Gout - also known as gouty arthritis - is a metabolic disease marked by monosodium urate deposits that cause red, swollen, and acutely painful joints. Gout can affect any joint but mostly affects those in the feet, especially the great toe, ankle, and midfoot.
Primary gout typically occurs in men over age 30 and in postmenopausal women who take diuretics. It follows an intermittent course that may leave patients symptom-free for years between attacks. Secondary gout occurs in older people.
In asymptomatic patients, serum urate levels rise but produce no symptoms. In symptom-producing gout, the first acute attack strikes suddenly and peaks quickly. Although it may involve only one or a few joints, this attack causes extreme pain. Mild, acute attacks usually subside quickly yet tend to recur at irregular intervals. Severe attacks may persist for days or weeks.
Intercritical periods are the symptom-free intervals between attacks. Most patients have a second attack between 6 months and 2 years after the first; in some patients, the second attack is delayed for 5 to 10 years. Delayed attacks, which may be polyarticular, are more common in untreated patients. These attacks tend to last longer and produce more symptoms than initial episodes. A migratory attack strikes various joints and the Achilles tendon sequentially and may be associated with olecranon bursitis.
Eventually, chronic polyarticular gout sets in. This final, unremitting stage of the disease (also known as tophaceous gout) is marked by persistent painful polyarthritis. An increased concentration of uric acid leads to urate deposits - called tophi - in cartilage, synovial membranes, tendons, and soft tissue.
Tophi form in the fingers, hands, knees, feet, ulnar sides of the forearms, pinna of the ear, Achilles tendon and, rarely, in such internal organs as the kidneys and myocardium. Renal involvement may adversely affect renal function.
Patients who receive treatment for gout have a good prognosis.
Although the underlying cause of primary gout is unknown, in many patients the disease results from decreased renal excretion of uric acid. In a few patients, gout is linked to a genetic defect in purine metabolism that causes overproduction of uric acid (hyperuricemia).
Secondary gout develops during the course of an other disease, such as obesity, diabetes mellitus, hypertension, polycythemia, leukemia, myeloma, sickle cell anemia, and renal disease. Secondary gout can also follow treatment with such drugs as hydrochlorothiazide or pyrazinamide.
Signs and Symptoms
The signs and symptoms of gout are almost always acute, occurring suddenly — often at night — and without warning. They include:
Needle aspiration of synovial fluid (arthrocentesis) or of tophaceous material for examination under polarized light microscopy reveals needlelike intracellular crystals of sodium urate. Monosodium urate monohydrate crystals in synovial fluid taken from an inflamed joint or tophus establish the diagnosis. If test results identify calcium pyrophosphate crystals, the patient probably has pseudogout, a disease similar to gout.
Serum uric acid levels may be normal, but the higher the level (especially when it's greater than 10 mg/dl), the more likely a gout attack.
Urine uric acid levels are high in about 20% of gout patients.
X-ray studies initially produce normal results but in chronic gout, X-ray findings show damage to the articular cartilage and subchondral bone. Outward displacement of the overhanging margin from the bone contour characterizes gout.
Correct management has three goals:
Treatment for an acute attack consists of bed rest: immobilization and protection of the inflamed, painful joints; and local application of cold. Analgesics such as acetaminophen relieve the pain associated with mild attacks. Acute inflammation requires nonsteroidal anti-inflammatory drugs or intramuscular corticotropin. Colchicine, oral or parenteral, or intra-articular corticosteroids are occasionally necessary to treat acute attacks.
Treatment for chronic gout involves decreasing the serum uric acid level to less than 6.5 mg/dl. This may be accomplished with various medications after a 24-hour urinalysis is used to determine whether the patient excretes too much or too little uric acid. If the patient overexcretes uric acid, he may be given allopurinol (in reduced doses if he has decreased renal function). If he underexcretes uric acid, he may be treated with probenecid or sulfinpyrazone (if he has no history of renal calculi). Taken once or twice daily, colchicine effectively prevents acute gout attacks, but it doesn't affect uric acid levels.
Adjunctive therapy emphasizes avoidance of alcohol (especially beer and wine) and sparing use of purine-rich foods, such as anchovies, liver, sardines, kidneys, sweetbreads, and lentils. Obese patients should begin a weight loss program because weight reduction decreases uric acid levels and eases stress on painful joints.
PreventionThere's no sure way to prevent initial or subsequent attacks of gout, but if you already have gout, your doctor may prescribe certain drugs to reduce the risk or lessen the severity of future episodes. These drugs include allopurinol (Zyloprim, Aloprim) and probenecid. Taken daily, they slow the rate at which uric acid is produced and speed its elimination from your body. In general, keeping uric acid levels within a normal range is the long-term key to preventing gout.
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