Primary gout is a metabolic disease marked by urate deposits that cause painfully arthritic joints. Secondary gout develops during the course of another disease. Gout most commonly affects the foot, especially the great toe, ankle, or midfoot, but it may affect any joint. Gout follows an intermittent course, and patients may be completely free of symptoms for years between attacks. The prognosis is good with treatment. However, renal-tubular damage by aggregates of urate crystals may result in progressively poorer excretion of uric acid and chronic renal dysfunction.
Age Alert
Primary gout usually occurs in men after age 30 (95% of cases) and in postmenopausal women; secondary gout occurs in elderly people.
Causes
Primary gout
· Possibly genetic defect in purine metabolism, causing overproduction of uric acid (hyperuricemia), retention of uric acid, or both
Secondary gout
· Obesity, diabetes mellitus, hypertension, sickle cell anemia, renal disease
· Drug therapy, especially hydrochlorothiazide or pyrazinamide, which decrease excretion of urate (ionic form of uric acid)
Pathophysiology
When uric acid becomes supersaturated in blood and other body fluids, it crystallizes and forms tophi—accumulations of urate salts in connective tissue throughout the body. The presence of the crystals triggers an acute inflammatory response in which neutrophils begin to ingest the crystals. Tissue damage begins when the neutrophils release their lysosomes, which not only damage the tissues, but also perpetuate the inflammation.
Signs and symptoms
· Joint pain, redness, swelling
· Tophi in great toe, ankle, pinna of ear
· Elevated skin temperature
· Hypertension
· Chills
· Fever
Diagnostic test results
· Needle aspiration of synovial fluid shows needlelike intracellular crystals.
· X-rays of the articular cartilage and subchondral bone shows evidence of chronic gout.
· Serum analysis reveals elevated uric acid levels and elevated white blood cell count.
· Urine analysis shows elevated uric acid levels.
Treatment
Acute gout
· Immobilization and protection of the inflamed, painful joints; local application of heat or cold
· Increased fluid intake to prevent kidney stone formation
· Colchicine (oral or I.V.) to inhibit phagocytosis of uric acid crystals by neutrophils (doesn't affect uric acid level)
· Nonsteroidal anti-inflammatory drugs for pain and inflammation.
Chronic gout
· Allopurinol to suppress uric acid formation or control uric acid levels, preventing further attacks (use cautiously in renal failure)
· Colchicine to prevent recurrent acute attacks until uric acid level subsides (doesn't affect uric acid level)
· Uricosuric agents (probenecid or sulfinpyrazone) to promote uric acid excretion and inhibit uric acid accumulation (of limited value in patients with renal impairment)
· Avoidance of alcohol and purine-rich foods (shellfish, liver, sardines, anchovies) that increase urate levels.
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GOUT OF THE KNEE
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GOUT OF THE FOOT
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