Gout (also called metabolic arthritis) is a disease created by a buildup of uric acid. In this condition, monosodium urate or uric acid crystals are deposited on the articular cartilage of joints, tendons and surrounding tissues due to elevated concentrations of uric acid in the bloodstream. This provokes an inflammatory reaction of these tissues.

Signs and symptoms

Gout usually attacks the big toe (approximately 75 percent of first attacks); however, it also can affect other joints such as the ankle, heel, instep, knee, wrist, elbow, fingers, and spine. In some cases, the condition may appear in the joints of small toes that have become immobile due to impact injury earlier in life, causing poor blood circulation that leads to gout.

Patients with long-standing hyperuricemia (see below) can have uric acid crystal deposits called tophi (singular: tophus) in other tissues such as the helix of the ear. Elevated levels of uric acid in the urine can lead to uric acid crystals precipitating in the kidneys or bladder, forming uric acid kidney stones.

Diagnosis

Clinically, gout can be hard to distinguish from several other conditions, including chondrocalcinosis. Chondrocalcinosis is a very similar disease, caused by deposition of calcium pyrophosphate rather than uric acid.

Hyperuricemia is a common feature of gout, so its presence supports a diagnosis of gout. However, gout can occur without hyperuricemia.

Hyperuricemia is defined as a plasma urate (uric acid) level greater than 420 μmol/L (7.0 mg/dL) in males, or 380 μmol/L in females. However, a high uric acid level does not necessarily mean a person will develop gout. Urate is within the normal range in up to two-thirds of cases.

If gout is suspected, the serum urate test should be repeated once the attack has subsided. Other blood tests commonly performed are full blood count, electrolytes, renal function, thyroid function tests and erythrocyte sedimentation rate (ESR). This helps to exclude other causes of arthritis, most notably septic arthritis, and to investigate any underlying cause for the hyperuricaemia.

A definitive diagnosis of gout is from light microscopy of fluid aspirated from the joints (this test may be difficult to perform) to demonstrate intracellular monosodium urate crystals in synovial fluid polymorphonuclear leukocytes. The urate crystal is identified by strong negative birefringence under polarised microscopy and its needle-like morphology. A trained observer does better in distinguishing them from other crystals.

Pathogenesis

Gout occurs when mono-sodium urate crystals form on the articular cartilage of joints, on tendons, and in the surrounding tissues. Purine metabolism gives rise to uric acid, which is normally excreted in the urine. Uric acid is likely to form into crystals when there is a hyperuricemia, although it is 10 times more common without clinical gout than with it.