eMedicine Specialties > Orthopedic Surgery > Systemic Diseases

Gout

Author: Bruce M Rothschild, MD, Professor of Medicine, Northeastern Ohio Universities College of Medicine; Adjunct Professor, Department of Biomedical Engineering, University of Akron; Adjunct Professor, Department of Anthropology, University of Kansas; Director, Arthritis Center of Northeast Ohio
Contributor Information and Disclosures

Updated: Jan 29, 2010

Introduction

Background

Gout is an inflammatory arthritis caused by cellular reaction to uric acid crystal deposition.1,2,3 Usually, gout is hyperacute in presentation, but it may progress to chronic arthritis.

Clinical Image Atlas

Click to view clinical images on the features and diagnosis of gout.



Diagnosis is based on identification of causative crystals or classic radiographic findings, but it 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 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.

Uric acid has been identified as a trigger of a cytosolic sensor called the inflammasome, thereby activating interleukin-1, an initiator of acute inflammation in gout.4

Gout-related images are provided below:

Gout. Radiograph of erosions with overhanging edg...

Gout. Radiograph of erosions with overhanging edges.

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Gout. Radiograph of erosions with overhanging edg...

Gout. Radiograph of erosions with overhanging edges.


Gout. Polarizing microscopy needles of urate.

Gout. Polarizing microscopy needles of urate.

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Gout. Polarizing microscopy needles of urate.

Gout. Polarizing microscopy needles of urate.


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.5 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

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).7,8

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 analog of uremia in humans.9 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)10 and 35 of 631 diseased Brown leghorn chickens and observed in a cassowary (Casuarius). Visceral gout, without articular (synovial) gout, has been reported in Ajaia (spoonbill), Cygnus (swan), Touraco (bird; synovial), Anser (goose), Anas (teal), Todorua species, and Casuarius (cassowary).

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),11 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. Dalmatian urate stones may be related to SLC2A mutations, which account for 1.7-5.3% of cases of human gout.12

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 the result of 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.13

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, as shown in the image below.

Gout. Polarizing microscopy needles of urate.

Gout. Polarizing microscopy needles of urate.

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Gout. Polarizing microscopy needles of urate.

Gout. Polarizing microscopy needles of urate.


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.4

Frequency

United States

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.

Frequency increased 40% from 1990 to 1999.14

International

International prevalence of gout is 0.3%.15 16 In the Maori people of New Zealand, 10.3% of men and 4.3% of women are affected.17,18,19

Mortality/Morbidity

  • Deposition of uric acid crystal in the kidneys may produce renal failure or obstruction.20
  • 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.
  • Gout is associated with hypertension and coronary artery disease.21,22

Race

The incidence of gout is 3.11 per 1000 person years in African Americans and 1.82 per 1000 person years in whites.23,24 In some populations (eg, Chamorros, Maori), frequency of gout is increased; in other populations, it is rarely represented. Frequency is increased in the Blackfoot and Pima.

Sex

  • Gout has a 90% male predominance.25,26
  • 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.27,28

Clinical

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.29
  • 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:30

  • Gout usually is monarticular, but 5% of cases are polyarticular and may even mimic rheumatoid arthritis.31,32
  • 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, carpal tunnel syndrome, neck stiffness, back pain, radiculopathy, neurologic compromise, sacroiliitis, and referred back, thigh, or hip pain.33
  • In monarticular 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:34

  • Hyperuricemia, including that produced by renal impairment
  • Genetic variants in SLC2A transportation
  • Reduced-carbohydrate beer
  • Obesity
  • High fructose corn syrup
  • Diabetes
  • End-stage renal disease
  • Organ transplantations
  • 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 and other agents, including the following:
    • Cyclosporine35
    • 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
    • Sucrose- or fructose-sweetened soft drinks
    • Purine-rich pancreatic therapy for cystic fibrosis

More on Gout

Overview: Gout
Differential Diagnoses & Workup: Gout
Treatment & Medication: Gout
Follow-up: Gout
Multimedia: Gout
References
Further Reading
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Keywords

gout, hyperuricemiaurate, crystal arthropathy, podagra, urate deposition disease, inflammatory arthritis, chronic arthritis, bursitis, rheumatoid arthritis

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Contributor Information and Disclosures

Author

Bruce M Rothschild, MD, Professor of Medicine, Northeastern Ohio Universities College of Medicine; Adjunct Professor, Department of Biomedical Engineering, University of Akron; Adjunct Professor, Department of Anthropology, University of Kansas; Director, Arthritis Center of Northeast Ohio
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.

Medical Editor

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, Ashford Specialist Centre
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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Paul E Di Cesare, MD, FACS, Chair and Professor, Department of Orthopedic Surgery, 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

CME Editor

Dinesh Patel, MD, FACS, Associate Clinical Professor of Orthopedic Surgery, Harvard Medical School; Chief of Arthroscopic Surgery, Department of Orthopedic Surgery, Massachusetts General Hospital
Dinesh Patel, MD, FACS is a member of the following medical societies: American Academy of Orthopaedic Surgeons
Disclosure: Nothing to disclose.

Chief Editor

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 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.

 
 
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