Gout
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Basics
Description
- Gout is 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)[C] 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)[C].
- Management involves treating acute attacks and preventing recurrent disease by long-term reduction of serum uric acid levels through pharmacology and lifestyle adjustments.
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)
- Prevalence increases with age and serum uric acid levels.
Etiology and Pathophysiology
- Hyperuricemia results from uric acid 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 uric acid solubility caused by local temperature decrease, trauma, or acidosis may lead to an acute gouty attack.
- Uric acid crystals that precipitate can trigger an immune response and inflammation in the affected joint.
- 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 uric acid excretion resulting in hyperuricemia (4)[A].
- Hypertension and renal disease reduce renal uric acid excretion due to glomerular arteriolar damage (4)[A].
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 and renal disease
- Smoking
- Diabetes mellitus
- Diuretics raise serum uric acid 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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Basics
Description
- Gout is 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)[C] 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)[C].
- Management involves treating acute attacks and preventing recurrent disease by long-term reduction of serum uric acid levels through pharmacology and lifestyle adjustments.
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)
- Prevalence increases with age and serum uric acid levels.
Etiology and Pathophysiology
- Hyperuricemia results from uric acid 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 uric acid solubility caused by local temperature decrease, trauma, or acidosis may lead to an acute gouty attack.
- Uric acid crystals that precipitate can trigger an immune response and inflammation in the affected joint.
- 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 uric acid excretion resulting in hyperuricemia (4)[A].
- Hypertension and renal disease reduce renal uric acid excretion due to glomerular arteriolar damage (4)[A].
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 and renal disease
- Smoking
- Diabetes mellitus
- Diuretics raise serum uric acid 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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