Pseudogout
Pseudogout, sometimes called calcium pyrophosphate dihydrate crystal deposition disease, is caused by deposits of these crystals in the cartilage and then in the fluid of the joints. These crystal deposits lead to intermittent attacks of painful joint inflammation.
Pseudogout usually occurs in older people and affects men and women equally. In most cases, joints heal without problems, but permanent joint damage can occur. Drug therapy is generally able to control symptoms.
Causes
The cause of pseudogout is unknown. It may occur in people who have other diseases, such as an abnormally high calcium level in the blood due to a high level of parathyroid hormone (hyperparathyroidism), an abnormally high iron level in the tissues (hemochromatosis), or an abnormally low magnesium level in the blood (hypomagnesemia). However, most people with pseudogout have none of these diseases. Pseudogout may be hereditary.
Symptoms
Symptoms vary widely but tend to resemble those of gout. Some people have attacks of painful joint inflammation, usually in the knees or wrists. Attacks may resemble those of gout but are usually less severe. Attacks of pseudogout, like those of gout, can cause fever. Some people have lingering, chronic pain and stiffness in joints of the arms and legs, including the shoulders, elbows, and hips. Other people have no pain between attacks, and some have no pain at any time, despite large deposits of crystals.
Diagnosis
A doctor diagnoses pseudogout by taking fluid from an inflamed joint through a needle (joint aspiration). The diagnosis is confirmed when calcium pyrophosphate crystals are identified in the joint fluid and viewed under a microscope. Calcium from calcium pyrophosphate crystals may be deposited in cartilage, joints, bursae (fluid-filled sacs near joints that help cushion movements), ligaments, and tendons. Deposition of calcium is called calcification, which can be seen on x-ray.
Prognosis and Treatment
Often, the inflamed joints heal without any residual problems, but many people experience permanent joint damage.
Usually, treatment can stop attacks and prevent new attacks but cannot prevent damage to the affected joints. Most often, nonsteroidal anti-inflammatory drugs (NSAIDs), including the cyclooxygenase-2 (COX-2) inhibitors (coxibs), are used to reduce the pain and inflammation. NSAIDs must be used with caution in older people, because these drugs pose a higher risk of side effects, such as bleeding in the digestive tract and kidney damage. One of the coxibs, rofecoxib (withdrawn from the market), appears to increase the risk of heart attack and stroke after long-term use. The risk with other coxibs is being studied. Because one recent study has shown a 2.5-fold increase in cardiovascular problems with another coxib, celecoxib, current FDA recommendations are to limit use of any coxib to people at high risk of gastrointestinal bleeding, who have a history of intolerance to other NSAIDs, or who are not doing well on other NSAIDs. Caution should be taken with use of coxibs for long periods or by people with risk factors for heart attack and stroke. Colchicine in low doses can be taken daily by mouth to prevent attacks. Sometimes, excess joint fluid is drained and a corticosteroid is injected into the joint to reduce the inflammation. No effective long-term treatment is available; however, physical therapy (such as muscle strengthening and range-of-motion exercises) may be helpful.
See the table Comparing Gout and Pseudogout.
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