• An inflammatory arthritis leading to an acutely red, hot, swollen joint, which can progress to a chronic tophaceous joint that is associated with pain, nodule formation, and cutaneous compromise
  • Characterized by deposition of monosodium urate (MSU) crystals in joints and soft tissues, resulting in acute and chronic arthritis, soft-tissue masses called tophi, urate nephropathy, and uric acid nephrolithiasis
  • The long limb, foot, ankle, and knee are preferentially involved, with the 1st metatarsophalangeal joint (podagra) characteristically affected.
  • Flares are usually monoarticular. Polyarticular flares can be associated with pronounced systemic symptoms, including fever, chills, and delirium.
  • Gout is related to a hyperuricemia (serum uric acid level >6.8 mg/dL).



  • Ranges between 0.68% and 3.9% in adults
  • Gout has a higher incidence in males than females.

Etiology and Pathophysiology

Four pathophysiologic stages:

  • Development of hyperuricemia (from uric acid overproduction and/or renal underexcretion)
  • Deposition of MSU crystals (Changes in uric acid solubility caused by local temperature decrease, trauma, or acidosis may precipitate out of solution and accumulate as crystals in joints and soft tissues.)
  • Clinical presentation of gout flares due to an acute inflammatory response to deposited crystals
  • Clinical presentation of advanced disease characterized by tophi and joint damage

Consider HLA-B*5801 mutation genotyping for people in Asian origin.

Risk Factors

  • Age >40 years
  • Excessive purine consumption from diet (alcohol [especially beer], red meat, seafood, sugar-sweetened beverages)
  • Diabetes mellitus, metabolic syndrome, obesity
  • Congestive heart failure, chronic kidney disease (CKD), dyslipidemia, hypertension
  • Smoking
  • Urate-elevating medications: thiazide diuretics, loop diuretics (less of a risk vs. thiazides), niacin, aspirin
  • Transplant-associated gout can happen in immunosuppressed solid organ transplant recipients on low-dose prednisolone and calcineurin inhibitors (cyclosporine and tacrolimus) as these medications increase uric acid (1).
  • Hyperuricemia from rapid cell turnover/tumor lysis syndrome (e.g. hemolysis, chemotherapy)

General Prevention

  • Diet modification: Avoid purine-rich foods like red meat and shellfish. Reduce alcohol consumption (beer and liquor).
  • Maintain fluid intake and avoid dehydration.

Commonly Associated Conditions

  • Nontraumatic joint disorders
  • Renal disease

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