Gout has been defined as one of the most painful rheumatic diseases. It results when crystals of uric acid are deposited in connective tissue, joint spaces, or both, and is due to a disorder of uric acid metabolism. It is caused by either an overproduction, or under excretion of uric acid and is manifested by hyperuricemia, acute or chronic recurrent arthritis, and deposits of monosodium urates.

Uric acid serves no bodily purpose and is the end product of purine metabolism. Purines are the end product of the digestion of protein. Gout occurs only in humans where there is a pool of uric acid. Under normal conditions, uric acid is dissolved in the blood and passes through the kidney and into the urine for elimination. The amount of cumulated uric acid in men is about 1,200mg and in women, about 600mg. These values are increased several-fold in individuals with gout.

Population studies have shown that serum urate concentrations (and consequently risk of gout) correlates with age, male gender, blood pressure, body weight, and alcohol intake. Prevalence increases with age, especially in men.(1) In fact, men are affected by gout approximately 10 times more often than women. Although no genetic marker has been isolated for gout, the familial nature of gout strongly suggests an interaction between genetic and environmental factors.(2)

This abnormally high level of uric acid in the blood, called hyperuricemia, may result when a person eats too many high-purine foods such as liver, dried beans and peas, anchovies, and gravies. Hyperuricemia is not a disease and by itself is not dangerous.

The purines, from which uric acid is produced, come from three sources: diet, conversion of tissue nucleic acids, and synthesis of purine bases. The purines derived from these three sources enter a common metabolic pathway, leading to either the production of nucleic acid or uric acid. Uric acid may accumulate excessively if more is produce than is excreted.(2) Several enzyme systems regulate the metabolism of purines, and a partial deficiency of one or more enzymes may be responsible for the increase in uric acid in otherwise normal individuals. Uric acid may also be overproduced as a consequence of certain metabolic disorders.

About two thirds of uric acid is eliminated through the kidneys. The remaining one third is eliminated through the GI tract as a result of the digestive process. There are a number of conditions that affect either uric acid clearance or increase its production. Therefore, a person with these conditions has a greater risk of developing gout.

In the absence of pre-existing conditions or drugs that may affect uric acid levels, the physician needs to determine whether the patient is over-producing or under excreting uric acid. This may be accomplished by placing the patient on a purine-free diet for three to five days, then measuring the amount of uric acid excreted in the urine in 24 hours.