What Causes Gout?

Gout is a metabolic disease characterized by the accumulation of excessive uric acid in the blood. Gout is associated with recurrent attacks of acute arthritis and in some cases with uric acid stones in the kidneys and large uric acid deposits in and around the joints. The most common form, primary gout, is inherited, but what is called secondary gout may be acquired as a complication of another disease. Although the gouty trait is probably as common in women as in men, the symptoms appear oftener in men.

Causes and Pathology of Gout

Uric acid is an end product of the metabolism of purines, a group of organic compounds found in nucleic acids. In the human body, uric acid is derived chiefly from the biosynthesis of purines from amino acids and in part from the degradation of ingested nucleic acids. Because the human body lacks an enzyme to break down uric acid, the acid is excreted, chiefly by the kidneys. Thus an excessive accumulation of uric acid (hyperuricemia) may result from an acceleration of purine biosynthesis (the basic cause of primary gout), an excessive dietary intake of nucleic acids or proteins, or an inadequate excretion of uric acid by the kidneys.

Uric acid is not very soluble; when it occurs in large amounts in the blood, it tends to precipitate out into the joints, initiating acute attacks of arthritis. In severe cases, uric acid forms large chalky deposits, called tophi, which may impair movement at the joints. High concentrations of uric acid in the urine may lead to the formation of uric acid stones in the kidneys.

Symptoms of Gout

In primary gout, hyperuricemia develops at puberty in males and much, later and to a lesser extent in females. In most cases, however, it does not produce any symptoms until middle age. Onset then is sudden, typically as an extremely painful acute arthritis involving the great toe or another area of the foot. The attacks recur and over several years spread to both feet, the knees, elbows, and hands. As the disease progresses, there is persistent joint stiffness and swelling. Tophi form in severe cases, producing chronic gouty arthritis.

Uric acid stones or gravel may produce some symptoms, but these usually occur later in the course of the disease. Kidney function may be impaired, but this is more often caused by associated hypertension (high blood pressure), vascular diseases, infection, or aging.

Treatment of Gout

Colchicine is the drug most often used to terminate acute attacks of gouty arthritis, but phenylbutazone and oxyphenbutazone are also effective, as is ACTH in treating unusually severe attacks. To prevent recurrent acute gouty arthritis colchicine may be given in low doses. Uric acid levels in the blood and urine can be lowered by allopurinol, a drug that reduces uric acid formation. Uricosuric drugs, such as probenecid and sulfinpyrazone, also decreases the blood level of uric acid, but they function by increasing uric acid excretion in the urine. The formation of uric acid kidney stones can be minimized by a high fluid intake, alkalizing salts, and allopurinol, and both allopUrinol and uricosuric drugs reduce tophi and prevent new ones from forming. The patient's diet is kept low in purine-rich foods, and in, more severe cases the diet may be limited in all proteins.

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