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- Gout refers to a group of disorders related to hyperuricemia. Although hyperuricemia is necessary for the development of gout, it is not the only determining factor.
- Characterized by deposition of monosodium urate (MSU) crystals in tissue, resulting in acute and chronic arthritis, soft-tissue masses called tophi, urate nephropathy, and uric acid nephrolithiasis
- Natural history involves 4 stages:
- Asymptomatic hyperuricemia
- Acute arthritis
- Intercritical gout
- Chronic tophaceous gout
- Acute gouty arthritis can affect ≥1 joints. The 1st metatarsophalangeal joint is most commonly involved at presentation (podagra).
- Other common sites include midtarsal, ankle, and knee joints.
- After an initial attack, patients can be attack-free for months or even years. Some patients will develop more frequent attacks or go on to develop chronic tophaceous gout.
- Management involves treating acute attacks and preventing recurrent disease by long-term reduction of serum uric acid (SUA) levels through pharmacology and lifestyle adjustments.
- Presentation may lack acute pain, swelling, and inflammation
- More common in women >80
- Can present with tophi and finger joint pain
- Commonly triggered by diuretic use, especially in women
Often due to an inborn error of metabolism or other disease
Increases with age, especially in women
6:1,000 population for men; 1:1,000 population for women
- Male gender (age <65)
- Increasing age
- Ethanol ingestion (beer and liquor > wine)
- Obesity (50%)
- Hypertension (HTN) (50%)
- Metabolic syndrome
- Medications: Diuretics induce 20% of secondary gout
- Diet: High-purine animal-origin foods (e.g., meats and seafood)
- Family history
- Keto- and lactic acidosis
- Surgery or trauma
- Renal impairment
- Parathyroid disease
- Hyperlipidemia types II, IV, V
- Paget disease
- Hyperproliferative skin disorders (psoriasis)
- Lymphoproliferative disorders, hemolytic anemia, hemoglobinopathies, pernicious anemia
- Glycogen storage diseases
- Primary gout runs in families and follows multifactorial inheritance.
- Phosphoribosyl pyrophosphate (PRPP) deficiency and hypoxanthine-guanine-phosphoribosyltransferase (HGPRT) deficiency are inherited enzyme defects associated with a primary overproduction of uric acid.
- URAT1 (urate transporter) deficiency is also a hereditary enzyme defect resulting in primary underexcretion of uric acid.
- Treat underlying cardiovascular risk factors.
- Maintain weight at optimal BMI of <26.
- Regular exercise
- Diet modification
- Reduce alcohol consumption (beer and liquor).
- Maintain fluid intake and avoid dehydration.
- Humans have a narrow window for urate to remain soluble before crystal precipitation due to lack of uricase enzyme.
- Precipitation of MSU crystals can occur in the synovium, joint cartilage, kidneys, and soft tissue.
- MSU crystals can initiate and sustain an inflammatory response, leading to an acute gout attack.
- Chronic and untreated hyperuricemia lead to tophi formation in and around the joint space.
- Tophi contribute to chronic synovitis, often resulting in joint damage.
- Increased uric acid production
- Renal underexcretion of uric acid
- Enzyme defects
- Increased purine turnover
- Dehydration or starvation
Commonly Associated Conditions
- Metabolic syndrome (obesity, hyperglycemia, hyperlipidemia, HTN)
- Myeloproliferative disorders
- Lymphoproliferative disorders
- Lesch-Nyhan syndrome