Medication Summary
Nonsteroidal anti-inflammatory drugs (NSAIDs) or, occasionally, low-dose prednisone may be beneficial for chronic arthropathies due to calcium pyrophosphate deposition (CPPD) disease. Medical therapy for acute pseudogout is similar to that for gout, including the use of NSAIDs; intra-articular or, occasionally, systemic corticosteroids; and, rarely, oral or intravenous colchicine.
Variable success in preventing acute attacks of pseudogout has been achieved with small doses of colchicine (0.6 mg once or twice daily) or NSAIDs.
Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)
Class Summary
NSAIDs are very effective for the treatment of acute pseudogout and may be used for prophylaxis to prevent recurrent attacks of pseudogout. These agents may also be useful for symptomatic treatment of chronic arthropathies associated with CPPD. NSAID use is limited by toxicity (eg, renal, gastrointestinal), which is common in elderly patients. COX-2 ̶ selective NSAIDs may be as effective as traditional NSAIDs but with less gastrointestinal toxicity (although this has not been rigorously tested).
Indomethacin (Indocin)
Indomethacin is a traditional NSAID used to treat acute gouty arthritis and is used in a similar fashion for acute pseudogout. It blocks COX and, as a result, the generation of proinflammatory prostaglandins. Use the maximum dose initially, tapering it over 2 weeks depending on clinical response.
Ibuprofen (Motrin, Advil, Addaprin, Caldolor)
Ibuprofen is the drug of choice for patients with mild to moderate pain. It inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
Naproxen sodium (Anaprox, Naprelan, Naprosyn, Anaprox)
This agent is used for the relief of mild to moderate pain. It inhibits inflammatory reactions and pain by decreasing the activity of cyclo-oxygenase, which results in a decrease in prostaglandin synthesis.
Diclofenac (Voltaren, Cataflam XR, Zipsor, Cambia)
Diclofenac inhibits prostaglandin synthesis by decreasing COX activity, which, in turn, decreases formation of prostaglandin precursors.
Ketoprofen
Ketoprofen is used for relief of mild to moderate pain and inflammation. Small dosages are indicated initially in small patients, elderly patients, and patients with renal or liver disease. Doses higher than 75 mg do not increase the therapeutic effects. Administer high doses with caution, and closely observe the patient's response.
Anti-Inflammatory Agents
Class Summary
If given orally or, rarely, intravenously, these agents can be used to treat acute pseudogout. Toxicity is significant; therefore, other therapies should be considered first. Low-dose colchicine may be useful for long-term prophylaxis of pseudogout attacks.
Colchicine
Colchicine inhibits microtubules and, as a result, may inhibit neutrophil chemotaxis and phagocytosis. It also may inhibit prostaglandin generation.
Corticosteroids
Class Summary
These agents are potent anti-inflammatories that are very useful in the treatment of acute pseudogout in patients who are not good candidates for NSAIDs; moreover, they are much less toxic than colchicine. Corticosteroids can be given orally, intravenously, or intra-articularly. Oral prednisone used for an acute attack of pseudogout is generally tapered over a 2-week period. Intra-articular corticosteroids (eg, methylprednisolone) are very effective for the treatment of acute pseudogout. However, intra-articular dexamethasone promotes calcium pyrophosphate crystal formation by chondrocytes.
The general dose for methylprednisone is 20-80mg or its equivalent, depending on the size of the joint. This treatment has minimal toxicity and few contraindications (septic arthritis). Low-dose prednisone may be used for long-term treatment of pseudorheumatoid arthritis.
Prednisone
Prednisone can be given orally to abort an attack of pseudogout. It can be given intravenously if the patient cannot take it by mouth. Intra-articular corticosteroids are the first choice of therapy due to their excellent safety profile.
Methylprednisolone (Medrol, Solu-Medrol, Depo-Medrol)
Methylprednisolone decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing increased capillary permeability.
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Calcium pyrophosphate deposition disease. Radiograph of the knee showing chondrocalcinosis involving the meniscal cartilage, as well as evidence of osteoarthritis.
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Calcium pyrophosphate deposition disease. Radiograph of the wrist and hand showing chondrocalcinosis of the articular disc of the wrist and atypical osteoarthritis involving the metacarpophalangeal joints in a patient with underlying hemochromatosis.
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Calcium pyrophosphate deposition disease. Appearance of calcium pyrophosphate dihydrate crystals obtained from the knee of a patient with pseudogout. The crystals are rhomboid-shaped with weakly positive birefringence, as seen by compensated polarized microscopy. The black arrow indicates the direction of the compensator.
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Calcium pyrophosphate deposition disease. High-powered view of calcium pyrophosphate dihydrate crystals with compensated polarized microscopy. The black arrow indicates the direction of the compensator. Crystals parallel to the compensator are blue, while those perpendicular to the compensator are yellow.
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Calcium pyrophosphate deposition disease. High-powered view of calcium pyrophosphate dihydrate crystals with compensated polarized microscopy. The crystals parallel to the compensator were blue, while those perpendicular to the compensator were yellow. However, the crystals have been rotated 90%, resulting in a color change in both of them. The direction of the compensator was not changed and is indicated by the black arrow.
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Calcium pyrophosphate deposition disease. Ultrasonography of the wrist demonstrates chondrocalcinosis.
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Intraoperative photographs demonstrate extensive precipitate deposition of the calcium pyrophosphate crystals in the articular cartilage, meniscus, and synovium of a knee. Left images depict femoral and tibial surfaces. Right images depict anterior cruciate ligament.
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Intraoperative photographs demonstrate extensive precipitate deposition of the calcium pyrophosphate crystals in the articular cartilage, meniscus, and synovium of a knee. Upper left image depicts anterior horn medial meniscus. Lower left image depicts undersurface of meniscus. Upper right image depicts medial femoral condyle. Lower right image depicts synovium.
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Calcium pyrophosphate deposition disease. Ultrasound scan of the triangular fibrocartilage complex (TFCC) of the wrist shows thin hyperechoic bands parallel to the surface of the hyaline cartilage. Other findings include a punctate pattern consisting of several hyperechoic spots and homogeneous hyperechoic nodular or oval deposits in the articular surface.
