Calcium Pyrophosphate Deposition Disease Medication

  • Author: Constantine K Saadeh, MD; Chief Editor: Herbert S Diamond, MD   more...
 
Updated: Apr 19, 2012
 

Medication Summary

NSAIDs or, occasionally, low-dose prednisone may be beneficial for chronic arthropathies due to calcium pyrophosphate deposition disease (CPDD). Medical therapy for acute pseudogout is similar to that for gout, including the use of NSAIDs, intraarticular or, occasionally, systemic corticosteroids, and, rarely, oral or IV colchicine.

Variable success in preventing acute attacks of pseudogout has been achieved with small doses of colchicine (0.6mg qd/bid) or NSAIDs.

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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 CPDD. 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.

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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.

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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 CPPD 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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Contributor Information and Disclosures
Author

Constantine K Saadeh, MD  President, Allergy ARTS, LLP; Principal Investigator, Amarillo Center for Clinical Research, Ltd

Constantine K Saadeh, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American College of Rheumatology, American Medical Association, Southern Medical Association, and Texas Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Herbert S Diamond, MD  Adjunct Professor of Medicine, Division of Rheumatology, University of Pittsburgh School of Medicine; Chairman Emeritus, Department of Internal Medicine, Western Pennsylvania Hospital

Herbert S Diamond, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology, American Medical Association, and Phi Beta Kappa

Disclosure: Merck Ownership interest Other; Smith Kline Ownership interest Other; Zimmer Ownership interest Other

Additional Contributors

Lawrence H Brent, MD Associate Professor of Medicine, Jefferson Medical College of Thomas Jefferson University; Chair, Program Director, Department of Medicine, Division of Rheumatology, Albert Einstein Medical Center

Lawrence H Brent, MD is a member of the following medical societies: American Association for the Advancement of Science, American Association of Immunologists, American College of Physicians, and American College of Rheumatology

Disclosure: Abbott Honoraria Speaking and teaching; Centocor Consulting fee Consulting; Genentech Grant/research funds Other; HGS/GSK Honoraria Speaking and teaching; Omnicare Consulting fee Consulting; Pfizer Honoraria Speaking and teaching; Roche Speaking and teaching; Savient Honoraria Speaking and teaching; UCB Honoraria Speaking and teaching

Kristine M Lohr, MD, MS Professor, Department of Internal Medicine, Center for the Advancement of Women's Health and Division of Rheumatology, Director, Rheumatology Training Program, University of Kentucky College of Medicine

Kristine M Lohr, MD, MS is a member of the following medical societies: American College of Physicians and American College of Rheumatology

Disclosure: Nothing to disclose.

Jan Malacara, PA-C Consulting Staff, Allergy ARTS, LLP

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Acknowledgments

The authors wish to thank Shannon Shaw and Michael Gaylor for their hard work in helping to prepare this article.

References
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Calcium pyrophosphate deposition disease. Radiograph of the knee showing chondrocalcinosis involving the meniscal cartilage, as well as evidence of osteoarthritis.
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.
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.
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.
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.
Wrist chondrocalcinosis.
 
 
 
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