Gout is diagnosed mainly in males. Males have higher levels of serum uric acid than women until menopause because estrogen has a uricosuric effect. Although the genetic factors underlying hyperuricemia are presumably present at birth, the disorder produces no clinical signs or symptoms until the hyperuricemia has persisted for years. Clinical manifestations of gout usually appear in middle age in males (age 30 to 50 years) and later in females (see Plate 5-38). Patients with severe hyperuricemia, and some others for unexplained reasons, may develop gout attacks at a younger age.
Pathogenesis. The excessive concentration of uric acid in the blood is responsible for gouty arthritis. Some of the factors contributing to hyperuricemia (in addition to the renal inefficiency in excreting uric acid) include obesity, meat and seafood ingestion, beer and liquor use, and low dairy intake. Factors that can induce an acute attack of gouty arthritis include sudden increase or decrease in the level of (chronically elevated) serum uric acid, surgery, fasting, alcohol ingestion, and joint trauma. The mechanisms of crystal nucleation are not fully understood, but formed urate crystals are phagocytosed by synovial cells and neutrophils, resulting in the release of proinflammatory mediators, including IL-1.
Clinical Manifestations. The first clinical evidence of gout is usually acute arthritis in one or a few peripheral joints. A fulminant synovitis begins abruptly, typically during the night, frequently involving the first metatarsophalangeal joint, midfoot, or other lower extremity joint. The acute involvement of the great toe is known as podagra. The affected joint becomes very swollen, red, hot, tender, and excruciatingly painful (see Plate 5-38). Fever and leukocytosis may accompany the attack, and the ESR may be increased. Hence, acute gout cannot be reliably distinguished from acute septic arthritis. If untreated, acute monarticular gouty arthritis lasts 3 or 4 days; if several joints are severely inflamed, the attack may persist 2 or 3 weeks. The patient may remain asymptomatic until the next attack. After several attacks the gouty episodes tend to be more severe, last longer, and involve several additional joints, tendons, or bursae.
After several years of persistent hyperuricemia, deposits of monosodium urate known as tophi form in joint structures (and other tissues). Tophi are the hallmark of chronic gout, occurring in a significant minority of patients. If tophi are periarticular, the affected joints show irregular knobby swelling and signs of chronic inflammation. Joint motion is limited and painful, deformities develop, and sinuses may form at the swollen joint, from which a chalky exudate drains from the underlying urate deposits. Tophi often form in extra-articular structures as well, especially in the extensor tendons of the fingers and toes, the olecranon and infrapatellar bursae, the calcaneal tendon, the cartilage of the external ear, and the parenchyma of the kidney (see Plate 5-39).
Gout in women may initially involve several joints and may include the distal interphalangeal finger joints. This latter pattern of acutely inflamed Heberden’s nodes mimics and is often misdiagnosed as inflammatory osteoarthritis. Thiazide diuretics may predispose to this form of gouty arthritis.
Radiographs show marked destruction of bone and cartilage and “punched-out” areas in the bone with adjacent bone proliferation stimulated by the urate deposits (see Plate 5-38).
Diagnosis. Diagnosis is problematic only in the first or early attacks of acute arthritis. Gout should always be suspected when acute synovitis develops in a few small joints, especially in the great toe of an older person, particularly a male. A history of gout in close relatives and the finding of hyperuricemia support the diagnosis but are certainly NOT definitive. Additional evidence is a quick and complete resolution of the synovitis after oral colchicine or NSAIDs. The presence of urate crystals in synovial fluid taken from the inflamed joint confirms the diagnosis and is the gold standard for the diagnosis, which should ideally be achieved before initiating lifetime therapy designed to lower serum uric acid levels and reduce attacks.
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