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Gout

Gout is a rheumatic disease resulting from deposition of uric acid crystals (monosodium urate) in tissues and fluids within the body. This process is caused by an overproduction or under excretion of uric acid. Certain common medications, alcohol, and dietary foods are known to be contributory factors. Acute gout will typically manifest itself as an acutely red, hot, and swollen joint with excruciating pain. These acute gouty flare-ups respond well to treatment with oral anti-inflammatory medicines and may be prevented with medication and diet changes. Recurrent bouts of acute gout can lead to a degenerative form of chronic arthritis called gouty arthritis.

I. Background

  • Gout is an ancient and common form of inflammatory arthritis, and is the most common inflammatory arthritis among men. Gout may remit for long periods, followed by flares for days to weeks, or can become chronic.
  • Gout is caused by an uncontrolled metabolic disorder, hyperuricemia, which leads to the deposition of monosodium urate crystals in tissue. Hyperuricemia means too much uric acid in the blood. Uric acid is a metabolic product resulting from the metabolism of purines (found in many foods and in human tissue).1,2
  • Hyperuricemia is caused by an imbalance in the production and excretion of urate, i.e., overproduction, underexcretion or both. Underexcretion is the most common cause, thought to account for 80–90% of hyperuricemia.3
  • Hyperuricemia is not the same as gout. Asymptomatic hyperuricemia does not need to be treated.
  • Risk factors for gout include being overweight or obese, having hypertension, alcohol intake (beer and spirits more than wine), diuretic use, a diet rich in meat and seafood, and poor kidney function.4-7
  • Weight loss lowers the risk for gout.5,6
  • Gout can be viewed in four stages:
    • Asymptomatic tissue deposition occurs when people have no overt symptoms of gout, but do have hyperuricemia and the asymptomatic deposition of crystals in tissues. The deposition of crystals, however, is causing damage.
    • Acute flares occur when urate crystals in the joint(s) cause acute inflammation. A flare is characterized by pain, redness, swelling, and warmth lasting days to weeks. Pain may be mild or excruciating. Most initial attacks occur in lower extremities. The typical presentation in the metatarsophalageal joint of the great toe (podagra) is the presenting joint for 50% of people with gout. About 80% of people with gout do have podagra at some point. Uric acid levels may be normal in about half of patients with an acute flare. Gout may present differently in the elderly, with many joints affected.
    • Intercritical segments occur after an acute flare has subsided, and a person may enter a stage with clinically inactive disease before the next flare. The person with gout continues to have hyperuricemia, which results in continued deposition of urate crystals in tissues and resulting damage. Intercritical segments become shorter as the disease progresses.
    • Chronic gout is characterized by chronic arthritis, with soreness and aching of joints. People with gout may also get tophi (lumps of urate crystals deposited in soft tissue)—usually in cooler areas of the body (e.g., elbows, ears, distal finger joints).8,9
  • Gout is also associated with an increased risk of kidney stones.10,11
  • The gold standard for diagnosing gout is aspiration and microscopic analysis for urate crystals in joint fluid or a tophus. Urate crystals are negatively birefringent under polarized light. Infection must be ruled out.8,12
  • The goals of treatment are to end the pain of acute flares, and to prevent future attacks and the formation of tophi and kidney stones. Therapy for acute flares consists of nonsteroidal anti-inflammatory drugs, steroids, and colchicine. Diet and lifestyle modifications (weight loss, avoiding alcohol, reducing dietary purine intake) may help prevent future attacks. Changing medications (e.g., stopping diuretics) associated with hyperuricemia may also help. Preventive therapy to lower blood uric acid levels in persons with recurrent acute flares or chronic gout usually involves allopurinol or a new drug (febuxostat).
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II. Prevalence

  • The prevalence of gout among US adults in 2007–2008 was 3.9% (8.3 million individuals) using nationally representative data (NHANES) from 2007–2008.13
    • The prevalence of gout among men was 5.9% (6.1 million), and the prevalence among women was 2.0% (2.2 million).
  • The prevalence of gout increased over the past 2 decades by an estimate of 1.2 percentage points.13

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III. Incidence

  • The incidence of gout among black men was almost twice that among white men (310 vs 180 per 100,000 person-years; follow up period 26 to 34 years). The cumulative incidence of gout was 10.9% among black men and 5.8% among white men.14
  • A Rochester Epidemiology Project study showed an increase in the incidence of gout from 45.0 per 100,000 in 1977-1978 to 63.3 per 100,000 in 1995-96. Male to female ratios were 3.3 to 1 at both time periods. Considering primary gout (excluding people with gout on diuretics), the incidence of gout increased from 20.2 to 45.9 per 100,000.15
  • An article using data from the Multiple Risk Factor Intervention Trial found that doctor-diagnosed gout incidence was 942 per 100,000 person-years, among 12,866 men aged 35–57 years at baseline (1973 to 1975), and followed for 7 years. 

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IV. Mortality

  • Using data from the Health Professionals Follow-Up Study researchers found that men with gout were shown to have an increased risk of all-cause mortality and cardiovascular disease (CVD) mortality compared with men without gout (the multivariate relative risks were 1.28 (95% confidence interval [CI], 1.15 to 1.41) for total mortality and 1.38 (95% CI, 1.15 to 1.66) for CVD deaths) over a 12-year follow-up period.16
  • However, gout as the underlying cause of death is very rare.17 

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V. Hospitalizations

  • In 2007, gout and other crystal arthropathies accounted for 1.5% of the 1.17 million nonfederal, short stay hospitalizations.18

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VI. Ambulatory Care

  • Gout was listed for 2.3 million ambulatory care visits annually from 2001-2005.19

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VII. Costs

  • Using data from the Medical Expenditure Panel Survey (MEPS) a nationally representative survey of the United States civilian, non-institutionalized population the estimated all-cause annual cost of gout in the US from 2005-2011 using 2011 inflation adjusted dollars was $31.8 billion or $11,663 per person.  The all-cause gout cost estimate includes ambulatory (office-based and hospital outpatient) inpatient, prescriptions, ER visits, other costs (home health, vision aids, dental, and medical devices).20
    • The estimated cost attributable to gout was 7.7 billion (24% of all-cause gout expenditures).20

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VIII. Impact on health-related quality of life (HRQOL)

  • A systematic review of 22 studies found that gout was associated with poor health-related quality of life.21

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IX. Unique characteristics

  • Unlike most types of arthritis, which are chronic, gout is typically episodic, characterized by painful flares lasting days or weeks followed by long periods without symptoms.

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X.  References

  1. Terkeltaub, RA. Gout: epidemiology, pathology and pathogenesis. In: J.H. Klippel, L.J. Crofford, J.H. Stone, C.D. Weyand (Eds.) Primer on the Rheumatic Diseases. 12th ed. Arthritis Foundation, Atlanta, GA; 2001: 307–312.
  2. Schumacher HR. Hyperuricemia and gout: a prevalent and chronic disease. JointandBone.org. January 2005. Accessed at info@JointandBone.org July 27, 2005.
  3. Edward NL. Treating hyperuricemia in gout: a review of goals and therapies. JointandBone.org. July 2005. Accessed at info@JointandBone.org July 27, 2005.
  4. Choi HK, Atkinson K, Karlson EW, Curhan G. Obesity, weight change, hypertension, diuretic use, and risk of gout in men. Arch Intern Med. 2005; 165: 742–748.
  5. Choi HK, Atkinson K, Karlson EW, Willet W, Curhan G. Alcohol intake and risk of incident gout in men: a prospective study. Lancet. 2004; 363: 1277–12781.
  6. Choi HK, Atkinson K, Karlson EW, Willet W, Curhan G. Purine-rich foods, dairy and protein intake, and the risk of gout in men. N Engl J Med. 2004; 350: 1093–1103.
  7. Krishnan E. Chronic Kidney Disease and the Risk of Incident Gout Among Middle-Aged Men. Arthritis Rheum. 2013; 65(12): 3271–3278.
  8. Weaver AL. Diagnosing Gout. JointandBone.org. May 2005. Accessed at info@JointandBone.org July 27, 2005.
  9. Bieber JD, Terkeltaub RA. Gout. On the brink of novel therapeutic options for an ancient disease. Arthritis Rheum. 2004; 50: 2400–2414.
  10. Kramer HM and Curhan G. The association between gout and nephrolithiasis: The National Health and Nutrition Examination Survey III, 1988–1994. Am J of Kid Dis. 2002; 40: 37–42.
  11. Kramer JH, Choi HK, Atkinson, K, Stampfer M, Curhan GC. The association between gout and nephrolithiasis in men: The Health Professionals’ Follow-up Study. Kid Int. 2003; 64: 1022–1026.
  12. Terkeltaub RA. Gout. N Engl J Med. 2003; 349(17): 1647–1655.
  13. 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. 2011; 63(10): 3136–3141.
  14. Hochberg MC, Thomas J, Thomas DJ, Mead L, Levine DM, Klag MJ. Racial difference in the incidence of gout. The role of hypertension. Arthritis Rheum. 1995; 38(5): 628–632.
  15. Arromdee E, Michet CJ, Crowson CS, O’Fallon WM, Gabriel SE. Epidemiology of gout: Is the incidence rising? J Rheumatol. 2002; 29: 2403–2406.
  16. Choi HK and Curhan G. Independent Impact of Gout on Mortality and Risk for Coronary Heart Disease. Circulation. 2007; 116: 894–900.
  17. Sacks JJ, Helmick CG, Langmaid G. Deaths from arthritis and other rheumatic conditions, United States, 1979–1998. J Rheumatol 2004;31(9):1823–1828.
  18. United States Bone and Joint Decade: The Burden of Musculoskeletal Diseases in the United States. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2008. Chapter 4. Arthritis and Related Conditions.
  19. Sacks JJ, Luo Y-H, Helmick CG. Prevalence of specific types of arthritis and other rheumatic conditions in the ambulatory health care system in the United States, 2001-2005. Arthritis Care Res. 2010; 62(4): 460-464.
  20. Cisternas MG, Murphy LB, Pasta DJ, Yelin EH, Helmick CG. Annual Medical Care Expenditures Among US adults with Gout, 2005–2011. Arthritis Rheum. 2014; 66(S10): S888.
  21. Chandratre P, Roddy E, Clarson L, Richardson J, Hider SL, Mallen CD. Health-related quality of life in gout: a systematic review. Rheumatology (Oxford). 2013; 52(11): 2031–2040.

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XI. Resources

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