Gout and Pseudogout 

  • Author: Bruce M Rothschild, MD; Chief Editor: Herbert S Diamond, MD   more...
 
Updated: Jan 24, 2012
 

Background

Gout and pseudogout are the 2 most common crystal-induced arthropathies. They are debilitating illnesses in which recurrent episodes of pain and joint inflammation are caused by the formation of crystals within the joint space and deposition of crystals in soft tissue.[1, 2, 3] If untreated, these disorders can lead to joint destruction and renal damage. Rarely, gout can produce significant ocular findings.[4] The incidence of age-related macular degeneration (ARMD) is higher in patients with gout.[5]

Gout is inflammation caused by monosodium urate monohydrate (MSU) crystals. Pseudogout is inflammation caused by calcium pyrophosphate (CPP) crystals and is sometimes referred to as calcium pyrophosphate disease (CPPD).

Gout-related images are provided below.

Gout. Acute podagra due to gout in an elderly man.Gout. Acute podagra due to gout in an elderly man. Gout. Radiograph of erosions with overhanging edgeGout. Radiograph of erosions with overhanging edges. Gout. Needles of urate on polarizing microscopy. Gout. Needles of urate on polarizing microscopy.

Although gout is associated with hyperuricemia, the level of uric acid does not itself precipitate gout; rather, acute changes in the level of uric acid cause gout. Most individuals with hyperuricemia do not have gout, but if high uric acid levels go untreated, 90% of patients develop gout within 30 years. Hyperuricemia is found in 90% of individuals with gout, but it is also found in patients taking diuretics and even in those taking low doses of aspirin.

Primary gout is related to underexcretion or overproduction of uric acid. Secondary gout is related to myeloproliferative diseases or their treatment, therapeutic regimens producing hyperuricemia, renal failure, renal tubular disorders, lead poisoning, hyperproliferative skin disorders, enzymatic defects (eg, deficient hypoxanthine-guanine phosphoribosyl transferase, and glycogen storage diseases).[6]

Gout is definitively diagnosed based on the demonstration of urate crystals in aspirated synovial fluid. Classic radiographic findings may also be diagnostic. (See Workup).

Improvements in early diagnosis and the availability of definitive treatment have significantly improved the prognosis of gout, as evidenced by the declining incidence of disabling chronic tophaceous gout. However, tophaceous gout may still develop because of misdiagnosis, poor management, medication intolerances, and/or poor patient compliance.

Treatment of gout is important to relieve pain, prevent disease progression, and prevent tissue deposition of uric acid (eg, in the kidneys) that may produce kidney stones or urate nephropathy.[7] (See Treatment.)

Treatment of the acute phase of pseudogout is identical to that of gout. Unlike gout, however, no specific therapeutic regimen exists to treat the underlying cause of pseudogout, but colchicine and hydroxychloroquine are effective for prophylaxis.

Historical background

Gout is one of the oldest diseases in the medical literature.[8, 9] Since the time of the Greeks, many authors have written about gout as the result of personal excess; its association with a diet rich in meat and alcohol gained it the sobriquet, “the king of diseases and the disease of kings”. However, among the abstinent was John Milton, who lived a life of rigorous self-discipline and yet, to his anger and despair, suffered from what commonly was regarded as just punishment of the dissolute.

Lowenhook described symptoms of gout in the 1600s. In 1848, Sir Alfred Garrod linked gout with hyperuricemia, but the pathophysiology of acute gouty arthritis was not described fully until 1962.

Since then, gout has been associated with a large number of different autoimmune and metabolic disorders. Specific therapies and prophylactic measures have been developed to address the underlying problem.

Pseudogout, which may be clinically indistinguishable from gout, was recognized as a distinct disease entity in 1962.

Next

Pathophysiology

Gout can be considered a disorder of metabolism that allows uric acid/urate to accumulate in blood and tissues. When tissues become supersaturated, the urate salts precipitate, forming crystals. In addition, the crystals also are less soluble under acid conditions, so any condition predisposing to acidosis also precipitates urate crystals.

Urate initially precipitates in the form of needlelike crystals. The light-retarding (phase-shifting) characteristics of urate crystals allow them to be recognized by polarizing microscopy, as shown in the image below.

Gout. Needles of urate on polarizing microscopy. Gout. Needles of urate on polarizing microscopy.

Many conditions and drugs have been associated with an increase in plasma (and subsequent synovial) urate levels. A genetic predisposition for the disease exists.[10]

The CPP crystals that produce pseudogout are produced by nucleoside triphosphate pyrophosphohydrolase (NTPPPH), a catalytic enzyme found in vesicles that develop within osteoarthritic cartilage. A genetic predisposition exists for the condition, but any process that leads to osteoarthritis also can be associated with subsequent pseudogout.

Although the presence of urate crystals in the soft tissues and synovial tissues is a prerequisite for a gouty attack, the fact that these crystals can also be found in synovial fluid in the absence of joint inflammation suggests that the mere presence of intrasynovial urate crystals is not sufficient to cause flares of gouty arthritis.

One explanation for this may lie in the observation that clumps or microtophi of highly negatively charged and reactive urate crystals are normally coated with serum proteins (apolipoprotein [apo] E or apo B) that physically inhibit the binding of the crystals to cell receptors.[11, 12] A gout attack may be triggered by either a release of uncoated crystals (eg, due to partial dissolution of a microtophus caused by changing serum urate levels) or precipitation of crystals in a supersaturated microenvironment (eg, release of urate due to cellular damage).

From either source, naked urate crystals are then believed to interact with intracellular and surface receptors of local dendritic cells and macrophages, serving as a danger signal to activate the innate immune system.[13]

This interaction may be enhanced by immunoglobulin G (IgG) binding.[14, 15] Triggering of these receptors, including Toll-like receptors, NALP3 inflammasomes, and the triggering receptors expressed on myeloid cells (TREMs) by MSU, results in the production of interleukin (IL)–1, which in turn initiates the production of a cascade of pro-inflammatory cytokines, including IL-6, IL-8, neutrophil chemotactic factors, and tumor necrosis factor (TNF)–alpha.[16, 17] Neutrophil phagocytosis leads to another burst of inflammatory mediator production.

Subsidence of an acute gout attack is due to multiple mechanisms, including the clearance of damaged neutrophils, recoating of urate crystals, and the production of anti-inflammatory cytokines including, IL-1RA, IL-10, and transforming growth factor (TGF)–beta.[15, 18, 19, 20]

Previous
Next

Etiology

Gout develops in the setting of excessive stores of uric acid in the form of monosodium urate. Uric acid is an end-stage by-product of purine metabolism. Humans remove uric acid primarily by renal excretion. When excretion is insufficient to maintain serum urate levels below the saturation level of 6.8 mg/dL (with some variability depending on temperature and pH), hyperuricemia may develop, and urate can crystallize and deposit in soft tissues.

Ninety percent of patients with gout develop excess urate stores due to an inability to excrete sufficient amounts of normally produced uric acid in the urine (underexcretion). The remaining patients either overconsume purines or produce excessive amounts of uric acid endogenously (overproduction).

In rare cases, overproduction of uric acid is primary, due to a genetic disorder. These disorders include hypoxanthine-guanine phosphoribosyltransferase deficiency (Lesch-Nyhan syndrome), glucose-6-phosphatase deficiency (von Gierke disease), fructose 1-phosphate aldolase deficiency, and PP-ribose-P synthetase variants.

It has been suggested that a link exists between several autosomal dominant disorders and the development of gout. However, there has not been a specific genetic marker for those predisposed to developing gout.

Overproduction of uric acid may also occur in disorders that cause high cell turnover with release of purines, which are present in high concentration in cell nuclei. These disorders include myeloproliferative and lymphoproliferative disorders, psoriasis, hemolytic anemias, pernicious anemia, and ineffective erythropoiesis (as in B-12 deficiency). Cell lysis from chemotherapy for malignancies, especially those of the hematopoietic or lymphatic systems, can raise uric acid levels, as can excessive exercise and obesity.

Common causes of secondary gout due to underexcretion of uric acid include renal insufficiency, lead nephropathy (saturnine gout), starvation or dehydration, hypothyroidism, hyperparathyroidism, drugs, and chronic ethanol (especially beer and hard liquor) abuse. These disorders should be identified and corrected, if possible.

Comorbidities, including hypertension, diabetes, renal insufficiency, hypertriglyceridemia, hypercholesterolemia, diabetes, obesity, and early menopause, are associated with a higher incidence of gout.

Foods that are rich in purines include anchovies, sardines, sweetbread, kidney, liver, and meat extracts. Consumption of fructose-rich foods and beverages (eg, those sweetened with high-fructose corn syrup) are associated with an increased risk of gout in both men and women.[21, 22]

Individual gout flares are often triggered by acute increases or decreases in urate levels that may lead to the production, exposure, or shedding of crystals that are not coated with apo B or apo E. This can result from acute alcohol ingestion, acute overindulgence in foods high in purines, rapid weight loss, starvation, trauma, emotional stress, or hemorrhage.

Similarly, flares can be precipitated by additions of or changes in dosage of medications that raise or lower uric acid levels, such as loop or thiazide diuretics, aspirin, allopurinol, or uricosurics. Medications that increase uric acid levels via effects on renal tubular transport include loop and thiazide diuretics, low-dose aspirin, and cyclosporine A.[23, 24] Agents that lower levels of uric acid include radiocontrast dyes, xanthine oxidase inhibitors (eg, allopurinol, febuxostat), and uricosurics (eg, probenecid, sulfinpyrazone).

Although the pathophysiology, clinical presentation, and acute-phase treatment of gout and pseudogout are very similar, the underlying causes of the 2 diseases are very different. Many cases of pseudogout are idiopathic, but pseudogout has also been associated with aging, trauma, and many different metabolic abnormalities, the most common of which are hyperparathyroidism and hemochromatosis. Pseudogout attacks have been reportedly induced by etidronate disodium therapy and angiography.[25, 26]

Gout and renal disease

Although patients with gout often have other risk factors for renal disease, including hypertension and diabetes, chronic urate nephropathy can contribute to renal insufficiency. Chronic urate nephropathy in patients with chronic tophaceous gout can result from the deposition of urate crystals in the medullary interstitium and pyramids, resulting in an inflammatory reaction that can lead to fibrotic changes. This process is characterized by hyperuricemia that is disproportional to the degree of renal impairment and is associated with a benign urinary sediment.

Previous
Next

Epidemiology

United States statistics

The prevalence of gout in men is 5-13.6 cases per 1000 population; the prevalence in women is 1.5-6.4 cases per 1000 population. The rate is 0.27% in the general population. Prevalence is approximately 20% in patients with a family history of gout. The incidence of gout has been increasing as American society grows older and heavier,[27] rising 40% from 1990 to 1999.[28] Approximately 750,000 people in the United States take medication to decrease serum uric acid levels.

The National Health and Nutrition Examination Survey (2007-2008) estimated a new prevalence for gout and hyperuricemia. Gout rates were reported as 5.9% among men and 2% among women. The prevalence rate of hyperuricemia was noted as 21.2% for men and 21.6% for women.[29]

The frequency of pseudogout varies with age. The annual incidence of acute attacks of arthritic pain and swelling is about 1.3 per 1000 adults, but nearly half of adults develop radiographic changes typical of CPPD by age 80 years.

Attacks of gout have been noted to occur more frequently in the spring and less frequently in the winter. The reason for this is unknown.

The incidence of significant eye symptoms or signs associated with gout or elevated uric acid levels is very low.

International statistics

Gout has a worldwide distribution. The international prevalence of gout is 0.3%,[30] [31] but the prevalence varies widely from country to country. Regional differences may reflect environmental, dietary, and genetic influences.

In England, gout affects 16.4 of every 1000 men and 2.9 of every 1000 women. In the Maori people of New Zealand, 10.3% of men and 4.3% of women are affected.[32, 33, 34]

Racial differences in incidence

Gout has an increased prevalence in some populations but is rare in others. For example, the frequency of gout is increased in populations such as the Chamorros and Maori and in the Blackfoot and Pima tribes. Racial differences may at least in part reflect differences in diet, which has a large influence on the clinical expression of gout.

In the United States, the incidence of gout is 3.11 per 1000 person-years in African Americans and 1.82 per 1000 person years in whites; the excess risk can be partly explained by explained, in part, by a greater risk of incident hypertension.[35, 36] In contrast, clinically recognized gout is extremely rare among blacks living in Africa.

Sex- and age-related differences in incidence

Gout has a male predominance.[22, 37] The prevalence of gout is 13.6 cases per 1000 men and 6.4 cases per 1000 women. This difference is largely a consequence of age at onset, because estrogenic hormones have a mild uricosuric effect; therefore, gout is unusual in premenopausal women. For pseudogout, the male-to-female ratio is 1.5:1.

The predominant age range is 30-60 years. As a rule, uric acid levels are elevated for 20 years before the onset of gout. In men, uric acid levels rise at puberty, and the peak age of onset of gout in men is in the fourth to sixth decade of life. However, onset may occur in men in their early 20s who have a genetic predisposition and lifestyle risk factors.[38] In women, uric acid levels rise at menopause, and peak age of onset in women is in the sixth to eighth decade of life.

Gout affects 1.3% of elderly patients.[39, 40] The higher prevalence of gout in elderly persons may also reflect an increased prevalence of metabolic syndrome, high rates of diuretic treatment for hypertension and congestive heart failure, and the use of low-dose aspirin. Tophi are typically detectable clinically approximately 10 years after the first gout attack.

Earlier onset of gout occurs in patients with renal insufficiency or a genetic abnormality of purine metabolism (eg, hypoxanthine-guanine phosphoribosyltransferase deficiency, phosphoribosylpyrophosphate synthetase superactivity). Cyclosporine A can cause an accelerated form of gout, even in premenopausal women, that can present after only a few years of hyperuricemia, particularly if the patient is also receiving diuretics.

Previous
Next

Prognosis

Gout is associated with considerable morbidity, with acute episodes often causing incapacitation. However, gout that is treated early and properly carries an excellent prognosis if patient compliance is good.

With early treatment, gout should be totally controlled. If attacks recur, successful uric acid adjustment (requiring lifelong use of uricosuric or allopurinol medication) usually suppresses further activity. During the first 6-24 months of uricosuric or allopurinol therapy, acute attacks of gout may occur.[41, 42]

Chronic injury to intra-articular cartilage leaves the joints more susceptible to subsequent joint infections. Draining tophi can become secondarily infected. Untreated chronic tophaceous gout can lead to severe joint destruction and renal impairment. Deposition of MSU crystals in the kidney can result in inflammation and fibrosis, leading to reduced renal function or chronic nephropathy.[43] Rarely, gout can produce spinal cord impingement when deposition in tissues produces a local mass.

Acute attacks of pseudogout usually resolve within 10 days. Prognosis for resolutions of acute attacks is excellent. Some patients experience progressive joint damage with functional limitation.

Hyperuricemia and gout are associated with an increased overall likelihood of mortality. Whether this is directly attributable to hyperuricemia or gout or to gout-associated diseases (eg, insulin resistance, type 2 diabetes mellitus, abdominal obesity, hypercholesterolemia, hypertension) has been much debated.[44, 45]

Although no evidence has shown that gout or hyperuricemia causes any of these disorders, elevated urate levels have been shown to correlate with blood pressure in adolescents.[46] Among middle-aged men, hyperuricemia with gout was a significant independent risk for death due to cardiovascular disease.[47]

In a 2010 study, Kuo et al demonstrated that gout, but not hyperuricemia, is associated with higher risk of death from all causes and cardiovascular diseases. Analysis of 1,383 deaths among 61,527 Taiwanese subjects showed that the hazard ratio (HR) of all-cause mortality was 1.46, and the adjusted HR of cardiovascular mortality was 1.97 in individuals with gout compared with those who had normal uric acid levels. Among individuals with hyperuricemia, the HR of all-cause mortality was 1.07 and the adjusted HR of cardiovascular mortality was 1.08.[48]

Patient Education

Patients with severe hyperuricemia should avoid food with high purine content. Moderation in food and alcohol is advised. Early recognition of acute attacks is critical, as intervention with medication is much more effective earlier in the attack.

For patient education information, see the Arthritis Center, as well as Gout. Online information and pamphlets on gout are also available from the Arthritis Foundation.

Previous
Proceed to Clinical Presentation
 
 
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.

References

  1. Currie WJ. The gout patient in general practice. Rheumatol Rehabil. Nov 1978;17(4):205-17. [Medline].

  2. Martinon F, Glimcher LH. Gout: new insights into an old disease. J Clin Invest. Aug 2006;116(8):2073-5. [Medline]. [Full Text].

  3. So A. Gout in the spotlight. Arthritis Res Ther. 2008;10(3):112. [Medline]. [Full Text].

  4. Knapp CM, Constantinescu CS, Tan JH, McLean R, Cherryman GR, Gottlob I. Serum uric acid levels in optic neuritis. Mult Scler. Jun 2004;10(3):278-80. [Medline].

  5. Klein R, Klein BE, Tomany SC, Cruickshanks KJ. Association of emphysema, gout, and inflammatory markers with long-term incidence of age-related maculopathy. Arch Ophthalmol. May 2003;121(5):674-8. [Medline].

  6. Edwards NL. Treatment-failure gout: a moving target. Arthritis Rheum. Sep 2008;58(9):2587-90. [Medline].

  7. Bluestone R, Waisman J, Klinenberg JR. The gouty kidney. Semin Arthritis Rheum. Nov 1977;7(2):97-113. [Medline].

  8. Choi HK, Atkinson K, Karlson EW, et al. Alcohol intake and risk of incident gout in men: a prospective study. Lancet. Apr 17 2004;363(9417):1277-81. [Medline].

  9. Choi HK, Curhan G. Gout: epidemiology and lifestyle choices. Curr Opin Rheumatol. May 2005;17(3):341-5. [Medline].

  10. Bleyer AJ, Hart TC. Genetic factors associated with gout and hyperuricemia. Adv Chronic Kidney Dis. Apr 2006;13(2):124-30. [Medline].

  11. Terkeltaub RA, Dyer CA, Martin J, et al. Apolipoprotein (apo) E inhibits the capacity of monosodium urate crystals to stimulate neutrophils. Characterization of intraarticular apo E and demonstration of apo E binding to urate crystals in vivo. J Clin Invest. Jan 1991;87(1):20-6. [Medline].

  12. Terkeltaub R, Smeltzer D, Curtiss LK, et al. Low density lipoprotein inhibits the physical interaction of phlogistic crystals and inflammatory cells. Arthritis Rheum. Mar 1986;29(3):363-70. [Medline].

  13. Liu-Bryan R, Scott P, Sydlaske A, et al. Innate immunity conferred by Toll-like receptors 2 and 4 and myeloid differentiation factor 88 expression is pivotal to monosodium urate monohydrate crystal-induced inflammation. Arthritis Rheum. Sep 2005;52(9):2936-46. [Medline].

  14. Nagase M, Baker DG, Schumacher HR Jr. Immunoglobulin G coating on crystals and ceramics enhances polymorphonuclear cell superoxide production: correlation with immunoglobulin G adsorbed. J Rheumatol. Jul 1989;16(7):971-6. [Medline].

  15. Ortiz-Bravo E, Sieck MS, Schumacher HR Jr. Changes in the proteins coating monosodium urate crystals during active and subsiding inflammation. Immunogold studies of synovial fluid from patients with gout and of fluid obtained using the rat subcutaneous air pouch model. Arthritis Rheum. Sep 1993;36(9):1274-85. [Medline].

  16. Akahoshi T, Murakami Y, Kitasato H. Recent advances in crystal-induced acute inflammation. Curr Opin Rheumatol. Mar 2007;19(2):146-50. [Medline].

  17. Martinon F. Mechanisms of uric acid crystal-mediated autoinflammation. Immunol Rev. Jan 2010;233(1):218-32. [Medline].

  18. Terkeltaub RA. What stops a gouty attack?. J Rheumatol. Jan 1992;19(1):8-10. [Medline].

  19. Yagnik DR, Evans BJ, Florey O, et al. Macrophage release of transforming growth factor beta1 during resolution of monosodium urate monohydrate crystal-induced inflammation. Arthritis Rheum. Jul 2004;50(7):2273-80. [Medline].

  20. Lioté F, Ea HK. Recent developments in crystal-induced inflammation pathogenesis and management. Curr Rheumatol Rep. Jun 2007;9(3):243-50. [Medline].

  21. Choi HK, Willett W, Curhan G. Fructose-rich beverages and risk of gout in women. JAMA. Nov 24 2010;304(20):2270-8. [Medline].

  22. Choi HK, Curhan G. Soft drinks, fructose consumption, and the risk of gout in men: prospective cohort study. BMJ. Feb 9 2008;336(7639):309-12. [Medline]. [Full Text].

  23. Hall AP, Barry PE, Dawber TR, McNamara PM. Epidemiology of gout and hyperuricemia. A long-term population study. Am J Med. Jan 1967;42(1):27-37. [Medline].

  24. Lin HY, Rocher LL, McQuillan MA, Schmaltz S, Palella TD, Fox IH. Cyclosporine-induced hyperuricemia and gout. N Engl J Med. Aug 3 1989;321(5):287-92. [Medline].

  25. Watanabe H, Yamada S, Anayama S, Sato E, Maekawa S, Sugiyama H, et al. Pseudogout attack induced during etidronate disodium therapy. Mod Rheumatol. 2006;16(2):117-9. [Medline].

  26. Taggarshe D, Ng CH, Molokwu C, Singh S. Acute pseudogout following contrast angiography. Clin Rheumatol. Feb 2006;25(1):115-6. [Medline].

  27. Kim KY, Ralph Schumacher H, Hunsche E, Wertheimer AI, Kong SX. A literature review of the epidemiology and treatment of acute gout. Clin Ther. Jun 2003;25(6):1593-617. [Medline].

  28. Terkeltaub RA. Gout: Recent advances and emerging therapies. Rheumatic Disease Clinics Update. 2008;3(1):1-9..

  29. Zhu Y, Pandya BJ, Choi HK. Prevalence of gout and hyperuricemia in the US general population: The National Health and Nutrition Examination Survey 2007-2008. Arthritis Rheum. Oct 2011;63(10):3136-41. [Medline].

  30. Miao Z, Li C, Chen Y, Zhao S, Wang Y, Wang Z, et al. Dietary and lifestyle changes associated with high prevalence of hyperuricemia and gout in the Shandong coastal cities of Eastern China. J Rheumatol. Sep 2008;35(9):1859-64. [Medline].

  31. Mould-Quevedo J, Peláez-Ballestas I, Vázquez-Mellado J, Terán-Estrada L, Esquivel-Valerio J, Ventura-Ríos L, et al. [Social costs of the most common inflammatory rheumatic diseases in Mexico from the patient's perspective]. Gac Med Mex. May-Jun 2008;144(3):225-31. [Medline].

  32. Reed D, Labarthe D, Stallones R. Epidemiologic studies of serum uric acid levels among Micronesians. Arthritis Rheum. Jul-Aug 1972;15(4):381-90. [Medline].

  33. Rose BS. Gout in Maoris. Semin Arthritis Rheum. Nov 1975;5(2):121-45. [Medline].

  34. Rothschild BM, Heathcote GM. Characterization of gout in a skeletal population sample: presumptive diagnosis in a Micronesian population. Am J Phys Anthropol. Dec 1995;98(4):519-25. [Medline].

  35. Hochberg MC, Thomas J, Thomas DJ, Mead L, Levine DM, Klag MJ. Racial differences in the incidence of gout. The role of hypertension. Arthritis Rheum. May 1995;38(5):628-32. [Medline].

  36. Mody GM, Naidoo PD. Gout in South African blacks. Ann Rheum Dis. Jun 1984;43(3):394-7. [Medline]. [Full Text].

  37. Choi HK, De Vera MA, Krishnan E. Gout and the risk of type 2 diabetes among men with a high cardiovascular risk profile. Rheumatology (Oxford). Oct 2008;47(10):1567-70. [Medline].

  38. Olaniyi-Leyimu BY. Consider gout in patients with risk factors, regardless of age. Am Fam Physician. Jul 15 2008;78(2):176. [Medline].

  39. Yarom A, Rennebohm RM, Strife F, Levinson JE. Juvenile gouty arthritis. Two cases associated with mild renal insufficiency. Am J Dis Child. Oct 1984;138(10):955-7. [Medline].

  40. Singh H, Torralba KD. Therapeutic challenges in the management of gout in the elderly. Geriatrics. Jul 2008;63(7):13-8, 20. [Medline].

  41. Schumacher HR, Taylor W, Joseph-Ridge N, Perez-Ruiz F, Chen LX, Schlesinger N, et al. Outcome evaluations in gout. J Rheumatol. Jun 2007;34(6):1381-5. [Medline].

  42. Becker MA, MacDonald PA, Hunt BJ, Lademacher C, Joseph-Ridge N. Determinants of the clinical outcomes of gout during the first year of urate-lowering therapy. Nucleosides Nucleotides Nucleic Acids. Jun 2008;27(6):585-91. [Medline].

  43. Yü T, Talbott JH. Changing trends of mortality in gout. Semin Arthritis Rheum. Aug 1980;10(1):1-9. [Medline].

  44. Forman JP, Choi H, Curhan GC. Uric acid and insulin sensitivity and risk of incident hypertension. Arch Intern Med. Jan 26 2009;169(2):155-62. [Medline]. [Full Text].

  45. Kim SY, De Vera MA, Choi HK. Gout and mortality. Clin Exp Rheumatol. Sep-Oct 2008;26(5 Suppl 51):S115-9. [Medline].

  46. Feig DI, Johnson RJ. The role of uric acid in pediatric hypertension. J Ren Nutr. Jan/2007;17(1):79-83. [Medline].

  47. Krishnan E, Svendsen K, Neaton JD, et al. Long-term cardiovascular mortality among middle-aged men with gout. Arch Intern Med. May 26 2008;168(10):1104-10. [Medline].

  48. [Best Evidence] Kuo CF, See LC, Luo SF, Ko YS, Lin YS, Hwang JS, et al. Gout: an independent risk factor for all-cause and cardiovascular mortality. Rheumatology (Oxford). Jan 2010;49(1):141-6. [Medline].

  49. Lin SH, Hsieh ET, Wu TY, Chang CW. Cervical myelopathy induced by pseudogout in ligamentum flavum and retro-odontoid mass: a case report. Spinal Cord. Nov 2006;44(11):692-4. [Medline].

  50. Puig JG, Michan AD, Jimenez ML, et al. Female gout. Clinical spectrum and uric acid metabolism. Arch Intern Med. Apr 1991;151(4):726-32. [Medline].

  51. Meyers OL, Monteagudo FS. Gout in females: an analysis of 92 patients. Clin Exp Rheumatol. Apr-Jun 1985;3(2):105-9. [Medline].

  52. Macfarlane DG, Dieppe PA. Diuretic-induced gout in elderly women. Br J Rheumatol. May 1985;24(2):155-7. [Medline].

  53. Taniguchi Y, Yoshida M, Tamaki T. Posterior interosseous nerve syndrome due to pseudogout. J Hand Surg Br. Feb 1999;24(1):125-7. [Medline].

  54. Dalbeth N, Schauer C, Macdonald P, Perez-Ruiz F, Schumacher HR, Hamburger S, et al. Methods of tophus assessment in clinical trials of chronic gout: a systematic literature review and pictorial reference guide. Ann Rheum Dis. Apr 2011;70(4):597-604. [Medline].

  55. Stocker SL, Graham GG, McLachlan AJ, Williams KM, Day RO. Pharmacokinetic and pharmacodynamic interaction between allopurinol and probenecid in patients with gout. J Rheumatol. May 2011;38(5):904-10. [Medline].

  56. Chehab MR, Goyal J, Schlesinger N. Tophaceous Pustule-like Rash in a Patient with Gout. J Rheumatol. Jan 2012;39(1):194-5. [Medline].

  57. Coassin M, Piovanetti O, Stark WJ, Green WR. Urate deposition in the iris and anterior chamber. Ophthalmology. Mar 2006;113(3):462-5. [Medline].

  58. Slansky HH, Kubara T. Intranuclear urate crystals in corneal epithelium. Arch Ophthalmol. Sep 1968;80(3):338-44. [Medline].

  59. Bernad B, Narvaez J, Diaz-Torné C, Diez-Garcia M, Valverde J. Clinical image: corneal tophus deposition in gout. Arthritis Rheum. Mar 2006;54(3):1025. [Medline].

  60. MCWILLIAMS JR. Ocular findings in gout; report of a case of conjunctival tophi. Am J Ophthalmol. Dec 1952;35(12):1778-83. [Medline].

  61. Morris WR, Fleming JC. Gouty tophus at the lateral canthus. Arch Ophthalmol. Aug 2003;121(8):1195-7. [Medline].

  62. Fishman RS, Sunderman FW. Band keratopathy in gout. Arch Ophthalmol. Mar 1966;75(3):367-9. [Medline].

  63. Julkunen H, Heinonen OP, Pyörälä K. Hyperostosis of the spine in an adult population. Its relation to hyperglycaemia and obesity. Ann Rheum Dis. Nov 1971;30(6):605-12. [Medline]. [Full Text].

  64. KOSKOFF YD, MORRIS LE, LUBIC LG. Paraplegia as a complication of gout. J Am Med Assoc. May 2 1953;152(1):37-8. [Medline].

  65. Nguyen C, Ea HK, Palazzo E, Lioté F. Tophaceous gout: an unusual cause of multiple fractures. Scand J Rheumatol. 2010;39(1):93-6. [Medline].

  66. Janssens HJ, Fransen J, van de Lisdonk EH, van Riel PL, van Weel C, Janssen M. A diagnostic rule for acute gouty arthritis in primary care without joint fluid analysis. Arch Intern Med. Jul 12 2010;170(13):1120-6. [Medline].

  67. Palestro CJ, Vega A, Kim CK, Swyer AJ, Goldsmith SJ. Appearance of acute gouty arthritis on indium-111-labeled leukocyte scintigraphy. J Nucl Med. May 1990;31(5):682-4. [Medline].

  68. Campion EW, Glynn RJ, DeLabry LO. Asymptomatic hyperuricemia. Risks and consequences in the Normative Aging Study. Am J Med. Mar 1987;82(3):421-6. [Medline].

  69. De Miguel E, Puig JG, Castillo C, Peiteado D, Torres RJ, Martín-Mola E. Diagnosis of gout in patients with asymptomatic hyperuricaemia: a pilot ultrasound study. Ann Rheum Dis. Jan 2012;71(1):157-8. [Medline].

  70. Barthelemy CR, Nakayama DA, Carrera GF, Lightfoot RW Jr, Wortmann RL. Gouty arthritis: a prospective radiographic evaluation of sixty patients. Skeletal Radiol. 1984;11(1):1-8. [Medline].

  71. Dalbeth N, Clark B, Gregory K, Gamble G, Sheehan T, Doyle A, et al. Mechanisms of bone erosion in gout: a quantitative analysis using plain radiography and computed tomography. Ann Rheum Dis. Aug 2009;68(8):1290-5. [Medline].

  72. Fodor D, Albu A, Gherman C. Crystal-associated synovitis- ultrasonographic feature and clinical correlation. Ortop Traumatol Rehabil. Mar-Apr 2008;10(2):99-110. [Medline].

  73. de Ávila Fernandes E, Kubota ES, Sandim GB, Mitraud SA, Ferrari AJ, Fernandes AR. Ultrasound features of tophi in chronic tophaceous gout. Skeletal Radiol. Mar 2011;40(3):309-15. [Medline].

  74. Fernandes EA, Lopes MG, Mitraud SA, Ferrari AJ, Fernandes AR. Ultrasound characteristics of gouty tophi in the olecranon bursa and evaluation of their reproducibility. Eur J Radiol. Jan 13 2011;[Medline].

  75. Thiele RG, Schlesinger N. Diagnosis of gout by ultrasound. Rheumatology (Oxford). Jul 2007;46(7):1116-21. [Medline].

  76. Dalbeth N, Clark B, Gregory K, Gamble G, Sheehan T, Doyle A, et al. Mechanisms of bone erosion in gout: a quantitative analysis using plain radiography and computed tomography. Ann Rheum Dis. Aug 2009;68(8):1290-5. [Medline].

  77. Al-Arfaj AM, Nicolaou S, Eftekhari A, Munk P, Shojani K, Reid G, et al. Utility of dual energy computed tomography (DECT) i8n tophaceous gout. Ann Rheum Dis. 2008;58:S878..

  78. Shimizu T, Hori H. The prevalence of nephrolithiasis in patients with primary gout: a cross-sectional study using helical computed tomography. J Rheumatol. Sep 2009;36(9):1958-62. [Medline].

  79. Poh YJ, Dalbeth N, Doyle A, McQueen FM. Magnetic Resonance Imaging Bone Edema Is Not a Major Feature of Gout Unless There Is Concomitant Osteomyelitis: 10-year Findings from a High-prevalence Population. J Rheumatol. Nov 2011;38(11):2475-81. [Medline].

  80. Oostveen JC, van de Laar MA. Magnetic resonance imaging in rheumatic disorders of the spine and sacroiliac joints. Semin Arthritis Rheum. Aug 2000;30(1):52-69. [Medline].

  81. Rothschild B, Yakubov LE. Prospective 6-month, double-blind trial of hydroxychloroquine treatment of CPDD. Compr Ther. May 1997;23(5):327-31. [Medline].

  82. Roddy E. Hyperuricemia, gout, and lifestyle factors. J Rheumatol. Sep 2008;35(9):1689-91. [Medline].

  83. Reber P, Crevoisier X, Noesberger B. Unusual localisation of tophaceous gout. A report of four cases and review of the literature. Arch Orthop Trauma Surg. 1996;115(5):297-9. [Medline].

  84. Schapira D, Stahl S, Izhak OB, Balbir-Gurman A, Nahir AM. Chronic tophaceous gouty arthritis mimicking rheumatoid arthritis. Semin Arthritis Rheum. Aug 1999;29(1):56-63. [Medline].

  85. Shogan CP, Folio CL. Tophaceous gout and rheumatoid arthritis awareness. J Am Osteopath Assoc. Jul 2008;108(7):352; author reply 352-3. [Medline].

  86. Riedel AA, Nelson M, Joseph-Ridge N, Wallace K, MacDonald P, Becker M. Compliance with allopurinol therapy among managed care enrollees with gout: a retrospective analysis of administrative claims. J Rheumatol. Aug 2004;31(8):1575-81. [Medline].

  87. Medsafe Pharmacovigilance Team. Colchicine: lower doses for greater safety. Available at http://www.medsafe.govt.nz/profs/puarticles/colchdose.htm. Accessed October 3, 2008.

  88. Nuki G. Colchicine: its mechanism of action and efficacy in crystal-induced inflammation. Curr Rheumatol Rep. Jul 2008;10(3):218-27. [Medline].

  89. [Best Evidence] Zhang W, Doherty M, Bardin T, et al. EULAR evidence based recommendations for gout. Part II: Management. Report of a task force of the EULAR Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT). Ann Rheum Dis. Oct 2006;65(10):1312-24. [Medline].

  90. Terkeltaub RA, Furst DE, Bennett K, Kook KA, Crockett RS, Davis MW. High versus low dosing of oral colchicine for early acute gout flare: Twenty-four-hour outcome of the first multicenter, randomized, double-blind, placebo-controlled, parallel-group, dose-comparison colchicine study. Arthritis Rheum. Apr 2010;62(4):1060-8. [Medline].

  91. Terkeltaub RA, Furst DE, Digiacinto JL, Kook KA, Davis MW. Novel evidence-based colchicine dose-reduction algorithm to predict and prevent colchicine toxicity in the presence of cytochrome P450 3A4/P-glycoprotein inhibitors. Arthritis Rheum. Aug 2011;63(8):2226-37. [Medline].

  92. FDA takes action to stop the marketing of unapproved injectable drugs containing colchicine. US Food and Drug Administration. Available at www.fda.gov/bbs/topics/news/2008/new01791.html. Accessed September 30, 2008.

  93. [Guideline] Wallace SL, Singer JZ, Duncan GJ, et al. Renal function predicts colchicine toxicity: guidelines for the prophylactic use of colchicine in gout. J Rheumatol. Feb 1991;18(2):264-9. [Medline].

  94. Yu T. The efficacy of colchicine prophylaxis in articular gout--a reappraisal after 20 years. Semin Arthritis Rheum. Nov 1982;12(2):256-64. [Medline].

  95. Perez-Ruiz F, Herrero-Beites AM, Carmona L. A two-stage approach to the treatment of hyperuricemia in gout: The "Dirty Dish" hypothesis. Arthritis Rheum. Dec 2011;63(12):4002-6. [Medline].

  96. Markel A. Allopurinol-induced DRESS syndrome. Isr Med Assoc J. Oct 2005;7(10):656-60. [Medline].

  97. Singer JZ, Wallace SL. The allopurinol hypersensitivity syndrome. Unnecessary morbidity and mortality. Arthritis Rheum. Jan 1986;29(1):82-7. [Medline].

  98. Vázquez-Mellado J, Morales EM, Pacheco-Tena C, et al. Relation between adverse events associated with allopurinol and renal function in patients with gout. Ann Rheum Dis. Oct 2001;60(10):981-3. [Medline].

  99. Fels E, Sundy JS. Refractory gout: what is it and what to do about it?. Curr Opin Rheumatol. Mar 2008;20(2):198-202. [Medline].

  100. Fam AG, Dunne SM, Iazzetta J, et al. Efficacy and safety of desensitization to allopurinol following cutaneous reactions. Arthritis Rheum. Jan 2001;44(1):231-8. [Medline].

  101. Walz-LeBlanc BA, Reynolds WJ, MacFadden DK. Allopurinol sensitivity in a patient with chronic tophaceous gout: success of intravenous desensitization after failure of oral desensitization. Arthritis Rheum. Oct 1991;34(10):1329-31. [Medline].

  102. Becker MA, Schumacher HR Jr, Wortmann RL, et al. Febuxostat compared with allopurinol in patients with hyperuricemia and gout. N Engl J Med. Dec 8 2005;353(23):2450-61. [Medline].

  103. Bieber JD, Terkeltaub RA. Gout: on the brink of novel therapeutic options for an ancient disease. Arthritis Rheum. Aug 2004;50(8):2400-14. [Medline].

  104. Sundy JS, Baraf HS, Yood RA, et al. Efficacy and tolerability of pegloticase for the treatment of chronic gout in patients refractory to conventional treatment: two randomized controlled trials. JAMA. Aug 17 2011;306(7):711-20. [Medline].

  105. Emmerson BT, Gordon RB, Cross M, et al. Plasma oxipurinol concentrations during allopurinol therapy. Br J Rheumatol. Dec 1987;26(6):445-9. [Medline].

  106. Huang HY, Appel LJ, Choi MJ, et al. The effects of vitamin C supplementation on serum concentrations of uric acid: results of a randomized controlled trial. Arthritis Rheum. Jun 2005;52(6):1843-7. [Medline].

  107. So A, De Smedt T, Revaz S, et al. A pilot study of IL-1 inhibition by anakinra in acute gout. Arthritis Res Ther. 2007;9(2):R28. [Medline].

  108. Lee YH, Lee CH, Lee J. Effect of fenofibrate in combination with urate lowering agents in patients with gout. Korean J Intern Med. Jun 2006;21(2):89-93. [Medline].

  109. Singh JA, Reddy SG, Kundukulam J. Risk factors for gout and prevention: a systematic review of the literature. Curr Opin Rheumatol. Mar 2011;23(2):192-202. [Medline].

  110. Dalbeth N, Horne A, Gamble GD, Ames R, Mason B, McQueen FM, et al. The effect of calcium supplementation on serum urate: analysis of a randomized controlled trial. Rheumatology (Oxford). Feb 2009;48(2):195-7. [Medline].

  111. Schumacher HR Jr, Becker MA, Lloyd E, MacDonald PA, Lademacher C. Febuxostat in the treatment of gout: 5-yr findings of the FOCUS efficacy and safety study. Rheumatology (Oxford). Feb 2009;48(2):188-94. [Medline].

  112. Hair PI, McCormack PL, Keating GM. Febuxostat. Drugs. 2008;68(13):1865-74. [Medline].

  113. Sundy JS, Becker MA, Baraf HS, Barkhuizen A, Moreland LW, Huang W, et al. Reduction of plasma urate levels following treatment with multiple doses of pegloticase (polyethylene glycol-conjugated uricase) in patients with treatment-failure gout: results of a phase II randomized study. Arthritis Rheum. Sep 2008;58(9):2882-91. [Medline].

  114. Becker MA, Schumacher HR Jr, Wortmann RL, et al. . A phase 3 study comparing the safety and efficacy of oral febuxostat and allopurinol in subjects with hyperuricemia and gout. Arthritis Rheum. 2004;50:4103-4..

  115. Fam AG. Should patients with interval gout be treated with urate lowering drugs?. J Rheumatol. Sep 1995;22(9):1621-3. [Medline].

  116. Groff GD, Franck WA, Raddatz DA. Systemic steroid therapy for acute gout: a clinical trial and review of the literature. Semin Arthritis Rheum. Jun 1990;19(6):329-36. [Medline].

  117. Konatalapalli RM, Demarco PJ, Jelinek JS, Murphey M, Gibson M, Jennings B, et al. Gout in the axial skeleton. J Rheumatol. Mar 2009;36(3):609-13. [Medline].

  118. Mayer MD, Khosravan R, Vernillet L, Wu JT, Joseph-Ridge N, Mulford DJ. Pharmacokinetics and pharmacodynamics of febuxostat, a new non-purine selective inhibitor of xanthine oxidase in subjects with renal impairment. Am J Ther. Jan-Feb 2005;12(1):22-34. [Medline].

  119. Primatesta P, Plana E, Rothenbacher D. Gout treatment and comorbidities: a retrospective cohort study in a large US managed care population. BMC Musculoskelet Disord. May 20 2011;12:103. [Medline]. [Full Text].

  120. Siegel LB, Alloway JA, Nashel DJ. Comparison of adrenocorticotropic hormone and triamcinolone acetonide in the treatment of acute gouty arthritis. J Rheumatol. Jul 1994;21(7):1325-7. [Medline].

  121. Singh JA, Hodges JS, Asch SM. Opportunities for improving medication use and monitoring in gout. Ann Rheum Dis. Aug 2009;68(8):1265-70. [Medline].

  122. Song EF, Xiang Q, Ren KM, Hu JC, Wu F, Gong MF, et al. Clinical effect and action mechanism of Weicao Capsule in treating gout. Chin J Integr Med. Jun 2008;14(2):103-6. [Medline].

  123. Wu EQ, Yu AP, Guerin A, et al. The costs of treatment failure gout: a claims-based analysis. ACR/ARHP Scientific Meeting 2009. Accessed January 28, 2010. Available at http://acr.confex.com/acr/2009/webprogram/Paper16451.htm.

 
Previous
Next
 
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.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2012 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.