Gout

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Basics

Description

  • An inflammatory arthritis 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
  • Acute gouty arthritis can affect ≥1 joint; the 1st metatarsophalangeal joint is most commonly involved at presentation (podagra).
  • Gout is related to a hyperuricemia (serum uric acid level >6.8 mg/dL) (1) and although hyperuricemia is necessary for the development of gout, it is not the only determining factor.
  • 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).

Epidemiology

Incidence
  • The incidence and prevalence of gout has been increasing over the past several decades (3).
  • Gout has a higher incidence in males than females.

Prevalence

Overall prevalence of gout is 3.9% (8.3 million people) 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 uric acid overproduction and/or renal underexcretion
  • Transient changes in uric acid solubility caused by local temperature decrease, trauma, or acidosis may also cause MSU to precipitate out of solution and to accumulate in joints and soft tissues, triggering an acute gouty attack.
  • Uric acid crystals are phagocytosed by macrophages inducing an inflammatory cascade (4).
  • Crystal deposition can lead to permanent joint damage and tophus formation.
  • Insulin resistance and renal disease can reduce renal uric acid excretion resulting in hyperuricemia (5).

Genetics
  • 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, renal disease
  • Smoking
  • Diabetes mellitus
  • Diuretics raise serum uric acid levels by increasing uric acid reabsorption and decreasing uric acid secretion in the kidneys (5).
  • Urate-elevating medications:
    • Thiazide diuretics: ethambutol
    • Loop diuretics (less of a risk vs. thiazides)
    • Niacin
  • Transplant-associated gout can happen in immunosuppressed solid organ transplant recipients on low-dose prednisolone and calcineurin inhibitors (cyclosporine and tacrolimus) because these medications increase uric acid (4).

General Prevention

  • Maintain optimal weight and perform regular exercise.
  • Diet modification
    • Avoid purine rich foods like red meat and shellfish.
    • Include certain food items shown to decrease serum uric acid (skim milk/yogurt, coffee, vitamin C (0.5 g/day) and cherries) (4).
  • 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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Basics

Description

  • An inflammatory arthritis 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
  • Acute gouty arthritis can affect ≥1 joint; the 1st metatarsophalangeal joint is most commonly involved at presentation (podagra).
  • Gout is related to a hyperuricemia (serum uric acid level >6.8 mg/dL) (1) and although hyperuricemia is necessary for the development of gout, it is not the only determining factor.
  • 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).

Epidemiology

Incidence
  • The incidence and prevalence of gout has been increasing over the past several decades (3).
  • Gout has a higher incidence in males than females.

Prevalence

Overall prevalence of gout is 3.9% (8.3 million people) 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 uric acid overproduction and/or renal underexcretion
  • Transient changes in uric acid solubility caused by local temperature decrease, trauma, or acidosis may also cause MSU to precipitate out of solution and to accumulate in joints and soft tissues, triggering an acute gouty attack.
  • Uric acid crystals are phagocytosed by macrophages inducing an inflammatory cascade (4).
  • Crystal deposition can lead to permanent joint damage and tophus formation.
  • Insulin resistance and renal disease can reduce renal uric acid excretion resulting in hyperuricemia (5).

Genetics
  • 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, renal disease
  • Smoking
  • Diabetes mellitus
  • Diuretics raise serum uric acid levels by increasing uric acid reabsorption and decreasing uric acid secretion in the kidneys (5).
  • Urate-elevating medications:
    • Thiazide diuretics: ethambutol
    • Loop diuretics (less of a risk vs. thiazides)
    • Niacin
  • Transplant-associated gout can happen in immunosuppressed solid organ transplant recipients on low-dose prednisolone and calcineurin inhibitors (cyclosporine and tacrolimus) because these medications increase uric acid (4).

General Prevention

  • Maintain optimal weight and perform regular exercise.
  • Diet modification
    • Avoid purine rich foods like red meat and shellfish.
    • Include certain food items shown to decrease serum uric acid (skim milk/yogurt, coffee, vitamin C (0.5 g/day) and cherries) (4).
  • 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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