• 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
  • Also 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
  • The long limb, foot, ankle, and knee is preferentially involved.
  • The involvement of the 1st metatarsophalangeal joint (podagra) is characteristic.
  • Gout flares can occur in the elbows, wrists and hand joints, but the upper limb involvement is usually only in patients with long-standing, poorly controlled disease. Axial skeleton involvement occurs occasionally.
  • 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).



  • Incidence ranges between 0.6 and 2.9 per 1,000 person-years.
  • Gout has a higher incidence in males than females.

Prevalence ranges between 0.68% and 3.9% in adults.

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.
  • 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
  • Excessive purine consumption from diet (alcohol [especially beer], red meat, seafood, sugar-sweetened beverages)
  • Metabolic syndrome/obesity (BMI >30)
  • Congestive heart failure
  • Chronic kidney disease (CKD)
  • Dyslipidemia, hypertension
  • Smoking
  • Dehydration (similar to diuretic effects)
  • Diabetes mellitus
  • 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
  • Metabolic syndrome, obesity (BMI >30)
  • Renal disease

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