Section 5. Bone, Joint, and Muscle Disorders

Chapter 70. Gout and Pseudogout

Topics: Introduction | Gout | Pseudogout

Gout

Gout is a disorder that results from deposits of sodium urate crystals, which accumulate in the joints because of high blood levels of uric acid (hyperuricemia), leading to attacks of painful joint inflammation.

Gout is more common in men than in women. Usually, gout develops during middle age in men and after menopause in women. Gout is rare in younger people but is often more severe in people who develop the disorder before age 30. Gout often runs in families.

Gout most often affects the joints in the feet, particularly at the base of the big toe (podagra). However, it also commonly affects other joints: the ankle, knee, wrist, and elbow. Urate crystals may form in these joints because the joints are cooler than the central part of the body, and urate crystals form readily at cooler temperatures. Gout rarely affects the joints of the spine, hips, or shoulders.

See the sidebar Risk Factors for the Development of Gout.

Causes

Normally, uric acid, a by-product of cell nucleic acid breakdown, is present in small amounts in the blood because the body continually breaks down cells and forms new cells. Also, the body readily transforms substances in foods called purines into uric acid. Foods high in purines include anchovies, asparagus, consommé, herring, meat gravies and broths, mushrooms, mussels, all organ meats, sardines, and sweetbreads. Most often, the uric acid level in the blood becomes abnormally high when the kidneys cannot eliminate enough uric acid in the urine. Too much uric acid in the blood can result in urate crystals being formed and deposited in joints. Additionally, combining a high-purine diet with alcohol can worsen matters, because alcohol both increases the production of uric acid and interferes with its elimination by the kidneys.

Less commonly, gout may be due to an identifiable underlying disorder; this is called secondary gout. For instance, large amounts of uric acid may be produced because of an inherited enzyme abnormality or a disease such as leukemia, in which cells multiply and are rapidly destroyed. Some types of kidney disease and certain drugs (eg, thiazide diuretics) impair the kidneys' ability to eliminate uric acid, so levels of uric acid rise. High levels of uric acid in the blood lead to high levels of uric acid in the joints; this process may then result in the formation of urate crystals in the joint tissue and the fluid within the joints (synovial fluid).

Symptoms

Attacks of gout (acute gouty arthritis) can occur without warning. They may be triggered by an injury, surgery, consumption of large quantities of alcohol or purine-rich food, fatigue, emotional stress, or illness. Typically, severe pain occurs suddenly in one or more joints, often at night (probably because of the metabolic changes that occur when a person lies down). The pain becomes progressively worse and is often excruciating, particularly when the joint is moved or touched. The joint becomes inflamed--it swells and feels warm, and the skin over the joint appears red or purplish, tight, and shiny.

Other symptoms of an attack can include fever (which may reach 102° F [38.9° C]), chills, a general sick feeling, and a rapid heartbeat. The first few attacks usually affect only one joint and last for a few days. The symptoms gradually disappear, joint function returns, and no symptoms appear until the next attack. However, if the disorder progresses, untreated attacks last longer, occur more frequently, and affect several joints.

After repeated attacks, gout can become severe and chronic and may lead to the destruction of tissue and a joint deformity.

Over time, joint motion becomes progressively restricted by damage caused by deposits of urate crystals in the joints and tendons. Hard lumps of urate crystals (tophi) are first deposited in the joint (synovial) lining or cartilage or in bone near the joints and then under the skin around joints. Tophi can also develop in the kidney and other organs, under the skin on the ears, in the tough band extending from the calf muscles to the heel (Achilles tendon), or around the elbows. If untreated, tophi can burst and discharge chalky masses of urate crystals through the skin.

About one fifth of people who have gout develop kidney stones (urolithiasis), which are composed of uric acid (see Section 11, Chapter 148). The stones may block the urinary tract, resulting in excruciating pain and, if untreated, infection and kidney damage. In people with gout who also have another disorder that damages the kidneys (such as diabetes or high blood pressure), increasingly poor kidney function reduces the excretion of uric acid and makes the gout and its joint damage progressively worse.

Diagnosis

Doctors often diagnose gout on the basis of its distinctive symptoms and an examination of the affected joints. A high uric acid level in the blood supports the diagnosis; however, this level is often normal, especially during an acute attack. A blood test may show increased numbers of white blood cells due to the inflammation caused by the urate crystals. The diagnosis is confirmed when needle-shaped urate crystals are identified in a sample of a tophus or in joint fluid removed (joint aspiration) with a needle and viewed under a microscope with polarized light. X-rays may show joint damage and the presence of tophi (urate crystal tophi that displace bone and produce cysts). Gout is often misdiagnosed as another type of arthritis.

Treatment

The first step is to relieve pain by controlling the inflammation.

Nonsteroidal anti-inflammatory drugs (NSAIDs), including the cyclooxygenase-2 (COX-2) inhibitors (coxibs), are often effective in relieving pain and swelling in the joint (see Section 6, Chapter 78). Rarely, additional analgesics such as codeine and meperidine are needed to control pain. The inflamed joint may be immobilized with a splint to reduce pain.

Colchicine is the traditional, but no longer the most common, first-step treatment. Usually, joint pain begins to subside after 12 hours of treatment with colchicine and is gone within 36 to 48 hours. Colchicine is usually taken in tablet form each hour until symptoms are relieved, but it can be given intravenously if the person cannot take drugs by mouth. Colchicine can cause abdominal pain and diarrhea. It can occasionally cause more serious side effects, including damage to the bone marrow.

Corticosteroids, such as prednisone, are sometimes useful to reduce joint inflammation (including the swelling) in people who cannot tolerate the other drugs. If only one or two joints are affected, a corticosteroid suspension, such as prednisolone tebutate, can be injected using the same needle that is used to remove fluid from the joint.

The second step is to prevent recurrences of gout attacks. Avoiding alcoholic beverages, losing weight, stopping drugs that cause elevated blood levels of uric acid, and eating smaller amounts of purine-rich foods may be all that is needed. Most people who have primary gout are overweight. As they gradually lose weight, their blood urate levels often return to normal or near normal, and gout attacks subsequently cease.

Preventive daily drug treatment may be needed for people who experience repeated, severe attacks. Colchicine may be taken daily to prevent attacks or to greatly reduce their frequency. Nonsteroidal anti-inflammatory drugs (NSAIDs) taken daily can also prevent attacks. However, preventing attacks does not prevent or heal existing joint damage caused by urate crystals because the crystals still persist in the joints, and the drugs do pose some risks for people who have kidney or liver disease.

Drugs that cause excretion of uric acid in the urine (uricosuric drugs), such as probenecid or sulfinpyrazone, can be used to lower the uric acid level in the blood (in people who have normal kidney function) by increasing the kidney's excretion of uric acid. Aspirin blocks the effects of probenecid and of sulfinpyrazone and should not be used at the same time as either of these drugs. If pain medication is needed, acetaminophen or other analgesics can be safely used instead.

Although uricosuric drugs lower the concentration of uric acid in the blood, they can increase the concentration of uric acid in the urine; drinking plenty of fluids--at least 3 quarts a day--may help reduce the risk of urate stones developing in the urinary tract. Making the urine alkaline (see Section 12, Chapter 159) by taking sodium bicarbonate or trisodium citrate (which increases the solubility of uric acid in the urine) can further help reduce the risk of urate stones forming in the urinary tract. However, if the urine becomes too alkaline, crystals or stones of another and more dangerous kind--calcium oxalate--may form. When starting a uricosuric drug, there is a risk of causing a gout attack. Because low-dose colchicine or an NSAID can decrease this risk, one of these drugs is usually given for a few months as well.

Allopurinol is another drug that is used to lower the blood level of uric acid. This drug blocks the production of uric acid in the body and is especially helpful for people who have a high blood uric acid level and urate stones or kidney damage. However, allopurinol can upset the stomach, cause a skin rash, decrease the number of white blood cells, or cause liver damage. As with uricosuric drugs, allopurinol can cause a gout attack when it is first taken. Low-dose colchicine or an NSAID is usually given at the same time, for a few months, to decrease this risk.

Most tophi on the ears, hands, or feet shrink slowly when the uric acid level becomes sufficiently low. However, extremely large tophi may have to be removed surgically.

Urate stones in the urinary tract can be broken up, and thereby washed out in the urine, using ultrasound directed at the stones from outside the body (extracorporeal shock wave lithotripsy (see Section 11, Chapter 148)).

See the drug table Drugs Used to Treat Gout.