Gout

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Gout
Gout
• The most common cause of inflammatory arthritis in US adults
(3.9% of Americans; approx. 8.3 million people; 2007-2008)
• Prevalence is greater in men (5.9%; 6.1 million) than women (2.0%;
2.2 million)
• Prevalence has increased by 1.2% points over the past 2 decades
• Incidence of gout 2x greater among black men than white men
• Men with gout have been shown to have an increased risk of allcause mortality and cardiovascular disease mortality
• Cost: 2.3 million ambulatory care visit annually from 2001-2005;
multiple hospitalizations; $7.7 billion attributable to gout between
2005-2011
Pathophysiology
• Caused by the deposition of monosodium urate crystals in
tissues
• Uric acid is a metabolic by-product of purine catabolism
• Purineshypoxanthinexanthineuric acid
• Reaction catalyzed by xanthine oxidase, found in the liver
• When the balance of dietary intake, synthesis and rate of
excretion are disrupted, hyperuricemia results
– Overproduction (10%)
– Underexcretion (90%)
• Results in arthritis, soft tissue masses, nephrolithiasis and
urate nephropathy
Pathophysiology
Rees, F. et al. (2014) Optimizing current treatment of gout
Nat. Rev. Rheumatol. doi:10.1038/nrrheum.2014.32
Risk Factors
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High Purine Diet (Red Meat, Fatty Poultry, High Fat Dairy, Seafood)
Alcohol Consumption
Trauma
Osteoarthritis
Surgery
Starvation
Dehydration
Obesity
Drugs (Allopurinol, uricosuric agents, thiazides, loop diuretics, low
dose aspirin)
• Renal Impairment
• Genetic Mutations (SLC22A9, SLC22A12, ABCG2)
Stages of Gout
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Asymptomatic tissue deposition
Acute Gouty Arthritis
Intercritical Gout
Chronic Articular and Tophaceous Gout
Acute Gout
• Often presents as involvement of a single joint or
multiple joints in the lower extremities: first
metatarsophalangeal (podagra; 50% of people
with gout), midtarsal, ankle and knee joints
• Characterized by pain, erythema, swelling and
warmth. Can have desquamation of skin.
• Can even cause fever and leukocytosis
• Maximal severity reached within 12-24 hours
• Even without treatment, attacks subside within
days to several weeks
Chronic Gout
• Characterized by chronic
arthritis and tophi, resulting
in chronic inflammatory and
destructive changes
Renal Complications
• Nephrolithiasis
– Risk factors: increase uric acid excretion, reduced urine
volume, and low urine pH
• Chronic urate nephropathy
– Urate crystals can deposit in renal medullary interstitium
producing inflammatory changes and fibrosis
– Clinical features are non specific: renal function
impairment, bland urinary sediment, mild proteinuria and
serum urate concentrations often higher than expected for
the degree of renal impairment.
– Biopsy confirms diagnosis
Diagnosis
• DDX: Pseudogout and Septic Arthritis
Diagnosis
• 5 clinical classification
criteria for gout currently
exist: Rome, New York, ACR,
Mexico and Netherlands
• These classification criteria
have not been extensively
validated
• Diagnosis should be based
on combination of clinical,
historical and laboratory
data if arthrocentesis cannot
be performed. Diagnosis is
considered provisional.
Diagnosis
• Arthrocentesis should be done in patients in
whom the diagnosis has not been previously
established .
• Labs: cell count with differential, gram stain,
culture, examination for crystals under
polarized light microscopy
Treatment
Treatment
Treatment
• When initiating urate lowering therapy, can
precipitate acute gouty arthritis. Therefore,
prophylaxis often given
Diet
Recommendations for Practice
References
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Mayo Clinic
UptoDate
CDC
Khanna,D., et. al. 2012 American College of Rheumatology
Guidelines for Management of Gout. Part 1: systematic
nonpharmacologic and pharmacologic therapeutic approaches to
hyperuricemia. Arthritis Care and Research, Vol. 64, No. 10, October
2012, pp 1431-1446
• Choi, H., et. al. Pathogenesis of Gout. Physiology in Medicine.
Annals of Internal Medicine. Vol. 143, 2005, pp 499-516
• Eggebeen, A. Gout: An Update. American Academy of Family
Physicians. 2007. http://www.aafp.org/afp/2007/0915/p801.html
• Dalbeth, N. et al. New Classification criteria for gout: a framework
for progress. Rheumatology (2013).
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