AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Background

Gout is an inflammatory arthritis caused by cellular reaction to uric acid crystal deposition. Usually, gout is hyperacute in presentation, but it may progress to chronic arthritis or even present as chronic arthritis. Diagnosis is based on identification of causative crystals or classic radiographic findings but is not based on hyperuricemia. The level of uric acid does not actually precipitate the 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 are untreated, 90% 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.

Treatment 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. 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, glycogen storage diseases).

Urate deposits have been reported in the pericardium of the Mexican lance-headed rattlesnake, Crotalus polystictus, as well as in Heloderma (Gila monster), Lampropeltis (milk snake), and Elaphe (rat snake). Actual articular gout was reported in Varanus exanthematicus (monitor lizard), Testudo sulcata (tortoise), Testudo radiata (tortoise; gout found in the forelimb, spine), Testudo graeca (tortoise), Testudo hermanni (tortoise), Kinixys belliana (tortoise), Alligator sclerops (lizard; gout found in the hip), Tupinambis (Teguixin lizards), and Crocodylus americanus (sharp-nosed crocodile).

Variation in susceptibility may relate to nitrogen excretory metabolism. Alligators predominantly excrete nitrogen in the form of ammonia (67-87%), aquatic tortoises excrete nitrogen as a mixture of urea and ammonia, Chrysemys turtles excrete nitrogen as urea (24-48%), and Phrynosoma turtles and terrestrial tortoises predominantly excrete nitrogen as uric acid. Dehydration appears especially to predispose animals to gout.

Gout in birds predominantly occurs from renal failure, as the analogue of uremia in humans. Visceral gout basically is a disorder of pericardial and pleuroperitoneal surfaces, whereas synovial gout predominantly produces nodules on the feet. Although osteoclastic resorption has been noted adjacent to such tophi, specific comment is unavailable on bone changes. Synovial gout has been reported in 13 of 2000 parakeets (Melopsittacus undulates) and 35 of 631 diseased Brown leghorn chickens. Visceral gout, without articular (synovial) gout, has been reported in Ajaia (spoonbill), Cygnus (swan), Touraco (bird; synovial), Anser (goose), Anas (teal), and Todorua species.

Urate arthritis or gout was reported in a rabbit but without documentation. Dissociation of visceral and articular gout apparently occurs in at least some mammals, as well as birds. Guanine gout has been reported in swine (which lack guanase), and xanthine deposits have been reported in the spleen, kidneys, and lymph nodes of cattle. Gout has not been reported in anthropoids, although oxalate kidney stones have been noted in Gorilla, Cercopithecus, and Gazella.

It is curious that among the dinosaurs, gout has only been found in carnosaurs, in spite of the larger available collections of herbivore skeletons for examination. This may be due to high levels of uric acid in raptors, in contrast to that in other birds. Gouty arthritis rarely has been noted in crocodilians, lizards, and turtles, but it has been reported in 1-5% of some birds. Contributing factors to occurrence of gout may be red meat in the diet; red meat was perhaps the foundation of the carnosaur diet.

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. Although increase in serum and tissue concentration may allow the crystals to precipitate, the crystals also are less soluble under acid conditions. 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.

Uric acid precipitates from supersaturated extracellular (ie, synovial) fluid. The resulting crystals stimulate phagocytosis by neutrophils and initiation of the inflammatory cascade. Interleukin-1 and tumor necrosis factor-a are involved in the inflammatory cascade.

Frequency

United States

The prevalence 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.

International

International prevalence is 0.3%. In the Maori people of New Zealand, 10.3% of men and 4.3% of women are affected.

Mortality/Morbidity

• Deposition of uric acid crystal in the kidneys may produce renal failure or obstruction.
• Deposition in tissues produces a mass with space-occupying or mass effects. This can produce spinal cord impingement (rarely).
• Joint damage may render the joint nonfunctional.

Race

Incidence of gout is 3.11 per 1000 person years in African Americans and 1.82 per 1000 person years in whites. In some populations (eg, Chamorros, Maori), frequency of gout is increased; in other populations, it is rarely represented. Frequency is increased in Blackfoot and Pima Indians.

Sex

• Gout has a 90% male predominance.
• Gout rarely occurs in women who are premenopausal.

Age

• Gout usually occurs in men older than 20 years. It also occurs in women who are postmenopausal. Gout affects 1.3% of elderly patients.

CLINICAL

Section 3 of 11  

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• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

History

• In hyperacute inflammatory arthritis, symptoms of redness, swelling, heat, tenderness, and interference with range of motion typically are most intense within 24 hours. Tenderness often is so exquisite that the affected individual cannot even tolerate the weight of bed sheets on the affected area. Attacks may be isolated (1-time) events or may occur repeatedly.
• Deposits forming a lump (tophus) also may be reported.

Physical

Gout usually is an inflammatory arthritis, with symptoms of redness, swelling, reduction of range of motion, and a hot and tender joint. Additional possible findings on physical examination include the following:

• Gout usually is monarticular, but 5% of cases are polyarticular and may even mimic rheumatoid arthritis.
• Chronic arthritis with tenderness and swelling, with or without redness, warmth, or joint damage, may be present.
• A tophus deposit may exist in the antihelix of the ear or subcutaneous regions (eg, olecranon, fingertips, cornea, aorta, CNS); an associated finding of a creamy discharge may be present (rarely).
• Other findings may include fever, chills, and carpal tunnel syndrome.
• In monoarticular gout, the first metatarsal phalangeal joint is most commonly affected (which leads to the appellation, podagra). Knee and ankle joints are the next most commonly affected, but any joints are susceptible. Polyarticular gout commonly involves the small joints of the fingers and toes, as well as the knees.

Causes

A cellular reaction to uric acid crystal deposition causes gout. Conditions and ingestions that may cause acute changes in the level of uric acid include the following:

• Hyperuricemia, including that produced by renal impairment
• Alcohol ingestion
• Dietary excess (especially of anchovies, sardines, sweetbread, kidney, liver, meat extracts)
• Fasting-induced ketosis
• Inborn errors of metabolism
• Lead poisoning (saturnine gout arising from ingestion of moonshine)
• Hypoparathyroidism
• Hyperlipidemia types 2, 4, and 5
• Paget disease
• Hyperproliferative skin disorders (eg, psoriasis)
• Calcium pyrophosphate deposition disease
• Sarcoidosis
• Hemolytic anemia
• Hemoglobinopathies
• Pernicious anemia
• Radiation treatment
• Glycogen storage disease (glycogenosis) type 1
• Down syndrome
• Gut sterilization by antibiotics
• Various medications, including the following:
• • Cyclosporine
  • Aminophylline
  • Caffeine
  • Corticosteroids
  • Cytotoxic drugs
  • Diazepam
  • Diphenhydramine
  • Diuretics
  • L-dopa
  • Dopamine
  • Epinephrine
  • Ethambutol
  • Methaqualone
  • Alpha-methyl dopa
  • Nicotinic acid
  • Probenecid (low dose)
  • Pyrazinamide
  • Salicylates ( <10/dL blood levels)
  • Sulfinpyrazone (low dose)
  • Vitamins B-12 and C

DIFFERENTIALS

Section 4 of 11  

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• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Other Problems to be Considered

Type IIA hyperlipoproteinemia
Amyloidosis
Multicentric reticulohistiocytosis
Hyperparathyroidism
Spondyloarthropathy
Sarcoid
Avascular necrosis
Tumor
Infectious arthritides
Malignant soft tissue tumors
Milk-alkali syndrome
Pigmented villonodular synovitis
Pseudogout
Psoriatic arthritis
Reiter syndrome
Renal osteodystrophy
Rheumatoid arthritis

WORKUP

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Lab Studies

• Synovial fluid wet mount examination reveals negatively birefringent urate crystals on polarizing examination in 85% of specimens. Synovial fluid WBC count usually is 10,000-70,000/µL, but it may be as low as 1000/µL.
• Peripheral WBC count often is elevated, with left shift during acute attacks.
• Erythrocyte sedimentation rate usually is elevated during acute attacks.
• Hyperuricemia is present in 95% of cases but is not diagnostic.
• Once the acute gout episode is controlled, 24-hour urine uric acid levels also are assessed for choosing medication to control the associated hyperuricemia.

Imaging Studies

• Routine radiographs reveal punched-out erosions or lytic areas with overhanging edges, but generally not within the first year of disease onset. Erosions with overhanging edges generally are considered pathognomonic for gout but also can be found in amyloidosis, multicentric reticulohistiocytosis, and type IIA hyperlipoproteinemia. Erosion with joint space preservation is typical.
• MRI depicts gouty tophi, which have low or intermediate signal intensity on T1-weighted spin echo images. Signal intensity also tends to be low on T2-weighted images. In the absence of inflammation, the tophi are sharply delineated. Presence of inflammation results in increased perilesional signal intensity related to inflammation. Tophi and the surrounding area of inflammation enhance with gadolinium.
• Indium-111–labeled leukocyte scans, usually used to identify infectious foci, also reveal intense accumulation in affected joints in gout.

Procedures

• Biopsy findings in synovial membrane or nodules include uric acid crystals if the biopsy is properly processed. As uric acid is water-soluble, the pathologic specimens need to be processed anhydrously.
• Arthrocentesis of the affected joint provides fluid for analysis under polarizing microscopy.

Histologic Findings

Polarizing microscopy reveals negatively birefringent crystals.

TREATMENT

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Medical Care

Treatment of gout is divided into 2 phases, namely, treatment of the acute attack and treatment of the underlying hyperuricemia. A nonsteroidal anti-inflammatory drug (NSAID) is 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. The latter is especially important when alteration in uric acid levels or load might be anticipated. As treatment of the underlying hyperuricemia (lowering of the uric acid levels) actually precipitates gout in up to 50% of individuals, anti-inflammatory therapy is continued (at low doses) for the first 6-18 months of hyperuricemia-directed treatment.

• Use of colchicine is controversial because of its toxicity. Oral administration generally has been discarded, as therapeutic doses usually produce diarrhea, and colchicine therapy must be initiated within 24 hours of onset of the acute attack to be effective. The therapeutic-toxic window is very narrow. Intravenous colchicine can also be prescribed.
• Intra-articular long-acting (depot) corticosteroids can be used for single joint involvement if infection is definitely ruled out. Use generally is limited to situations in which nonsteroidal anti-inflammatory agents and colchicine are contraindicated.
• Therapy to control the underlying hyperuricemia generally is contraindicated until the acute attack is controlled (unless kidneys are at risk due to 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.
• • Any contributing medication regimens are altered first, and any predisposing medical conditions or habits are addressed.
  • The patient then 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 to 2 mg/dL less than the levels during which attacks were noted.
  • If the patient has tophaceous disease, probenecid should not be used. Urinary alkalization and the recommendation to ingest copious amounts of fluid are adjunctive. If the patient is a hyperexcreter or has tophi or renal disease, the drug of choice is allopurinol.
  • As both probenecid and allopurinol change serum and tissue uric acid levels, they may predispose patients to acute gouty attacks. A low-dose nonsteroidal anti-inflammatory agent is used for 6-24 months to reduce this undesired effect.
• No role exists for probenecid or allopurinol in treatment of an acute gouty attack. If the patient has been on a consistent dose of one of those agents for more than 2 weeks at the time of the acute attack, probenecid or allopurinol should be continued at that dose during the attack.

Consultations

If the gout attack does not respond to nonsteroidal anti-inflammatory agents within 2 days or to colchicine within 1 day, consultation with a rheumatologist may prove helpful. If the hyperuricemia is not controlled, similar consultation may be helpful.

Diet

Treatment adjuvants include weight reduction if the patient has obesity, but ketosis-inducing diets (eg, fasting) should be avoided. As uric acid is a breakdown product of the purine component of DNA, any high-purine foods should be consumed only in moderation. Sweetbread (eg, pancreas, thymus), liver, kidney, brain, meat extracts, meats, and shellfish are high in purine content. Alcohol intake should be minimized.

Activity

The acute attack is sufficiently limiting to activity that additional limitations on activity are not necessary. The patient should avoid trauma to the affected joint.

MEDICATION

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The goals of pharmacotherapy are to reduce morbidity and prevent complications.

Drug Category: Nonsteroidal anti-inflammatory drugs

Choice of NSAID is more habit than science; use of concomitant misoprostol gastric protection or consideration of a COX-2–specific NSAID might be considered if the patient has gastrointestinal risk; 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.

Drug Category: Anti-inflammatories

Reduce formation of uric acid crystals in affected joint, thereby reducing amount of acute inflammation and pain; also decreases uric acid levels in blood.

Drug Category: Uricosurics

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

Note that febuxostat is a potential alternative to allopurinol. Currently, it is an experimental inhibitor of xanthine oxidase and has been used to lower uric acid levels. Dosed at 80-120 mg/d. Most common adverse events were upper respiratory tract infections, arthralgias, diarrhea, headache, and liver function abnormalities.

Drug Category: Intra-articular corticosteroids

Used for single joint involvement if infection is excluded; water-soluble steroids (eg, Decadron) are teleologically inappropriate for use as a depot steroid treatment.

Drug Category: Corticosteroid stimulating hormones

Stimulate synthesis and release of corticosteroid hormones.

Drug Category: Uric acid oxidizers

Metabolizes uric acid to a soluble form, thus preventing acute renal failure.

FOLLOW-UP

Section 8 of 11  

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• Follow-up
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Further Outpatient Care

• Serum uric acid levels are assessed at monthly intervals, and dosages of the suppressive agent (eg, probenecid, allopurinol) are modified to achieve goals.

Deterrence/Prevention

• Patients should avoid exacerbating medications, diets, and habits when possible

Complications

• Patients may experience the following complications:
• • Increased susceptibility to infection
  • Urate nephropathy
  • Uric acid nephropathy
  • Renal stones
  • Nerve or spinal cord impingement

Prognosis

• 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 gout may occur.

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 excellent patient education resources, visit eMedicine's Arthritis Center. Also, see eMedicine's patient education article Gout.

MISCELLANEOUS

Section 9 of 11  

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• Miscellaneous
• Multimedia
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Medical/Legal Pitfalls

• Attentiveness to medication interactions (eg, allopurinol with methotrexate) is critical in treatment of hyperuricemia.
• Be alert to the possibility of associated infection complicating or initiating an acute gouty attack.
• Be very circumspect if colchicine is used.

MULTIMEDIA

Section 10 of 11  

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• Differentials
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• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  Gout. Radiograph of erosions with overhanging edges.
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Media type:  X-RAY

Media file 2:  Gout. Polarizing microscopy needles of urate.
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Media type:  Photo

REFERENCES

Section 11 of 11

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• References

• Appleby EC, Siller WG. Some cases of gout in reptiles. J Pathol Bacteriol. Oct 1960;80:427-30. [Medline].
• Barthelemy CR, Nakayama DA, Carrera GF, et al. Gouty arthritis: a prospective radiographic evaluation of sixty patients. Skeletal Radiol. 1984;11(1):1-8. [Medline].
• 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.
• Bluestone R, Waisman J, Klinenberg JR. The gouty kidney. Semin Arthritis Rheum. Nov 1977;7(2):97-113. [Medline].
• Canoso JJ, Yood RA. Acute gouty bursitis: report of 15 cases. Ann Rheum Dis. Aug 1979;38(4):326-8. [Medline].
• Currie WJ. The gout patient in general practice. Rheumatol Rehabil. Nov 1978;17(4):205-17. [Medline].
• Fam AG. Should patients with interval gout be treated with urate lowering drugs?. J Rheumatol. Sep 1995;22(9):1621-3. [Medline].
• 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].
• Hadler NM, Franck WA, Bress NM, Robinson DR. Acute polyarticular gout. Am J Med. May 1974;56(5):715-9. [Medline].
• 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].
• Hochberg MC, Thomas J, Thomas DJ, et al. Racial differences in the incidence of gout. The role of hypertension. Arthritis Rheum. May 1995;38(5):628-32. [Medline].
• Jubb KV, Kennedy PC. Pathology of Domestic Animals. New York: Academic Press;. 1970.
• Julkunen H, Heinonen OP, Pyorala 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].
• Koskoff YD, Morris LE, Lubic LG. Paraplegia as a complication of gout. JAMA. 1953;152:37-8.
• Lawry GV 2d, Fan PT, Bluestone R. Polyarticular versus monoarticular gout: a prospective, comparative analysis of clinical features. Medicine (Baltimore). Sep 1988;67(5):335-43. [Medline].
• Lin HY, Rocher LL, McQuillan MA, et al. Cyclosporine-induced hyperuricemia and gout. N Engl J Med. Aug 3 1989;321(5):287-92. [Medline].
• Martinon F, Glimcher LH. Gout: new insights into an old disease. J Clin Invest. Aug 2006;116(8):2073-5. [Medline].
• Mendelson W. On guanin gout in the hog, and its relations to the sodium urate gout of man. Amer J Med Sci. 1888;95:109-22.
• Mody GM, Naidoo PD. Gout in South African blacks. Ann Rheum Dis. Jun 1984;43(3):394-7. [Medline].
• 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].
• Palestro CJ, Vega A, Kim CK, et al. Appearance of acute gouty arthritis on indium-111-labeled leukocyte scintigraphy. J Nucl Med. May 1990;31(5):682-4. [Medline].
• Pund EE Jr, Hawley RL, McGee HJ. Gouty heart. N Engl J Med. Oct 27 1960;263:835-8. [Medline].
• 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].
• 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].
• Resnick D, Niwayama G. Diagnosis of Bone and Joint Disorders. Philadelphia, Pa: Saunders;. 1988.
• Rose BS. Gout in Maoris. Semin Arthritis Rheum. Nov 1975;5(2):121-45. [Medline].
• Rothschild BM, Tanke D, Carpenter K. Tyrannosaurs suffered from gout. Nature. May 22 1997;387(6631):357. [Medline].
• 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].
• Schapira D, Stahl S, Izhak OB, et al. Chronic tophaceous gouty arthritis mimicking rheumatoid arthritis. Semin Arthritis Rheum. Aug 1999;29(1):56-63. [Medline].
• Schlumberger HG. Synovial gout in the parakeet. Lab Invest. Nov-Dec 1959;8:1304-18. [Medline].
• Schmidt RE, Hubbard GB. Atlas of Zoo Animal Patholology. II. Avian, Reptile and Miscellaneous Species. London: CRC Press;. 1987.
• Schumacher HR, Jiminez SA, Gibson T. Acute gouty arthritis without urate crystals identified on initial examination of synovial fluid. Arthritis Rheum. 1975;18:603-12.
• 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].
• Siller WG. Avian nephritis and visceral gout. Lab Invest. Nov-Dec 1959;8:1319-57. [Medline].
• Virchow R. Ueber Concretionen im Schweinfleisch, welche wahrscheinlich aus Guanin bestehen. Virchows Arch Pathol Anat Physiol. 1866;36:358-9.
• 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].
• Yu T, Talbott JH. Changing trends of mortality in gout. Semin Arthritis Rheum. Aug 1980;10(1):1-9. [Medline].

Article Last Updated: Sep 13, 2006