Gout is a type of arthritis that is characterized by sudden, severe attacks of joint pain with tenderness, redness, warmth, and swelling in the affected area. It usually attacks only one joint at a time. It most often strikes the joint of the big toe, in which case it is also known as podagra, but other joints can also be involved.
Gout is typically a condition that occurs in middle age, and is unusual in people under the age of 30. It is twice as common in men as in premenopausal women. Women develop gout as often as men after menopause (estrogens, which are at higher levels before menopause, appear to play a protective role).
Certain medications and diseases can bring on gout in anyone of any age or gender. A first gout attack most commonly occurs in the mid-40s. It is found globally and has been described as far back as the time of Hippocrates, 2,500 years ago. It affects about 3% of the population.
The pain and swelling of a gout attack are caused by uric acid crystals building up in the joint and leading to inflammation. The body normally forms uric acid when breaking down protein. The uric acid usually stays dissolved in the blood and ends up being flushed out by the kidneys.
If there’s too much uric acid in the blood, called hyperuricemia, or if the kidneys can’t get rid of it quickly enough, the blood levels of uric acid rises beyond what the blood can hold. As a result, crystals form and may be deposited in joints or other storage areas like the skin. Excess uric acid in the urine can also crystallize and deposit in the kidneys, acting as a seed to form kidney stones.
In severe cases, the uric acid deposits are so large that they can extend out to the skin and beyond. These large deposits around the joints and cartilage (such as the outer ear) are called tophi. Gout can also cause severe bursitis, which is inflammation of the fluid-filled sacs that cushion and protects tissues.
Most people with gout have elevated uric acid levels for a long time, often up to 20 years, before the first gout attack.
Certain high-protein foods can make the body produce too much uric acid, triggering gout. Beverages such as tea, coffee, cocoa, and especially alcohol in any form lead to extra water loss from the body, which can cause an attack. Certain medications can hamper the kidneys’ ability to clear out uric acid, including low-dose ASA* (Apirin) and diuretics (“water pills”). Certain conditions can also increase your risk of developing gout such as obesity, chronic kidney disease type 2 diabetes, high blood pressure and high cholesterol. Sudden changes in diet and weight gain or loss can also lead to gout.
Gout occurs often in joints that have previously been injured. 95% of gout patients have had an attack in a large toe at some point, since almost everyone has injured their big toe repeatedly over their lives.
The symptoms of a gout attack are almost unmistakeable. Typically, a person will go to bed feeling fine, then wake up during the night with intense pain in the big toe (more than half of first-time gout cases involve this joint). At first it feels like a bucket of cold water has been poured over the joint, but soon there’s an agonizing sensation of stretching and tearing, along with pressure and tightness. The affected area also becomes red, hot, and extremely sensitive to touch – even a bed sheet can make it hurt more. The swelling often spreads over more of the foot, making it impossible to put on a shoe. A low-grade fever may also develop.
An attack will usually taper off on its own in 3 to 10 days, but prompt treatment can end it faster. After such an attack, called acute gout or acute gouty arthritis, most sufferers will have another episode within the next two years. Attacks tend to strike more often, last longer, and affect more joints over time.
Very rarely, however, the attacks don’t go away – instead, they linger on to become chronic gout. The inflammation persists, while the crystals can permanently damage and deform the affected joints. As well, uric acid crystals can build up in tissues other than the joints, forming deposits called tophi that can show up as whitish or yellowish chalky lumps under the skin, typically in the fingers, toes, back of the elbow, behind the heel, and around the outer edge of the ear. The tophi sometimes poke through the skin, leading to ulcerations or sores.
People with gout are at higher risk of cardiovascular disease, including atherosclerosis (hardening of the arteries, which can lead to heart attack and stroke). It is not clear whether high uric acid levels play a role in developing atherosclerosis, but most people with gout also have high visceral fat and other risk factors for atherosclerosis, such as high blood pressure, blood sugar, and blood cholesterol. These risks can be markedly reduced by a healthy lifestyle and medications as indicated.
Gout can cause kidney stones, which can cause symptoms such as severe flank or groin pain, and sometimes blood in the urine. It is unclear as to what degree gout can damage the kidneys besides the effects of kidney stones.
The symptoms and signs of an acute gout attack are normally obvious enough that a doctor can usually be quite sure of the diagnosis just from your history and physical exam. Doctors will also consider other causes such as infection when making the diagnosis.
Blood tests showing hyperuricemia can support the diagnosis, but aren’t necessary for it. To confirm the diagnosis, your doctor may insert a needle into the joint and draw out some fluid to examine under a microscope. If it’s gout, needle-shaped uric acid crystals show up when the fluid is viewed under polarizing light. This is a definitive diagnostic test.
The first priority is to relieve pain and shorten the acute attack. NSAIDs (nonsteroidal anti-inflammatory drugs) such as naproxen*, indomethacin, and celecoxib can be used. These medications help with the swelling and pain. Another medication called colchicine can be prescribed instead of an NSAID at the first sign of an attack. Corticosteroids, either injected directly into the joint or taken orally, can control the inflammation. Your doctor may prescribe one or more of these medications to treat your gout attack.
Someone who gets a gout attack once or twice a year and does not have kidney stones or high urine levels of uric acid usually does not need chronic treatment. When attacks are more frequent or kidney damage is a concern, then medications such as allopurinol and febuxostat can be used to help reduce uric acid levels. These medications need to be taken daily, usually for the rest of the person’s life. One concern with these medications is that for the first 6 months gout attacks can actually increase while the medication tries to clear extra uric acid. Because of this, many people will take colchicine as well for the first 6 months.
Prevention is an important part of managing gout. It’s crucial to control weight and blood pressure and to be well-hydrated. A healthy diet is important and can help minimize attacks. This includes avoiding alcohol overuse. There are diets specific to reducing uric acid by limiting purines and pyramidines. However, these diets can be hard to follow and may only have a small effect on lowing uric acid levels.
With early diagnosis and treatment, it’s possible to control gout, prevent joint damage, and live a normal life.
*All medications have both common (generic) and brand names. The brand name is what a specific manufacturer calls the product (e.g., Tylenol®). The common name is the medical name for the medication (e.g., acetaminophen). A medication may have many brand names, but only one common name. This article lists medications by their common names. For information on a given medication, check our Drug Information database. For more information on brand names, speak with your doctor or pharmacist.
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