Gout: Arthritis

by Food and Drug Administration (FDA)

Say the word "gout" and some people will think of a bloated king surveying the remains of a sumptuous feast, wine glass in hand, swollen foot propped on a pillow — looking for all the world like the dismal product of a grossly overindulgent life.

There are a couple of flaws in that conventional image. We know, for example, that gout doesn't afflict only the privileged classes and that women, too, are susceptible, though a lot less than men.

But still there's a good deal right with that picture. It correctly reflects that:

About 90 percent of people afflicted with gout are men over 40.

Obesity in general, and in particular excessive weight gain in men between ages 20 and 40, has been shown to increase the risk of gout. In fact, about half of all gout sufferers are overweight.

Alcohol abuse and so-called "binge" drinking are associated with gout, as is eating purine-rich foods such as brains, kidneys, liver, sardines, anchovies, and dried beans and peas.

In addition, careful scientific surveys have shown that occupational exposure to lead, the use of certain drugs to control high blood pressure, some surgical procedures, family history (possibly a genetic predisposition), and trauma are all linked to an increased risk of gout. Indeed, the prevalence of gout — the number of gout sufferers for each 100,000 people — is rising rapidly in the United States and other developed countries. Some authorities believe the increase is related to higher living standards.

Our fanciful image of a gouty Henry VIII (or other bloated monarch) can't show, however, the one common denominator that ties together this mixed bag of risk factors: failure of the metabolic process that controls the amount of uric acid in the blood. For most people, the process works just fine. But in some 1 million Americans, uric acid metabolism has gone seriously haywire. As a result, they suffer from gout.

And suffer they do. An Englishman, Thomas Sydenham, writing in the 17th century, left this unfortunately all-too-accurate description of a typical attack of gout:

The victim goes to bed in good health. About two o'clock in the morning, he is awakened by a severe pain in the great toe; more rarely in the heel, ankle, or instep. The pain is like that of a dislocation. [It] becomes more intense. So exquisite and lively meanwhile is the feeling of the part affected, that it cannot bear the weight of the bed-clothes nor the jar of a person walking in the room. The night is passed in torture.

A Crystal Culprit

In spite of the agony and havoc it can cause, uric acid is a normal constituent of the human body. Ordinarily about one-third of the uric acid in our system comes from food, especially foods like those noted earlier that are rich in purines. The rest we produce ourselves through ordinary metabolism.

The body converts purines to uric acid. The level of uric acid in the blood fluctuates in response to diet, fluid intake, overall health status, and other factors. Men normally have somewhat more uric acid than women do (although the difference begins to narrow after menopause), and in both sexes it tends to increase with advancing age.

Higher-than-normal amounts of uric acid in the blood, a condition called hyperuricemia, is quite common and only rarely warrants medical treatment. On the other hand, sustained hyperuricemia is the primary risk factor for gout. It's safe to say that, while not all people with hyperuricemia develop gout, virtually everyone with gout is hyperuricemic. It works this way:

At normal and even somewhat elevated levels, uric acid stays in solution in the blood. It moves through the circulation, gets filtered by the kidneys, and is excreted in the urine. When, however, blood uric acid levels rise above a certain concentration (which varies with temperature and blood acidity), it forms needle-like crystals that lodge in or around a joint.

In response to irritation caused by uric acid crystals, the skin covering the affected area rapidly becomes tight, inflamed, swollen, and red or purplish. These classical signs of inflammation, together with sudden and extreme pain (just as Thomas Sydenham described), strongly suggest an acute attack of gout. The diagnosis is confirmed by laboratory finding of uric acid crystals in fluid taken from the affected joint.

Why is the big toe the most common site for an initial gout attack? Perhaps because first, the extremities are a bit cooler than other parts of the body, and uric acid crystals form more readily at lower temperatures; and second, normal walking and standing subject the feet to considerable stress. Together, these factors might explain why the big toe, heel, instep, and Achilles tendon are among the places that gout attacks first. Other targets, especially in untreated patients who have recurrent attacks of gout, are the knee, elbow, wrist, fingers and, less often, the shoulder, pelvis, spine, and internal organs.

Gout is classified as a form of arthritis because it is initially and predominantly a disease of the joints. Other similar conditions exist; one called flpseudogoutfl is somewhat milder than true gout and is caused by calcium rather than uric acid crystals. Infection or trauma to the affected area can mimic gout and mislead both patients and health professionals. Accurate diagnosis is essential for appropriate treatment.

Without treatment, an initial acute attack of gout will run its painful course within several days or a few weeks, by which time all outward evidence of the disease disappears. The next acute attack — 50 or more percent of gout sufferers will have a second attack — may not occur for months or years. Subsequent attacks, however, are likely to be more frequent, more severe, and more destructive to joints and other tissue unless the problem is treated. Over time, uric acid crystals accumulate in the body, causing gritty, chalky deposits called tophi that are sometimes visible under the skin, particularly around joints and in the edges of the ears. Tophi may also form inside bone near the joints, in the kidneys, and in other organs and tissues, causing permanent damage. Advances in treatment, fortunately, have made this kind of chronic gout extremely rare.

About the Author

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