Although the underlying cause of primary gout remains unknown, in many patients the disease results from decreased renal excretion of uric acid. In other 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 another 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.

Potential complications include renal disorders such as renal calculi; circulatory problems, such as atherosclerotic disease, cardiovascular lesions, stroke, coronary thrombosis, and hypertension; and infection that develops with tophi rupture and nerve entrapment.

The patient’s history may reveal a sedentary lifestyle and a history of hypertension and renal calculi. He may report waking during the night with pain in his great toe or another part of the foot. The patient may complain that the initially moderate pain has grown so intense that he can’t bear the weight of bed sheets or the vibrations of a person walking across the room. He may also report accompanying chills and a mild fever.

Inspection typically reveals a swollen, dusky red or purple joint with limited movement. You may also notice tophi, especially in the outer ears, hands, and feet. Tophi may also form in the myocardium and kidneys, although this is rare. Renal involvement may impair renal function.

Late in the chronic stage of gout, the skin over the tophi may ulcerate and release a chalky white exudate or pus. Chronic inflammation and tophaceous deposits prompt secondary joint degeneration, which may be followed by erosions, deformity, and disability.

Palpation may reveal warmth over the joint and extreme tenderness. Assessment of vital signs may disclose fever and hypertension. If the patient has a fever, the possibility of occult infection must be investigated.

In an asymptomatic patient, 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 but 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, however, 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 the initial episodes. A migratory attack strikes various joints and the Achilles’ tendon sequentially and may be associated with olecranon bursitis.