surgeons, and Sigma Xi

Disclosure: Stryker Consulting fee Consulting

Steven C Dronen, MD, FAAEM Chair, Department of Emergency Medicine, LeConte Medical Center

Steven C Dronen, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Gino A Farina, MD, FACEP, FAAEM Associate Professor of Clinical Emergency Medicine, Albert Einstein College of Medicine; Program Director, Department of Emergency Medicine, Long Island Jewish Medical Center

Gino A Farina, MD, FACEP, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Harris Gellman, MD Consulting Surgeon, Broward Hand Center; Voluntary Clinical Professor of Orthopedic Surgery and Plastic Surgery, Departments of Orthopedic Surgery and Surgery, University of Miami, Leonard M Miller School of Medicine

Harris Gellman, MD is a member of the following medical societies: American Academy of Medical Acupuncture, American Academy of Orthopaedic Surgeons, American Orthopaedic Association, American Society for Surgery of the Hand, and Arkansas Medical Society

Disclosure: Nothing to disclose.

Joseph Kaplan, MD, MS, FACEP Attending Physician, Department of Emergency Medicine, Martin Army Community Hospital, Fort Benning

Joseph Kaplan, MD, MS, FACEP is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Jegan Krishnan, MBBS, FRACS, PhD Professor, Chair, Department of Orthopedic Surgery, Flinders University of South Australia; Senior Clinical Director of Orthopedic Surgery, Repatriation General Hospital; Private Practice, Orthopaedics SA, Flinders Private Hospital

Jegan Krishnan, MBBS, FRACS, PhD, is a member of the following medical societies: Australian Medical Association, Australian Orthopaedic Association, and Royal Australasian College of Surgeons

Disclosure: Nothing to disclose.

Edward A Michelson, MD Associate Professor, Program Director, Department of Emergency Medicine, University Hospital Health Systems of Cleveland

Edward A Michelson, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Hampton Roy Sr, MD Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

R Christopher Walton, MD Professor, Director of Uveitis and Ocular Inflammatory Disease Service, Department of Ophthalmology, Assistant Dean for Graduate Medical Education, University of Tennessee College of Medicine; Consulting Staff, Regional Medical Center, Memphis Veterans Affairs Medical Center, St Jude Children's Research Hospital

R Christopher Walton, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Healthcare Executives, American Uveitis Society, Association for Research in Vision and Ophthalmology, and Retina Society

Disclosure: Nothing to disclose.

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Gout. Acute podagra due to gout in an elderly man.
Gout. Tophaceous deposits in ear.
Gout. Tophaceous deposits on elbow.
Gout. Chronic tophaceous gout in an untreated patient with end-stage renal disease.
Gout. Fluid obtained from a tophaceous deposit in a patient with gout.
Gout. Strongly negative birefringent, needle-shaped crystals diagnostic of gout obtained from an acutely inflamed joint.
Gout. Plain radiograph showing typical changes of gout in the first metatarsophalangeal joint and fourth interphalangeal joint.
Gout. Plain radiograph showing chronic tophaceous gouty arthritis in the hands.
Gout. Radiograph of erosions with overhanging edges.
Gout. Needles of urate on polarizing microscopy.
 
 
 
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