CDC - Arthritis - Basics - Definition

Arthritis

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, and a diet rich in meat and seafood. (4,5,6)
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). (7,8)
Gout is also associated with an increased risk of kidney stones. (9,10)
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. (7,11)
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 (weight loss, avoiding alcohol, reducing dietary purine intake) modifications 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

A study of gout and kidney stones among male health professionals showed that 5% of the 49,717 providing information reported gout at baseline. [Data source: Health Professionals’ Follow-up Study; gout: self reported physician diagnosed. (10)]
One study in a managed care population showed an increase in prevalence of gout from 2.9 to 5.2 per 1000 enrollees in the time period 1990 to 1999. For those under age 65, rates among men were 4 times those of women; over age 65 rates among men were 3 times greater. Most of the increase occurred among enrollees over the age of 65: among those over age 75, the prevalence increased (1990 to 1999) from 21 to 41 per 1000 enrollees. Among those 65 to 74, prevalence increased from 21 to 31 per 100 enrollees. [Gout was defined by ICD-9-CM codes 274xx or use of uric acid lowering drugs. (12)]
One-year period prevalence estimates ("Have you or any member of your household had gout within the past year?") derived from the NHIS were 0.94% for those 18 and older in 1996, thereby affecting about 3.0 million adults in 2005. (18)
Lifetime prevalence estimates (“Has a doctor ever told you that you had gout?”) from NHANES III (1988-1994) were 2.6% overall for those aged ≥20 years with a low of 400/100,000 in adults aged 20-29 years and a peak of 8,000/100,000 in adults aged 70-79 years, thereby affecting about 6.1 million adults in 2005. Gout was reported more often in men than in women overall, but prevalence increased with age for both, especially for women after menopause. (17)
Both the above are likely overestimates because they are based on self-reported data, but nationally gout appears to be increasing in frequency, with one-year prevalence estimates up from 0.85% in 1998. (17)

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III. Incidence

The incidence of gout among black men was almost twice that among white men (3.1 vs. 1.8 per 1,000 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. [Data source: medical students/physicians enrolled in the Mehary-Hopkins Study providing information. Gout: “Have you ever had gout?” (13)]
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. (14)

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IV. Mortality

Mortality is very low. (15)

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V. Hospitalizations

In 2004, gout and other crystal arthropathies accounted for 1.5% of 922,000 hospitalizations for a principal diagnosis of arthritis and other rheumatic conditions. (16)

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VI. Ambulatory Care

Gout was listed for 2.3 million ambulatory care visits annually from 2001-2005. (18)

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VII. Costs

No gout specific costs studies were identified.

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

No gout specific quality of life studies were identified.

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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/weeks followed by long periods without symptoms.

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X. References

Terkeltaub RA.Gout A. Epidemiology, pathology, and pathogenesis. (Chapter 15) in Primer on the Rheumatic Diseases, 12th edition. Klippel J (ed). 2001 Arthritis Foundation, Atlanta GA 30309.
Schumacher HR. Hyperuricemia and gout: a prevalent and chronic disease. JointandBone.org. January 2005. accessed at info@JointandBone.org July 27, 2005
Edward NL. Treating hyperuricemia in gout: a review of goals and therapies. JointandBone.org. July 2005. accessed at info@JointandBone.org July 27, 2005
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.
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.
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.
Weaver AL. Diagnosing Gout. JointandBone.org. May 2005. accessed at info@JointandBone.org July 27, 2005
Bieber JD, Terkeltaub RA. Gout. On the brink of novel therapeutic options for an ancient disease. Arthritis Rheum 2004;50:2400–2414.
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.
Kramer JH, Choi HK, Atkinson, K, Stampfer M, Curhan GC. The association between gout and nephrolithiasis in men: The Health Professionals’ Follow-up Study. Kidney International 2003; 64:1022–1026.
Terkeltaub RA Gout. N Engl J Med 2003. 349(17):1647–1655.
Wallace Kl, Riedel AA, Joseph-Ridge N, Wortmann R. Increasing prevalence of gout and hyperuricemia over 10 years among older adults in a managed care population. J Rheumatol 2004; 31:1582–1587.
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.
Arromdee E, Michet CJ, Crowson CS, O’Fallon WM, Gabriel SE. Epidemiology of gout: Is the incidence rising? J Rheumatol 2002;29:2403–2406.
Sacks JJ, Helmick CG, Langmaid G. Deaths from arthritis and other rheumatic conditions, United States, 1979–1998. J Rheumatol 2004;31(9):1823–1828.
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.
Lawrence RC, Felson DT, Helmick CG, et al. Estimates of the prevalence of arthritis and other rheumatic conditions in the United States. Part II. Arthritis Rheum 2008;58(1):26–35.
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 & Research 2010;62(4):460-464.