Gout and Pseudogout Treatment & Management

  • Author: Bruce M Rothschild, MD; Chief Editor: Herbert S Diamond, MD   more...
 
Updated: Feb 9, 2012
 

Approach Considerations

Gout is managed in 3 stages: (1) treating the acute attack, (2) providing prophylaxis to prevent acute flares, and (3) lowering excess stores of urate to prevent flares of gouty arthritis and to prevent tissue deposition of urate crystals.

Asymptomatic hyperuricemia should generally not be treated. However, patients with levels higher than 11 mg/dL who overexcrete uric acid are at risk for renal stones and renal impairment; therefore, renal function should be monitored in these individuals.[68] In one study, ultrasound identified urate crystal deposition in 11 of 26 individuals having asymptomatic gout for 2-28 years (average, 6.2 y), affecting the knee in 9 individuals and the first metatarsal phalangeal joint in 6. These results document that asymptomatic gout may not be as innocuous as once perceived.[69]

In patients with gout that is diagnosed and treated early, orthopedic surgery is usually unnecessary. Tophi should not be surgically removed unless they are in a critical location or drain chronically.

Surgery may be indicated for tophaceous complications, including infection, joint deformity, compression (eg, cauda equina or spinal cord impingement), and intractable pain, as well as for ulcers related to tophaceous erosions. Delayed healing is noted in 50% of patients.

A deterrent regimen for patients with idiopathic pseudogout can be obtained with hydroxychloroquine or colchicine.[81] If an underlying metabolic problem is responsible for pseudogout, the arthritis may be cured when the underlying problem is addressed.

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Treatment of Acute Attacks

The temptation to treat patients without a proven diagnosis must be resisted, as septic arthritis may clinically resemble gout or pseudogout. Unrecognized septic arthritis can lead to loss of life or of limb. Distinguishing septic arthritis from crystal-induced arthritis is not possible without an examination of joint fluid.

Acute treatment of proven crystal-induced arthritis is directed at relief of the pain and inflammation. Nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, and ACTH are the mainstays of treatment. The choice is based primarily on any concomitant health problems (eg, renal insufficiency, peptic ulcer disease). Colchicine, a classic treatment, is now rarely indicated.

When comorbidities limit the use of NSAIDs or colchicine, a preferred option may be an intra-articular steroid injection, particularly when a large, easily accessible joint is involved.

Any contributing medication regimens are altered first, and any predisposing medical conditions or habits are addressed.[82] Patients should be instructed to go on a diet if obese, to stop drinking beer, and to avoid purine-rich foods.

Therapy to control the underlying hyperuricemia generally is contraindicated until the acute attack is controlled (unless kidneys are at risk because of unusual uric acid load). Further, control of hyperuricemia generally is not pursued for a single attack. If attacks are recurrent or evidence of tophaceous or renal disease is present, therapy for control of hyperuricemia is indicated.[83, 84, 85]

Starting therapy to control hyperuricemia during an acute attack may intensify and prolong the attack. If the patient has been on a consistent dose of probenecid or allopurinol for more than 2 weeks at the time of the acute attack, the drug should be continued at that dose during the attack.

For urate crystals within the ocular tissue, treatment is directed at reducing both hyperuricemia and ocular inflammation.

In 2010, an 8-week, single-blind, double-dummy, dose-ranging study showed that the selective interleukin 1β selective binder canakinumab yielded fast and lasting relief of pain in patients with acute gouty arthritis flares refractory to NSAIDs or colchicine.[86] However, in June 2011, canakinumab was denied approval by the US Food and Drug Administration.[87] (See FDA Panel Says No to Canakinumab for Gout Attacks.)

Nonsteroidal anti-inflammatory drugs

NSAIDs are the drugs of choice in most patients with acute gout who do not have underlying health problems. Although indomethacin is the traditional NSAID of choice for acute gout (unless the patient is elderly, because of the potential for adverse CNS effects in this age group), most NSAIDs can be used. Select an agent with a quick onset of action, but do not use aspirin because it can alter uric acid levels and potentially prolong and intensify an acute attack. Cyclooxygenase-2 (COX-2) inhibitors have been used with success.

Avoid NSAIDs in patients who have a history of peptic ulcer disease or GI bleeding, patients with renal insufficiency, patients with abnormal hepatic function, patients taking warfarin (selective COX-2 inhibitors can be used), and patients in the intensive care unit who are predisposed to gastritis. Use NSAIDs cautiously in patients with diabetes and those who are receiving concomitant angiotensin-converting enzyme (ACE) inhibitors.

NSAIDs are prescribed at full dosage for 2-5 days to control the acute attack, and the dose is reduced to approximately one half to one fourth of that amount once the acute attack is controlled. Taper the dose down over approximately 2 weeks.

Gout symptoms should be absent for at least 2 days before the NSAID is discontinued. Anti-inflammatory therapy is continued (at low doses) for 6-18 months in patients starting medication to lower uric acid levels, as this treatment precipitates gout in up to 50% of patients.

Patient compliance of only 20% indicates that repeated reinforcement of the treatment regimen is necessary.[88]

Colchicine

Although colchicine was once the treatment of choice for acute gout, it is now a second-line approach because of its narrow therapeutic window and risk of toxicity.[89, 90] Colchicine therapy must be initiated within 24 hours of onset of the acute attack to be effective. When used in classic hourly dosing regimens in acute gout, colchicine causes adverse GI effects, particularly diarrhea and vomiting, in 80% of patients. This dosing regimen has been superseded (see below).

Dosing recommendations for colchicine in acute gout therapy have been modified in recent years because of an increased awareness of its toxicities. The most recent recommendations have been trending toward lowered daily and cumulative doses.

A task force of the European League Against Rheumatism (EULAR) Standing Committee for International Clinical Studies has developed evidence-based guidelines that recommend colchicine dosing in acute gout of 0.5 mg tid (0.6 mg tid in the United States).[91] An alternative regimen suggested by the New Zealand Medicines and Medical Devices Safety Authority is as follows: 1 mg loading dose followed by 0.5 (0.6) mg every 6 hours, up to a maximum of 2.5 mg/24 hours and 6 mg over 4 days.[89] This regimen also has been superseded (see below).

In a multicenter, randomized, double-blind, placebo-controlled, parallel-group study, Terkaltaub et al found that low-dose colchicine (1.8 mg total over 1 h) yielded both maximum plasma concentration and early gout flare efficacy comparable with that of high-dose colchicine (4.8 mg total over 6 h).[92] The safety profile of the low-dose treatment was indistinguishable from that of placebo. This is the favored regimen.

Evidence from 7 separate drug-to-drug interaction (DDI) studies indicates colchicine dose reductions of 33-66% for the treatment of acute gout and 50-75% for prophylaxis when colchicine therapy is used in combination with the extended-release calcium channel blockers verapamil and diltiazem. Doses of colchicine did not need to be adjusted when used in combination with azithromycin.[93]

Colchicine should not be used if the glomerular filtration rate (GFR) is less than 10 mL/min, and the dose should be decreased by at least half if the GFR is less than 50 mL/min. Colchicine should also be avoided in patients with hepatic dysfunction, biliary obstruction, or an inability to tolerate diarrhea.

A clinical response to colchicine is not pathognomonic for gout and may occur in patients with pseudogout, sarcoid arthropathy, psoriatic arthritis, or calcific tendonitis.

In February 2008, the US Food and Drug Administration (FDA) ruled that intravenous colchicine can no longer be produced or shipped in the United States because of its toxicities. Because of this, intravenous colchicine is no longer advocated for the treatment of acute gout in the United States.[94]

Prophylaxis

The standard dose of colchicines for prophylaxis is 0.6 mg bid, but lower doses have also been suggested. In patients with renal insufficiency, this dose may need to be decreased to daily or every-other-day administration. Even in prophylactic doses, colchicines can cause marrow toxicity and neuromyopathy in the setting of renal insufficiency.

Compared with the 80% risk of adverse GI effects in patients using classic hourly colchicine for the treatment of acute gout, the prophylactic dose of colchicine induces adverse GI effects in only 4% of patients.

Long-term use of colchicine can lead to a muscle weakness associated with elevated levels of creatine kinase due to a drug-induced neuromyopathy, particularly in patients with renal insufficiency.[95]

Prophylaxis with colchicine can be started during an acute attack. Lowering uric acid with either allopurinol or probenecid can precipitate attacks of gout. When used prophylactically, colchicine can reduce such flares by 85%.[96] Patients with gout may be able to abort an attack by taking a single colchicine tablet at the first twinge of an attack.

Corticosteroids

Corticosteroids can be given to patients with gout who cannot use NSAIDs or colchicine, but adrenocorticotropic hormone (ACTH) would be preferred. Steroids can be given orally, intravenously, intramuscularly, intra-articularly, or indirectly via ACTH.

ACTH at 40 IU IM can be given to induce corticosteroid production by the patient's own adrenal glands. Such a regimen does not depend on the patient to properly taper prednisone.

Prednisone can be given at a dose of approximately 40 mg for 1-3 days and then tapered over approximately 2 weeks. Tapering more rapidly can result in a rebound flare. Prophylaxis for steroid adverse effects (eg, osteoporosis) is recommended.

Using parenteral corticosteroids confers no advantage unless the patient cannot take oral medications.

Intra-articular, long-acting (depot) corticosteroids are particularly useful in patients with a monoarticular flare to help reduce the systemic effects of oral steroids. Ensuring that the joint is not infected prior to injecting intra-articular corticosteroids is particularly important.

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Treatment of Chronic Gout

In many cases, patients who have a first attack of gout should undergo therapy with agents that lower uric acid, given the high risk for further inflammatory attacks and the potential for destructive tophaceous deposition in the bone, synovium, and kidney, even without episodes of acute inflammation. However, some rheumatologists advocate waiting for the second attack to initiate therapy to lower uric acid levels because not all patients experience a second attack and because some patients may need to be convinced they need life-long therapy.

The risk of a second attack of gout after the first attack is 62% after 1 year, 78% after 2 years, and 93% after 10 years. The decision to begin therapy depends partly on the baseline serum uric acid levels (>9 mg/dL denotes a higher risk for recurrent gouty arthritis and tophi).

Long-term management of gout is focused on lowering uric acid levels. The goal of therapy is to lower serum uric acid levels to approximately 6 mg/dL or less. A prospective cohort study of 211 patients with gout found that maintenance of serum uric acid levels below 6 mg/dl resulted in disappearance of urate crystals in synovial fluid, resorption of tophi and cessation of acute attacks. Maintenance for 5 years is apparently sufficient in the absence of tophi to permit complete dissolution of all urate crystals. Use of diuretics is to be avoided, as they reduced ability to lower uric acid levels below 7 mg/dl in 17% of study participants.[97]

Avoiding the use of medications that elevate uric acid in patients with gout is prudent. Thus, in patients with hypertension, other agents are preferable to a thiazide diuretic. The angiotensin receptor blocker losartan should be considered. Losartan (is uricosuric at 50 mg/d. However, medications that elevate uric acid can still be used, if required, by making appropriate adjustments of allopurinol or probenecid doses.

The patient is tested for uric acid excretion. If the patient excretes less than 600 mg of uric acid per 24-hour period on a purine-free diet or less than 800 mg per 24-hour period on an unrestricted diet, the patient is considered a hypoexcreter. Probenecid is administered, and the dosage is increased at monthly intervals until the uric acid is lowered to reference range or at least lowered by 2 mg/dL less than the levels during which attacks occurred.

If the patient has tophaceous disease, probenecid should not be used. Urinary alkalization and the recommendation to ingest copious amounts of fluid are adjunctive.

Gout patients who have a 24-hour urinary excretion of uric acid above 1100 mg have a 50% risk of developing urate and oxalate kidney stones. Those with a measured urate excretion greater than 800 mg per 24 hours may benefit from allopurinol prophylaxis to prevent urate nephropathy. Allopurinol is also the drug of choice in patients with existing renal disease.

As both probenecid and allopurinol change serum and tissue uric acid levels, they may predispose patients to acute gouty attacks. Colchicine or low-dose NSAID treatment is used for 6-24 months to reduce this undesired effect. In patients who cannot take colchicine or NSAIDs, low doses of prednisone can be considered.

Monotherapy with colchicine may help prevent flares of inflammatory arthritis but does not prevent the accumulation of uric acid in the joints, which can lead to further joint destruction. In all cases, the risks and benefits need to be judged based on the individual patient. For instance, in an elderly patient with multiple underlying medical problems and renal insufficiency, the risks of therapy to lower uric acid levels may outweigh the benefits.

Agents that lower uric acid levels should not be initiated during an acute attack, because this may lead to a more intense and prolonged attack. Typically, they should be started a few weeks after the attack has resolved and with the protection of prophylactic colchicine to prevent another attack. If the patient develops a gout flare after beginning therapy with a uric acid–lowering agent, the agent should not be discontinued because this will only cause another flux in the uric acid level, which may prolong and intensify the attack.

Some rheumatologists prefer probenecid whenever possible because it has fewer significant adverse effects than allopurinol. Probenecid can be used in most middle-aged patients with gout who are otherwise healthy. Patients who use probenecid need to drink 2 L of fluid daily at the inception of therapy in order to reduce their urinary concentration and thereby reduce the risk of renal stones. Drug interactions may occur with probenecid (see Medication).

Indications for the use of allopurinol instead of probenecid include renal insufficiency (GFR < 50 mL/min), renal stones, use of aspirin (blocks the effect of probenecid), overproduction of uric acid, and unresponsiveness to probenecid.

Allopurinol

Allopurinol blocks xanthine oxidase and thus reduces the generation of uric acid. Therefore, it should be used in patients who overproduce uric acid and in patients at risk of tumor lysis syndrome to prevent renal toxicity during therapy for malignancies. It is the most effective urate-lowering agent. However, alcohol can interfere with the effectiveness of allopurinol.

Approximately 3-10% of patients taking allopurinol develop dyspepsia, headache, diarrhea, and/or pruritic maculopapular rash. Less frequently, patients taking allopurinol can develop allopurinol hypersensitivity, which carries a mortality rate of 20-30%.[98] Features of allopurinol hypersensitivity include fever, toxic epidermal necrolysis, bone marrow suppression, eosinophilia, leukocytosis, renal failure, hepatic failure, and vasculitis. Corticosteroids are often used to treat allopurinol hypersensitivity.

Allopurinol hypersensitivity is more likely to occur in patients with renal insufficiency, patients who are taking a diuretic, and patients begun on 300 mg of allopurinol.[99] Although allopurinol hypersensitivity is more common (although still rare) in patients with renal insufficiency, this effect does not appear to be dose-related.[100] Thus, a slow and careful titration of allopurinol dosing sufficient to achieve uric acid levels of less than 6 mg/dL is also recommended in these patients.[101]

Allopurinol is also associated with the drug rash with eosinophilia and systemic symptoms (DRESS) syndrome. DRESS syndrome affects the liver, kidney, and skin. It is a delayed-hypersensitivity response occurring 6-8 weeks after beginning allopurinol. The underlying mechanism is thought to be a cell-mediated immunity to allopurinol and its metabolites. Although occurrence is 0.4 %, the rate of organ failure and death is high. Treatment is with intravenous N- acetyl cysteine and steroids.

Allopurinol should be discontinued in patients who develop a rash. In patients with a history of drug eruptions due to allopurinol, both oral[102] and intravenous[103] desensitization regimens can be considered.

In most patients, start at 100 mg per day (50 mg in patients with renal insufficiency) and adjust the dose monthly according to the uric acid level until the goal of a uric acid level of 6 mg/dL or less is achieved.

Beware of drug interactions. For example, allopurinol prolongs the half-life of azathioprine and 6-mercaptopurine. It enhances the bone marrow toxicity of cyclophosphamide. Patients taking concomitant ampicillin are at an increased risk of rash.

Once the target uric acid level is achieved and maintained for 6 months, discontinue colchicine prophylaxis.

Allopurinol can be used in combination with probenecid. However, note that allopurinol increases the half-life of probenecid, whereas probenecid increases the excretion of allopurinol.

Febuxostat

Febuxostat, a nonpurine selective inhibitor of xanthine oxidase, is a potential alternative to allopurinol in patients with gout. Febuxostat is administered orally and is metabolized mainly in the liver. In contrast, allopurinol and its metabolites are excreted primarily by the kidney. Therefore, febuxostat can be administered in patients with renal insufficiency with no dosage adjustment. Its efficacy and side-effect profile otherwise appears similar to that of allopurinol.[104]

Uricase

Nonrecombinant urate-oxidase (uricase) is used in Europe to prevent severe hyperuricemia induced by chemotherapy in patients with malignancies, as well as in selected patients with treatment-refractory gout. Short-term use of such agents in patients with severe tophaceous could debulk the total-body urate load, allowing for maintenance with probenecid or allopurinol.

In 2009, the FDA approved recombinant Aspergillus flavus uricase (rasburicase [Elitek]) for the prevention of tumor lysis syndrome. However, it is highly immunogenic and may cause anaphylaxis.[105] A polyethylene-glycol–conjugated uricase (pegloticase [Krystexxa]) was approved by the FDA in 2010. Pegloticase, an enzymatically metabolizing uric acid, is a biologic agent to be considered when adjustment of contributing medications (eg, diuretics), allopurinol, febuxostat, and uricosuric agents is insufficient to appropriate reduction of serum uric acid levels. At this time, substantial expense compromises cost-effectiveness as an initial approach.[106]

Other therapeutic options

Patients with allopurinol hypersensitivity can often tolerate oxypurinol, which is a metabolite of allopurinol.[107] It is available on a "compassionate use" basis. Cross-reactivity with allopurinol can occur.

Benzbromarone is an effective uricosuric agent that may eventually become available. However, it can cause fulminant hepatotoxicity.

The angiotensin receptor blocker losartan and the triglyceride-lowering agent micronized fenofibrate have moderately potent uricosuric effects. They should therefore be considered in patients with gout who also require treatment for hypertension and hypertriglyceridemia.[105]

Vitamin C, with its uricosuric effect, may reduce the serum concentration of uric acid. In one study, 500 mg/day for 2 months reduced uric acid by a mean of 0.5 mg/dL.[108] Vitamin C treatment should be avoided with nephrolithiasis or urate nephropathy, cystinuria, or penicillamine.

In an open-label pilot study of 10 patients with refractory acute gout treated with the interleukin-1 (IL-1) antagonist anakinra, pain was substantially reduced in all patients within 2 days, without side effects. Clinical signs of inflammation had disappeared in 9 of 10 patients by the third day of treatment.[109]

Research has indicated that the lipid-lowering drug fenofibrate, a fibric acid derivative, will lower serum uric acid levels while reducing very-low-density lipoprotein (VLDL), total cholesterol, and triglyceride levels.[110] However, the creatinine level increases, and all effects are negated once the drug has been discontinued.

Rilonacept, a fusion protein designed to attach to and neutralize circulating IL-1 before it can attach to cell-surface receptors and generate signals that can trigger inflammation, has been shown in phase 3 studies to reduce the incidence of gout flares induced by the initiation of urate-lowering drug therapy.

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Diet and Activity

As uric acid is a breakdown product of purine, high-purine foods should be avoided, or consumed only in moderation. Foods very high in purines include hearts, sweetbreads (eg, pancreas, thymus), smelt, sardines, and mussels. Foods moderately high in purines include anchovies, trout, haddock, scallops, mutton, veal, liver, bacon, salmon, kidneys, and turkey.

Purines are found in all protein foods. All sources of purines cannot and should not be eliminated, but a low-protein diet may be helpful.

Overall, purine restriction reduces serum uric acid levels by only 1 mg/ml, at significant psychological impact. Diet modifications are rarely able to lower uric acid levels sufficiently to prevent further attacks and accumulation of urate.

Patients with gout should avoid beer and hard liquor because they elevate levels of uric acid and therefore can precipitate attacks of gout. Indeed, heavy drinkers are much more likely to have recurrent gout attacks, even with allopurinol therapy. Moderate wine intake is not associated with an increased gout flares.[8]

Increasing dairy intake, folic acid intake, and coffee consumption may reduce gout flares.[111]

Particularly because of the association of gout with atherosclerosis, the diagnosis of gout may be a good time to advise a low-cholesterol, low-fat diet if otherwise appropriate for the patient. While such a diet may help uric acid levels, such advice should be given primarily to help prevent atherosclerosis.

Weight reduction in patients who are obese can improve hyperuricemia. Ketosis-inducing diets (eg, fasting) should be avoided, however.

Ingestion of fructose-containing beverages should be reduced, and ingestion of milk and calcium should be increased.[112] If hyperphosphatemia is present, phosphate-binding agents should be used. Maintaining a high level of hydration with water (at least 8 glasses of liquids per day) is helpful in avoiding attacks of gout.

Because acute attacks are sufficiently limiting to activity, additional limitations of activity are not necessary. The patient should avoid trauma to the affected joint. Otherwise, they should be active.

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Consultations

Rheumatologists should be involved in the care of patients with gout. They can establish the diagnosis with arthrocentesis and synovial fluid analysis for crystals. They also are skilled in the management of this disorder, and consultation may be helpful in patients with an acute gout attack that does not respond to NSAIDs within 2 days or to colchicine within 1 day, or patients with refractory hyperuricemia.

Rheumatology or orthopedic consultation is indicated for any patient with septic arthritis or for any patient in whom a septic arthritis cannot be ruled out.

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Long-Term Monitoring

After diagnosis and treatment of an acute gouty arthritis episode, the patient should return for a follow-up visit in approximately 1 month to be evaluated for therapy to lower serum uric acid levels.

If uric acid–lowering therapy is begun, patients should be seen every 1-2 months while adjusting the dose of medications to achieve the target uric acid level of 5-6 mg/dL. Once this level is achieved and maintained, patients can be seen every 6-12 months.

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Proceed to Medication
 
 
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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