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.

Untreated cases may develop chronic gouty arthritis in which multiple joints are involved by a long-term destructive process. Tophi, small nodules consisting of uric acid and inflammatory tissues, may be seen on the ear cartilage and along tendons.

Diagnosis
Since several other kinds of arthritis can mimic a gout attack, and since treatment is specific to gout, proper diagnosis is essential. The definitive diagnosis of gout is dependent on finding uric acid crystals in the joint fluid during an acute attack. However, uric acid levels in the blood alone are often misleading and may be transiently normal or even low. Additionally, uric acid levels are often elevated in individuals without gout. While sudden swelling and pain in a joint, especially the big toe, suggests the diagnosis of gout, many other arthritic conditions and some infections present themselves in a similar manner. Gout is the diagnosis if gout medications resolve the symptoms. Uric acid levels are usually elevated around an attack, and reduced when treated successfully.

Gout in women occurs nearly always after menopause. Women develop gout at an older age than men and have twice the prevalence of hypertension, renal insufficiency and exposure to diuretics. The onset of gout before age 30 in men or before menopause in women is unusual and raises concern about an associated inherited enzyme defect or renal disease.

Comparison with 220 male patients with gout showed that female patients developed gout significantly later, more frequently had associated diseases, and more often were receiving diuretics, whereas significantly more male than female patients had alcoholism. The articular features of gout were similar in both groups. However, the prevalence of tophi was higher and its localization different in female than in male patients. Female patients with gout had a higher mean serum urate concentration and a lower mean urinary uric acid excretion than did male patients with gout. These differences were significant and independent of the effects of age, renal insufficiency, alcoholism, or previous diuretic intake. Renal underexcretion of uric acid appears to be more severe in female than in male patients with gout. [Arch Int Med Vol. 151 No. 4, April 1, 1991]

Treatment
Aside from those mentioned below, also avoid purine-rich foods: anchovies, asparagus, crab, fish roe, herring, kidney, liver, meat gravies and broth, mushrooms, mussels, peas & beans, and sardines.