Gout and crystal arthritis

Only a minority of people with elevated blood levels of uric acid develop gout. For this reason, people who have never had an attack of gout should not be prescribed medication to reduce uric acid levels, as it may cause undesirable consequences.

Elevated uric acid levels in people who are predisposed to developing gout may be caused by:

• Increased production or decreased renal elimination;
• excessive consumption of substances such as red meat and game, from which uric acid is derived (a rarer cause).

Excess uric acid circulates in the blood (hyperuricemia) and is deposited as crystals in various tissues, including the kidneys (gouty nephropathy) and joints (gouty arthritis). Uric acid is excreted in the urine; if it is present in excessive concentrations, it can lead to stone formation.

The cause of calcium deposition in other crystalline arthritis has not been established.

This pathology is characterized by very intense and sudden signs, such as:

• rapid swelling;
• redness;
• fever;
• pain in the affected joint.

Usually the first joint of the toe (tarsometatarsal joint) is the first to be involved. Other joints may be the wrists, finger joints, knees, or ankles.

If the inflammation is left untreated, it persists for a few days or weeks and then goes away. After the first attack, if the uric acid level in the blood does not decrease, gout often flares up again in the same or other joints. A granulomatous inflammatory reaction (tophus) forms around the deposits of uric acid crystals, which corrodes the bone of the joint (chronic tophus gout).

Arthropathies with calcium crystal deposition cause calcification of periarthritic tissues (calcified periarthritis), calcium deposition in articular cartilage (chondrocalcinosis) and acute arthritis (pseudopodagra).