Hyperuricemia - Gout

Diagnosis

Indications for Testing

• Swollen, erythematous joint(s)

Criteria for Diagnosis

• Diagnosis based on criteria from the American College of Rheumatology (Wallace, 1977); however, recent guidelines from the European League Against Rheumatism (EULAR) (Zhang, 2006) may be more applicable

Laboratory Testing

• Synovial fluid examination
  • Essential if chief differential diagnosis is between gout and septic joint
  • Cell count – may see predominantly polymorphonuclear cells; absolute count usually <50,000
  • Crystals – gold standard for diagnosis is presence of uric acid crystals in fluid
  • Gram stain – rule out septic arthritis
  • Culture – rule out septic arthritis
• Serum uric acid – may be elevated; however, lack of elevation does not rule out gout
  • Elevated in only 50% of those with acute attacks
  • Best time to measure may be 2 weeks after a flare-up
  • If performed during acute attack and normal, repeat when joint normalizes
• CBC – modest leukocytosis may be present
  • May be helpful in discriminating septic joint from gout if significant leukocytosis is present
• BUN and creatinine – evaluate renal function
  • Drugs used to treat acute and chronic gout may affect renal function

Imaging Studies

•  Acute gout – not useful
• Chronic gout – may demonstrate tophi

Differential Diagnosis

• Calcium pyrophosphate dihydrate disease
• Reactive arthritis (eg, Campylobacter jejuni)
• Septic arthritis
• Cellulitis
• Osteoarthritis
• Rheumatoid arthritis
• Internal ligaments derangement
• Hemarthropathy

Monitoring

Clinical Background

Gout is a type of arthritis caused by hyperuricemia (high serum uric acid) leading to deposits of urate crystals in tissues and joints.

Epidemiology

• Prevalence – 2% in males >30 years and females >50 years
• Age – unusual <30 years
• Sex – M>F; 4-9:1

Risk Factors

• Hyperuricemia
• Obesity
• Diuretic therapy
• High purine diet
• Alcohol use
• Common triggers in patients with a history of gout – trauma, surgery, psoriasis exacerbations, diuresis, starting or stopping allopurinol, infections

Pathophysiology

• Uric acid – final byproduct of purine metabolism; poorly soluble
• Hyperuricemia (common in gout) – caused by altered purine metabolism leading to increased levels of urate
  • Decreased excretion, increased production, or a combination of factors may be involved
  • When solubility limits exceeded, monosodium urate crystals can deposit in joints, kidneys, and soft tissues

Clinical Presentation

• Usually involves single joint
  • More common in lower extremities – typical joints include first metatarsophalangeal, midfoot, ankle
• Pain, erythema, and swelling of joint – abrupt onset; usually takes <24 hours to go from no pain to maximum pain
• May cause fever, leukocytosis, and/or cellulitis over joint
• Chronic gout
  • Tophi – nodular mass of urate crystals in soft tissue
  • Joint erosion and destruction
  • More susceptible to septic joints – knee and olecranon bursa common

Treatment

• Acute therapy – includes nonsteroidal anti-inflammatory drugs (NSAIDS), steroids, and colchicine
• Chronic therapy – includes urate-lowering drugs, dietary adjustment, adequate fluid intake

Indications for Laboratory Testing

• Tests generally appear in the order most useful for common clinical situations
• Click on number for test-specific information in the ARUP Laboratory Test Directory

Click the plus sign to expand the table of additional tests.

Test Name and Number	Comments
Uric Acid, Urine 0020481 Method: Quantitative Spectrophotometry
Uric Acid, Body Fluid 0020513 Method: Quantitative Spectrophotometry