Pain-Free Living

The Good News and Bad News on Gout

By Kurt Ullman, RN

Gout is a type of inflammatory arthritis caused by crystals of uric acid (UA) that accumulate in the joints. Gout has been around as long as humans have been writing about health—it was first described in Egypt nearly 4,000 years ago.

“We have chemicals within our bodies called purines that are very important for many cellular functions, from energy generation to making DNA,” says Bruce N. Cronstein, MD, professor of medicine at the New York University School of Medicine in New York City. “In humans, these purines are metabolized to UA, which is then excreted mainly through the kidneys.”

According to the Centers for Disease Control and Prevention (CDC), gout affects approximately three million people in the United States each year, and overall, more than five million American adults have had gout at least once. Some indicators suggest that the number may be rising.

“Many researchers, including myself, think gout is on the rise,” says Angelo L. Gaffo, MD, assistant professor of medicine in the Division of Rheumatology at the University of Alabama at Birmingham and a rheumatologist at the Birmingham Veteran’s Administration. “The best research suggests that five million or so people in the United States have gout, and when you look at large databases from America and Europe, the numbers seem to be rising.”

UA crystals
Since UA can only minimally dissolve in water, it tends to crystalize into a salt (monosodium urate) when not eliminated through urination. When either too much UA is manufactured as purines are metabolized (the case in 10% of people with gout), or too little is excreted by the kidneys (90%), the crystals can deposit in the joints and other tissues. This causes the inflammation, swelling, and pain that are the hallmarks of gout.

“The joint becomes swollen, warm, and red,” says Emilio B. Gonzalez, MD, professor and director of the Division of Rheumatology at the University of Texas Medical Branch in Galveston. “But what usually brings a patient to my office is the intense pain.”

For most people, the first joints affected are those in the big toe. (This phenomenon even has its own name, podagra.) Other joints and areas around them also can be affected, including ankles, heels, the insteps of the feet, wrists, fingers, and elbows.

In addition to the joints, deposits of UA known as tophi can be seen as lumps under the skin around the joints and rim of the ear. Finally, UA crystals can collect in the kidneys and produce stones that can damage them.

Stages of gout
There are four stages of gout.

• Asymptomatic gout. In this stage, you have too much UA in the blood (also called hyperuricemia) but no other symptoms. Because of this, you seldom need the attention of a doctor, and no is treatment needed.

• Acute gout or “flares.” At this point, deposits of UA crystals have accumulated in the joint spaces, which results in a very sudden onset of intense pain and swelling. The joints may be warm to the touch and very tender—many people complain that even just having sheets touch their big toe hurts. Untreated, these attacks usually fade within 10 days, and it may be months or even years until the next one. However, attacks usually come closer together over time if left untreated.

• Interval or intercritical gout. This is the “quiet time” between acute attacks. You have no symptoms.

• Chronic or tophaceous gout. This is the most disabling stage and takes a long time to develop. If you reach this stage, you probably will have permanent damage to the joints, and possibly to your kidneys from stone formation. With proper treatment, few people get to this stage.

You are more likely to develop gout when you have high levels of uric acid in your body. That raises the question of what factors increase the UA level.

Risk factors
Two important factors are age and sex. Your likelihood of having gout is much higher throughout your life if you are male. Estrogen appears to be protective against hyperuricemia, so gout in women is very rare until menopause. Postmenopausal women see an increase in gout, although they don’t catch up with men.

Age itself is thought to increase the likelihood of gout. Even in very healthy people, the kidneys become less efficient in excreting uric acid as a person ages.

Diet can be important. One high in meat, seafood, and beverages containing high levels of fructose will increase the uric acid in your body. Beer and liquor consumption can also up your chances of developing gout. Wine does not seem have an impact.

Closely related to diet is obesity. When you’re overweight, your body produces more UA and may overwhelm the kidneys’ ability to filter it out. For reasons not completely understood, very rapid weight loss may also trigger gout flares.

Some medical conditions make it more likely you’ll develop gout. Obviously, anything that limits the kidney’s ability to get rid of uric acid will cause problems; others include high blood pressure, diabetes, and heart diseases. Surgery and trauma are common triggers of gout attacks in people with hyperuricemia.

Medications have been linked to additional risk of gout. Thiazide diuretics, or “water pills” that are used to treat high blood pressure, and low-dose aspirin to prevent heart attacks or strokes can add to your risk for gout. Some transplant anti-rejection medications are implicated in increased UA levels.

Family history can be a factor. If members of your family have had gout, you’re more likely to develop it. However, while some cases may be hereditary (especially if your family comes from certain areas of southeast Asia), much of the genetic link is not well understood.

“If you have gout and a strong family history of it, my first reaction is to tell you that genetics could be playing an important role,” says Dr. Gaffo. “However, we really still don’t understand which genes contribute the most to having UA and gout. It is also hard to tease out how much is related to genetics versus a shared environment. For instance, children and parents might share similar dietary factors.”

Diagnosis is key
Sometimes discerning gout as a condition separate from other kinds of arthritis is difficult. Proper diagnosis is a key issue.

Your doctor will start looking for gout when you have joint swelling and intense pain in one or two joints, followed by pain-free times between attacks. Unlike some other forms of arthritis, gout usually has a sudden onset of pain and symptoms.

“The gold standard is doing a joint tap also known as arthrocentesis, which takes some fluid from the joint,” says Dr. Gonzalez. “When we see urate crystals under a microscope, we know you have gout.” Uric acid levels in the blood serum are often drawn, with normal considered to be at or under 5.0 mg/dL.

Of course, this is not useful during an acute attack. “While an attack is ongoing, the body releases inflammatory mediators in an effort to defend itself,” notes Dr. Gonzalez. “The mediators increase the excretion of UA, which can result in very low blood serum readings. Blood tests for UA are much more important and useful when the acute phase is over.”

X-rays may show joint damage, but this tends to be in gout of long-standing. Ultrasound and CT scans show earlier features of gouty joints and are more useful during diagnosis.

Medications for treatment
Gout medications can be used to treat acute attacks, prevent future attacks, and reduce your risk of complications such as the development of tophi from crystal deposits. What medications you and your doctor choose will be based on your current health and your own preferences.

There are two targets for treating gout. One is to stop the current acute attack; the second step focuses on long-term care by getting your blood serum UA levels to around 5.0 and keeping them there.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are used in both acute and chronic care. This class of drugs lowers the inflammation caused by crystals in the joint, but have no effect on the levels of uric acid. Over-the-counter options include ibuprofen (Advil, Motrin IB, others) and naproxen sodium (Aleve, others), as well as more powerful prescription medicines including indomethacin (Indocin) or celecoxib (Celebrex).

Another medication frequently used is colchicine (Colcrys, Mitigare), a special type of anti-inflammatory that effectively reduces gout pain when used during an attack. The best use for this medication is to prevent attacks. One pill a day will stop future attacks and still be well tolerated in most users.

Heat is another useful treatment, especially for the pain associated with acute attacks. Keeping the joint immobilized and elevated is suggested as well.

Corticosteroid medications such as prednisone may control gout inflammation and pain. They can be given by mouth or injected directly into the joint. Because of their adverse effects, corticosteroids are generally reserved for people who can’t take either NSAIDs or colchicine. In very severe cases, they may be used short term to help calm the storm.

Medicines to prevent further attacks
You may be one of the lucky ones and have only one acute attack, with no further need for treatment—these cases are rare, but they do happen. For most people, however, the attacks increase in both frequency and severity if left untreated. In those instances, medications will be prescribed to help prevent complications of gout, and you likely will have to take them for the rest of your life.

One class is medications that lower UA levels by blocking uric acid production in the body. Drugs called xanthine oxidase inhibitors—including allopurinol (Aloprim, Lopurin, and Zyloprim) and febuxostat (Uloric)—limit the amount of uric acid your body makes. This may lower your blood’s uric acid level and reduce your risk of gout attacks.

The other group works to improve your kidney’s ability to rid the body of uric acid. Probenecid (Probalan) lowers your uric acid levels and reduces risk of gout, but increases uric acid in your urine, which can lead to kidney stones.

“Your doctor will track serum UA levels over time to see how well you’re doing, and medications will usually be titrated to where the level is less than 6 mg/dL,” says Dr. Cronstein. “If it stays at that level, the crystals in the joints will be reabsorbed and eliminated entirely from your body. We try to give you the lowest dose of medication that meets that goal.”

Other options
Other approaches are available to lower your uric acid levels. With the exception of those with borderline high results, though, medications will still be needed to stay gout free.

Lifestyle changes can be very important. If you are obese, losing weight can bring down UA levels. So can limiting the amount of beer, red meat, seafood, and high fructose soft drinks you consume.

“‘Moderation’ is the key in diet changes,” says Dr. Gaffo. “For most patients, it isn’t that you can’t have beer—just that you should limit yourself to no more than a serving or two each week. Same with red meats, where you can enjoy a weekly small steak.”

Some research suggests that a half a cup of cherries and dark berries daily helps reduce uric acid levels. Greater vitamin C intake is another possibility, as is up to 5 cups of dairy products daily. Drinking 8 to 10 glasses of water will increase the filtering of the kidneys and flush out uric acid.

The future
Developments currently on the horizon could impact gout diagnosis and treatment over the next three to five years. Multiple medications are being studied that increase the efficiency of kidney excretion, and one or more of these could be released to the market soon.

“Some of the most exciting areas are looking at how we can treat gout better,” says Dr. Gaffo. “We have medications that work well, but the fact that some patients don’t take their medicines correctly, or at all, leaves a big gap in our understanding.”

Another area of interest centers on finding out why some people can have very high uric acid levels for many years, along with deposits in their joints, and yet never exhibit the inflammation and damage seen in others. Discovering what protects these patients may lead to newer treatments and interventions in the long run.

“Gout is a disease that we can cure and make sure attacks either come less often or go away altogether,” says Dr. Cronstein. “I think this is a very hopeful time for our patients.”

Last Reviewed September 2, 2015

Kurt Ullman has been a medical writer for 30 years. He is based in Indiana.

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