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National Center for Chronic Disease Prevention and Health Promotion
Division of Adult and Community Health
Health Care and Aging Studies Branch
Arthritis Program
Mailstop K-51
4770 Buford Highway NE
Atlanta, GA 30341-3724
Phone: 770.488.5464
Fax: 770.488.5964
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Arthritis Types — Overview
Gout
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 a chronic disease 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 (masses 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.
Therapy for persons with recurrent acute flares or chronic gout
usually involves allopurinol.
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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
(Lawrence, 2008), 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.
- 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
1998.18
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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
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V. Hospitalizations
- In 1997, gout and other crystal arthropathies accounted for only
1% of 744,000 hospitalizations for a principal diagnosis of
arthritis and other rheumatic conditions.16
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VI. Ambulatory Care
- In 1997, gout accounted for 3% of 36.5 million visits for
arthritis and other rheumatic conditions as a primary diagnosis.17
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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
often 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 inof@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.
- Lethbridge-Cejku M, Helmick CG, Popovic JR. Hospitalizations for
arthritis and other rheumatic conditions: data from the 1997
National Hospital Discharge Survey. Med Care 2003
Dec;41(12):1367–73.
- Hootman JM, Helmick CG, Schappert SM. Magnitude and
characteristics of arthritis and other rheumatic conditions on
ambulatory medical care visits, United States, 1997. Arthritis
Care Res 2002;47(6):571–581.
- 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.
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XI. Resources
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* Links to non-Federal
organizations are provided solely as a service to our users. Links do not
constitute an endorsement of any organization by CDC or the Federal
Government, and none should be inferred. The CDC is not responsible for
the content of the individual organization Web pages found at this link.
Page last reviewed: June 8, 2008
Page last modified: January 11, 2008 Content Source:
Division of
Adult and Community Health, National Center for Chronic Disease Prevention and Health Promotion
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