Gout attacks can come on quickly and keep returning over time, slowly harming tissues in the region of the inflammation, and can be extremely painful. Hypertension, cardiovascular, and obesity are risk factors for gout.
Gout is a general term for a variety of conditions caused by a buildup of uric acid. This buildup usually affects your feet. Men are three times more likely than women to develop gout. It tends to affect men after age 40 and women after menopause. Gout symptoms can be confused with another type of arthritis called calcium pyrophosphate deposition (CPPD). However, the crystals that irritate the joint in this condition are calcium phosphate crystals, not uric acid.
Gout is a common and complex form of arthritis that can affect anyone. It’s characterized by sudden, severe attacks of pain, swelling, redness and tenderness in one or more joints, most often in the big toe
It is the most common form of inflammatory arthritis in men, and although it is more likely to affect men, women become more susceptible to it after the menopause.
What Is Gout?
Gout is a very painful form of arthritis caused by crystals that form in and around the joints.
It’s the most common type of inflammatory arthritis. It’s more common in men and you’re more likely to get it as you get older.
Gout occurs in people who have high levels of urate in their blood, but having urate in your blood doesn’t mean you’ll develop gout. It’s normal and healthy to have some urate in your bloodstream.
Urate is created every day when our bodies break down purines. Purines are chemicals that are naturally created in our body, but they are also present in certain foods.
People used to think that gout was caused by overeating and drinking too much alcohol. While this can make attacks of gout more likely, it’s not the whole story.
The signs and symptoms of gout almost always occur suddenly, and often at night. They include:
- Intense joint pain. Gout usually affects the big toe, but it can occur in any joint. Other commonly affected joints include the ankles, knees, elbows, wrists and fingers. The pain is likely to be most severe within the first four to 12 hours after it begins.
- Lingering discomfort. After the most severe pain subsides, some joint discomfort may last from a few days to a few weeks. Later attacks are likely to last longer and affect more joints.
- Inflammation and redness. The affected joint or joints become swollen, tender, warm and red.
- Limited range of motion. As gout progresses, you may not be able to move your joints normally.
These symptoms and signs usually affect a single joint. The pain is typically severe, reflecting the severity of inflammation in the joint. The affected joint is often very sensitive to touch to the point that some people with gout attacks experience pain from something as simple as pulling the bedsheets over the inflamed joint. The affected joint becomes swollen. The medical term for excessive fluid in a joint is a “joint effusion.”
Gout frequently involves joints in the lower extremities. The classic location for gout to occur is the big toe (first metatarsophalangeal joint). Podagra is the medical term for inflammation at the base of the big toe. Gout can also affect the foot, knee, ankle, elbow, wrist, hands, or nearly any joint in the body. When gout is more severe or longstanding, multiple joints may be affected at the same time. This causes pain and joint stiffness in multiple joints.
Another sign of gout is the presence of tophi. A tophus is a hard nodule of uric acid that deposits under the skin. Tophi can be found in various locations in the body, commonly on the elbows, upper ear cartilage, and on the surface of other joints. When a tophus is present, it indicates that the body is substantially overloaded with uric acid. When tophi are present, the uric acid level in the bloodstream typically has been high for years. The presence of tophi indicates tophaceous gout and treatment with medications is necessary.
Longstanding untreated gout can lead to joint damage and physical deformity.
Kidney stones may be a sign of gout as uric acid crystals can deposit in the kidney and cause kidney stones.
The human body makes uric acid during the breakdown of chemicals called purines found in certain food and drinks. This normal byproduct goes through the kidneys and exits the body when you pee.
Sometimes the body produces too much uric acid. Or the kidneys can’t do a good job handling it. When the body has high levels of uric acid, or hyperuricemia, uric acid crystals can concentrate in the joints. The sharp, needle-like crystals cause gout. However, many people with higher uric acid levels never get gout.
Who Gets Gout?
Gout can develop in a person either because they are producing too much uric acid or because they are unable to put enough of it into the urine (or both). The most common cause of gout (about 90% of cases) is the inability to excrete enough uric acid in the urine. This inability may occur for a number of reasons.
The most common is a genetic defect in substances referred to as organic anion transporters in the kidney, which leads to an excessive reabsorption of uric acid from the kidney – and thus too much uric acid in the blood. However, a defect in excretion of uric acid can also occur due to medications, such as diuretics, low dose aspirin, or alcohol. Defective uric acid excretion also occurs when the kidneys are functioning poorly.
About 10% of cases of gout are due to overproduction of uric acid. When uric acid is overproduced, it is high not only in the blood but in the urine, raising the risk of both gout and kidney stone. Some people overproduce uric acid due to a genetic defect in an enzyme in the purine breakdown pathway (See Figure 4) which leads to overactivity of this pathway. Since cells contain DNA, and DNA contains purines, anything that increases the breakdown of cells in the body can lead to more uric acid and gout.
For example, if a patient is receiving chemotherapy for a tumor, as the treatment kills the tumor cells a gout attack or kidney stone can develop as a result of the breakdown of the purines from those cells.
Foods can also lead to overproduction of uric acid, such as meats and meat gravies and beer, which contain high levels of purines.
Men get gout more than women, and at younger ages; the male to female ratio is 9:1. The most common age of onset is from age 40 to 60 years. Gout is fairly rare in women until they reach menopause. One theory is that estrogen blocks the anion exchange transporter (see above) in the kidney, causing more uric acid to be excreted in the urine, and thus lowering the level of uric acid in the blood. Gout most commonly starts in a person’s 40’s to 60’s, although it can start earlier than the 40’s for those with a genetic predisposition, and it can also occur for the first time when someone is in their 80’s.
In some cases, injuries can set off an attack of gout. A “stub of the toe” can lead to a gout attack if there were already enough uric acid crystals saturating the cartilage.
Whatever the mechanism of the elevated uric acid, the key event in gout is the movement of uric acid crystals into the joint fluid. The body’s defense mechanisms, including the white blood cells (neutrophils) engulf the uric acid crystals, which leads to a release of inflammatory chemicals (called cytokines) which cause all the signs of inflammation, including heat, redness, and swelling and pain. This cycle also recruits more white blood cells to the joint, which accelerates the inflammatory process.
When thinking of gout, a useful model has been proposed by Wortmann.1 Uric acid crystals can be thought of like matches, which can sit quietly or can be ignited. Crystals can be present for years in the cartilage, or even in the joint fluid, without causing inflammation. Then, at some point, due to increasing number of crystals or other inciting factor, the matches are “struck” and the inflammation begins.
This analogy is important both for conceptualizing the uric acid crystals in the joint and for understanding the various types of gout treatment (see below), some of which attack the inflammation (pour water on the flaming matches) and some of which remove the uric acid crystals (take away the matches).
Some other kinds of arthritis can mimic gout, so proper diagnosis (detection) is key. At first, gout attacks may start at night. Acute attacks are typically followed by periods of no symptoms. In addition to being located in the joints, crystals can form tophi, or swollen growths, under the skin, often located over a joint or on the outer ear. Urate crystals and tophi can damage the joints over time. A rheumatologist can diagnose gout and make sure symptoms are not due to some other type of arthritis or an injury.
Diagnosis of gout can be made in several ways. Gout is often diagnosed upon the finding of uric acid based crystals. The physician may use a needle to extract fluid from an affected joint and will study that fluid under a microscope to find whether urate crystals are present. Crystals also can be found in deposits (called tophi) that can appear under the skin. These tophi occur in advanced gout.
Gout can also be diagnosed based on the pattern of joint involvement, characteristic symptoms, time course, blood tests for uric acid, and advanced imaging tests.
Uric acid levels in the blood are important to measure but can sometimes be misleading, especially if measured at the time of an acute attack. Levels may be normal for a short time or even low during attacks. Even people who do not have gout can have increased uric acid levels.
X-rays may show joint damage in gout of long duration. Ultrasound and dual energy computed tomography (commonly called dual energy CT) can show early features of gouty joint involvement. These imaging techniques also can help suggest the diagnosis.
The majority of gout cases are treated with medication. Medication can be used to treat the symptoms of gout attacks, prevent future flares, and reduce the risk of gout complications such as kidney stones and the development of tophi.
Commonly used medications include nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, or corticosteroids. These reduce inflammation and pain in the areas affected by gout and are usually taken orally.
Medications can also be used to either reduce the production of uric acid (xanthine oxidase inhibitors such as allopurinol) or improve the kidney’s ability to remove uric acid from the body (probenecid).
Without treatment, an acute gout attack will be at its worst between 12 and 24 hours after it began. A person can expect to recover within 1 to 2 weeks without treatment, but there may be significant pain during this period.
When gout is mild, infrequent, and uncomplicated, it can be treated with diet and lifestyle changes. However, studies have shown that even the most rigorous diet does not lower the serum uric acid enough to control severe gout, and therefore medications are generally necessary. When attacks are frequent, uric acid kidney stones have occurred, tophi are present, or there is evidence of joint damage from gout attacks, medications are typically used to lower the uric acid blood level.
Medications for the treatment of gout generally fall into one of three categories: uric-acid-lowering medications, prophylactic medications (medications used in conjunction with uric-acid-lowering medications to prevent a gout flare), and rescue medications to provide immediate relief from gout pain.
Urate-lowering medications are the primary treatment for gout. These medications decrease the total amount of uric acid in the body and lower the serum uric acid level. For most patients, the goal of uric-acid-lowering medication is to achieve a serum uric acid level of less than 6 mg/dl. These medications also are effective treatments to decrease the size of tophi, with the ultimate goal of eradicating them. Uric-acid-lowering medications include allopurinol (Zyloprim, Aloprim), febuxostat (Uloric), probenecid, and pegloticase (Krystexxa).
Prophylactic medications are used during approximately the first six months of therapy with a medication to lower high levels of uric acid to either prevent gout flares or decrease the number and severity of flares. This is because any medication or intervention that either increases or decreases the uric acid level in the bloodstream can trigger a gout attack.
Colcrys (colchicine) and any of the NSAIDs (nonsteroidal anti-inflammatory drugs) such as indomethacin (Indocin, Indocin-SR), diclofenac (Voltaren, Cataflam, Voltaren-XR, Cambia), ibuprofen (Advil), or naproxen sodium (Aleve) are frequently used as prophylactic medications to prevent gout flares during uric-acid lowering. By taking one of these prophylactic or preventative medications during the first six months of treatment with allopurinol, febuxostat, or probenecid, the risk of having a gout attack during this time is decreased. Prophylactic medications are not used in combination with Krystexxa.
The third category of medications are those used during attacks of acute gout to decrease pain and inflammation. Both colchicine (Colcrys) and NSAIDs can be used during an acute gout attack to decrease inflammation and pain. Corticosteroids such as prednisone, methylprednisolone (Medrol), and prednisolone (Orapred), also can be used during an acute gouty flare. However, the total dose of steroids is generally limited due to potential side effects such as cataract formation and bone loss. Steroid medications are extremely helpful in treating gout flares in patients who are unable to take colchicine or NSAIDs.
Home remedies for an acute gout attack include drinking plenty of water. Over-the-counter NSAIDs (nonsteroidal anti-inflammatory drugs), such as ibuprofen (Advil, Motrin) and naproxen sodium (Aleve), can be used when there are no contra-indications, such as decreased kidney function or stomach ulcers.
Home remedies may be very beneficial for the management of chronic gout, as well. The dietary modifications detailed above can be very effective in certain patients. Drinking plenty of water to remain well-hydrated can be beneficial in preventing gout attacks.
Some gout-relief methods don’t come in a bottle from your pharmacy. Evidence from studies suggests that these natural remedies may help lower uric acid levels and prevent gout attacks:
- tart cherries
- apple cider vinegar
- nettle tea
- milk thistle seeds
You can make certain lifestyle changes to help prevent gout:
- Drink plenty of water to help your kidneys function better and avoid dehydration.
- Exercise regularly to stay at a healthy weight. Extra weight increases uric acid in your body and puts more stress on joints.
Do your best to limit the purines in your body, since these chemicals can trigger uric acid buildup. Foods and drinks containing high purine levels include:
- Red meat and organ meats (liver, for example).
- Drinks and foods high in fructose (fruit sugar).
- Protein from animal sources. All protein from animal flesh can potentially lead to elevated uric acid levels.
Certain medications can lead to elevated uric acid levels. These medications include:
Diuretics, also known as “water pills.”
Immunosuppressants, or drugs used to slow the immune system (common in organ transplants, for example).