Hyperuricemia - Gout

Hyperuricemia - Gout

 

Gout is caused by crystalline deposition in tissues and joints.

Epidemiology

  • Prevalence – 2% in males >30, females >50
  • Age – unusual in patients <30 years
  • Sex – M>F

Risk Factors

  • Elevated uric acid
  • Obesity
  • Diuretic therapy
  • High purine diet
  • Alcohol use
  • Common triggers in patients with a history of gout – trauma, surgery, psoriasis, flare-ups, diuresis, starting or stopping allopurinol, infections

Pathophysiology

  • Uric acid is a byproduct of purine catabolism
  • Hyperuricemia is common in gout and is caused by altered purine metabolism
  • When solubility limits of uric acid or urate are exceeded, monosodium urate crystals deposit in joints, kidneys and soft tissue

Clinical Presentation

  • Usually single joint involvement
    • More common in lower extremities
    • Most common in first metatarsophalangeal (MTP) joint
  • Pain, erythema and swelling of joint
  • May cause fever, leukocytosis and/or cellulitis over joint
  • Chronic gout
    • Tophi depositions in soft tissue
    • Joint destruction and erosion

Diagnosis

  • Use criteria from the American College of Rheumatology (1977)
American College of Rheumatology Criteria for Gout
Gout may be diagnosed if one of the following criteria is present:
  • Monosodium urate crystals in synovial fluid present during an attack
  • Tophi confirmed with crystal examination
  • At least six of the following findings:
    • Asymmetric swelling within a joint on a radiograph
    • First metatarsophalangeal joint is tender or swollen (ie, podagra)
    • Hyperuricemia
    • Maximal inflammation developed within one day
    • Monoarthritis attack
    • More than one acute arthritis attack
    • Redness observed over joints
    • Subcortical cysts without erosions on a radiograph
    • Suspected tophi
    • Synovial fluid culture negative for organisms during an acute attack
    • Unilateral first metatarsophalangeal joint attack
    • Unilateral tarsal joint attack
(Adapted with permission from "Gout:  An Update," September 15, 2007, American Family Physician. ©2007 American Academy of Family Physicians. All Rights Reserved.)
  • Laboratory testing
    • Synovial fluid examination for cells and crystals; gold standard for diagnosis is presence of uric acid crystals in fluid
    • Serum uric acid; may be elevated; however, lack of elevation does not rule out gout
    • Complete blood count (CBC); modest leukocytosis may be present; may be helpful in discriminating septic joint from gout
    • Blood urea nitrogen (BUN) and creatinine to evaluate renal function

Differential Diagnosis

  • Other crystalline arthritis; eg, pseudogout
  • Reactive arthritis
  • Cellulitis
  • Septic arthritis

Treatment

  • Acute therapy includes NSAIDS, steroids and colchicine
  • Chronic therapy includes urate-lowering drugs