Gout (also called metabolic arthritis) is a disease due to an inborn uric acid metabolism. In this condition sodium urate crystals are deposited on the particular cartilage of joints and in the particular tissue like tendons. This provokes an inflammatory reaction of these tissues. These deposits often increase in size and burst through the skin to form sinuses discharging a chalky white material.

Normally, the human bloodstream only carries small amounts of uric acid. However, if the blood has an elevated concentration of uric acid, uric acid crystals are deposited in the cartilage and tissue surrounding joints. Elevated blood levels of uric acid can also result in uric kidney stones.

The classic picture is of excruciating and sudden pain, swelling, redness, warmness and stiffness in the joint. Low-grade fever may also be present. The patient usually suffers from two sources of pain. The crystals inside the joint cause intense pain whenever the affected area is moved. The inflammation of the tissues around the joint also causes the skin to be swollen, tender and sore if it is even slightly touched. For example, a blanket draping over the affected area would cause extreme pain.

Gout usually attacks the big toe (approximately 75% of first attacks), however it can also 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 the small toes which have become immobile due to impact injury earlier in life, causing poor blood circulation that leads to gout.

Patients with longstanding hyperuricemia (see below) can have uric acid crystal deposits called tophi (singular: tophus) in other tissues e.g. the helix of the ear. Uric acid stones can form as one kind of kidney stone in some occasions.

The diagnosis is generally made on a clinical basis, although tests are required to confirm the disease.

Hyperuricemia is a common feature; however, urate levels are not always raised. Hyperuricemia is defined as a plasma urate (uric acid) level greater than 420 μmol/L (7.0 mg/dL) in males ( the level is around 380 μmol/L in females ); despite the above, high uric acid level does not necessarily mean a person will develop gout. Additionally, urate falls to within the normal range in up to two-thirds of cases. If goutis suspected, the serum urate should be repeated once the attack has subsided. Other blood tests commonly performed are full blood count, electrolytes, renal function and erythrocyte sedimentation rate (ESR). This serves mainly to exclude other causes of arthritis, most notably septic arthritis.

A definitive diagnosis of goutis from light microscopy of joint fluid aspirated from the joint (this test may be difficult to perform) to demonstrate intracellular monosodium urate crystals in synovial fluid polymorph nuclear leukocytes. The urate crystal is identified by strong negative bi-refringence under polarized microscopy, and their needle-like morphology. A trained observer does better in distinguishing them from other crystals.

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