Known as "the disease of kings and the king of diseases", gout has been studied by physicians and has caused suffering in countless humans since at least the days of Hippocrates. Formerly a leading cause of painful and disabling chronic arthritis, gout has been all but conquered by advances in research. Unfortunately, many people with gout continue to suffer because knowledge of effective treatments has been slow to spread to patients and their physicians. The inflammatory process in gout is unrelated to infection. Rather, it is incited by the deposition in the joint of uric acid crystals usually due to an excess of uric acid in the bloodstream. This can be caused by an increase in production by the body, by under-elimination of uric acid by the kidneys or by increased intake of foods containing purines which are metabolized to uric acid in the body. Certain meats, seafood, dried peas and beans are particularly high in purines. Alcoholic beverages may also significantly increase uric acid levels and precipitate gout attacks. Gout is strongly associated with obesity, hypertension, hyperlipidemia, diabetes and dehydration. A familial pattern is observed in 5-15% of cases.

The four phases of gout include elevated uric acid levels without symptoms, acute gouty arthritis, multiple attacks with intervals between attacks, and chronic tophaceous (nodular masses of uric acid crystals (tophi) deposited in different soft tissue areas of the body) gout. Patients with asymptomatic hyperuricemia do not require treatment, but efforts should be made to lower their urate levels by encouraging them to make changes in diet or lifestyle.

Uric acid is a product of the chemical breakdown of the purine bases that compose the genetic material, DNA. As cells die and release DNA from their chromosomes, purines are converted into uric acid which is excreted in the urine and, to a lesser extent, the intestinal tract. The level of uric acid dissolved in the bloodstream is directly related to this delicate balance between uric acid production and excretion. The normal level is approximately 2-7mg/dl.

In most cases, an under-excretion of uric acid by the kidneys is responsible. Among the more common predisposing factors are kidney failure from any cause, diuretics, dehydration, hormonal diseases, alcohol consumption and using low doses of aspirin. About 10% of people with hyperuricemia are overproducers of uric acid. For some of these patients, diseases of the blood and bone marrow or inherited enzyme abnormalities can be implicated. Some are associated with metabolic alterations due to obesity, but for most the exact cause is indeterminable.

An attack of acute gouty arthritis is caused by the body's inflammatory reaction to intermittent deposition of needle-like uric acid crystals. When these crystals are ingested by white blood cells, the cells release enzymes that evoke inflammation. Attacks are usually marked by intermittent joint pain, swelling, redness and warmth. In some individuals, it is a progressive, crippling chronic disease that also damages the kidneys. Gout is from 5 to 20 times more common in men than in women and afflicts an estimated 840 out of 100,000 people. Gout and its complications occur more commonly and at a younger age in males.

Signs and Symptoms

• Rapid onset of severe joint pain, swelling and redness, often beginning at night after ingestion of alcoholic beverages, uric acid-elevating medications or high-purine foods.
• In 90% of initial episodes a single joint is involved - especially the joint at the base of the big toe. Gouty arthritis of the big toe afflicts some 90% of patients some time during the course of their disease. The foot, heel, ankle, knee, hands, wrists and elbows are some of the other joints that are frequently involved.
• Attacks tend to last a few days to a few weeks.
• Attacks respond well to medications.
• The frequency of subsequent attacks is variable. 5-10% of patients will never be bothered again, but most relapse within a year.