– A primary or secondary recurrent, acute arthritis of the peripheral joints, particularly the great toe.
Causes and Incidence
The precise causal mechanism in gout is unknown. However, a host of factors act as precursors to overproduction or undersecretion of uric acid, including genetic factors (hyperactivity of hypoxanthine guanine phosphoribosyl transferase, superactivity of phosphoribosyl pyrophosphate, fructose intolerance); environmental factors (ethanol abuse, diuretic use, severe muscle exertion); underlying disease processes (diabetes mellitus, polycythemia, hypertension, renal disease, leukemia, sickle cell anemia); and the evolutionary absence of the enzyme uri-case. Gout occurs most often in men. The incidence in the United States is about 14 per 1,000 in men and 6 per 1,000 in women. Gout is rare in women before menopause. The incidence of gout is increasing in developed countries.
Some factor triggers an overproduction or undersecretion of uric acid. The plasma becomes supersaturated with uric acid, and a crystal urate precipitate is formed and deposited in avascular tissues (e.g., cartilage, tendons, and ligaments of peripheral joints) and in cooler tissues (e.g., the ears). Through some undefined mechanism, the crystals are released at various times, causing an acute inflammatory reaction in the joint with extension to the periarticular tissues. Repeated acute attacks lead to chronic arthritis and deformed joints.
Acute pain, redness, swelling, tenderness, and heat at the affected joint are typical presenting features. Fever, chills, and malaise may also be present. Limited motion is present in the affected joint or joints.
Complications include infection of ruptured deposits, renal involvement with formation of renal calculi, and secondary degenerative arthritis.
A tentative diagnosis is made by clinical examination and elevated serum uric acid levels and confirmed with needle aspiration of synovial fluid, which is positive for urate crystals.
Treatment is aimed at terminating the acute attack and preventing future attacks by lowering uric acid levels and resolving existing deposits.
Removal of large crystal deposits (tophi).
Colchicine for long-term prophylaxis and to reduce inflammation in acute attack; nonsteroidal antiinflammatory agents to reduce inflammation in established gout; antihyperuricemic drugs for those with frequent attacks or chronic disease to reduce uric acid levels or increase excretion of uric acid (lifelong treatment); sodium bicarbonate to alkalize urine in patients who form calculi.
Rest of joint; avoidance of alcohol and purinerich foods; weight reduction if necessary to reduce wear and tear on joints; increased fluid intake; instruction in long-term use of medications and their side effects.