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  • Gout is an inflammatory arthritis related to a hyperuricemia (serum uric acid [SUA] level >6.8 mg/dL) (1)[C].
  • Acute gouty arthritis can affect ≥1 joint; the 1st metatarsophalangeal joint is most commonly involved at presentation (podagra).
  • Although hyperuricemia is necessary for the development of gout, it is not the only determining factor.
  • Characterized by deposition of monosodium urate (MSU) crystals that accumulate in joints and soft tissues, resulting in acute and chronic arthritis, soft-tissue masses called tophi, urate nephropathy, and uric acid nephrolithiasis
  • After an initial flare, a second flare occurs in ~60% of patients within 1 year and 78% within 2 years of the initial attack (2)[C].
  • Management involves treating acute attacks and preventing recurrent disease by long-term reduction of SUA levels through pharmacology and lifestyle adjustments.



Annual incidence of gout (3):

  • Uric acid 7.0 to 8.9 mg/dL is 0.5%.
  • Uric acid >9 mg/dL is 4.5%.

  • Increasing prevalence over the past decades (3)
  • Overall prevalence of 3.9% (8.3 million) in the United States in 2008 (3):
    • Men 5.8% (6.1 million)
    • Women 2.0% (2.2 million)

Etiology and Pathophysiology

  • Hyperuricemia results from urate overproduction, underexcretion, or often a combination of the two.
  • Gout occurs when MSU, a product of purine metabolism, precipitates out of solution and accumulates in joints and soft tissues.
  • Transient changes in urate solubility caused by local temperature decrease, trauma, or acidosis may lead to an acute gouty attack.
  • Urate crystals that precipitate trigger an immune response.
  • Left untreated, this crystal deposition leads to permanent joint damage and tophus formation.
  • Obesity predisposes to gout by promoting insulin resistance, which in turn reduces renal urate excretion resulting in hyperuricemia (4)[A].
  • Hypertension and renal disease reduce renal urate excretion due to glomerular arteriolar damage (4)[A].

  • Phosphoribosyl pyrophosphate (PRPP) deficiency and hypoxanthine guanine phosphoribosyltransferase (HGPRT) deficiency (Lesch-Nyhan syndrome) are inherited enzyme defects associated with overproduction of uric acid.
  • Polymorphisms in the URAT1 and SLC2A9 (GLUT9) renal transporters are hereditary enzyme defects resulting in primary underexcretion of uric acid.

Risk Factors

  • Age >40 years
  • Male gender
  • Increased purine uptake (meats and seafood)
  • Alcohol intake (especially beer)
  • Obesity (BMI >30)
  • Heart disease and congestive heart failure
  • Dyslipidemia
  • Hypertension and renal disease
  • Smoking
  • Diabetes mellitus
  • Diuretics raise SUA levels by increasing uric acid reabsorption and decreasing uric acid secretion in the kidneys (4)[A].
  • Urate-elevating medications:
    • Thiazide diuretics: ethambutol
    • Loop diuretics (less of a risk vs. thiazides)
    • Niacin
    • Calcineurin inhibitors (cyclosporine and tacrolimus)

General Prevention

  • Maintain optimal weight.
  • Regular exercise
  • Diet modification (purine-rich foods)
  • Reduce alcohol consumption (beer and liquor).
  • Smoking cessation
  • Maintain fluid intake and avoid dehydration.

Commonly Associated Conditions

  • Hypertension
  • Dyslipidemia
  • Nontraumatic joint disorders
  • Heart disease
  • Diabetes mellitus
  • Metabolic syndrome
  • Obesity (BMI >30)
  • Renal disease

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