Calcium Pyrophosphate Deposition Disease Treatment & Management

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

Approach Considerations

Management of calcium pyrophosphate deposition disease (CPDD) depends on the clinical manifestations.

Asymptomatic (lanthanic) CPDD should not be treated unless it is a possible manifestation of other syndromes, such as hyperparathyroidism or hemochromatosis (treatment of which is important to prevent further end-organ damage but cannot reverse the joint disease).

Acute pseudogout may be treated by joint aspiration and intra-articular corticosteroid injection, systemic corticosteroids, nonsteroidal anti-inflammatory drugs (NSAIDs), or, occasionally, high-dose colchicine.

Treatment for pseudo-osteoarthritis is similar to that for typical osteoarthritis. Patients with a pseudorheumatoid arthritis can be treated with small doses of corticosteroids, such as prednisone at 5mg daily.

Methotrexate was effective in isolated observations in patients who had severe disease with particular emphasis on joint destruction. However, this treatment was attempted only in patients with the pseudorheumatoid presentation.[10]

Studies have suggested that the inflammasome complex plays a pivotal role for interleukin-1 in pseudogout attacks, which means that anakinra (Kineret) is a potential alternative for treating patients with calcium pyrophosphate disease.[11] This was reported in a single individual, a 71-year-old man with recurrent pseudogout attacks in multiple joints that were resistant to therapy with anti-inflammatory drugs, including glucocorticoids. This could also be important in patients with renal insufficiency (such as this patient), in whom nonsteroidal drugs can be problematic.[11]

Surgical care

Theoretically, surgically removing calcifications from an affected joint could be beneficial, but this is currently considered an experimental procedure.

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Pharmacotherapy for Pseudogout

Intra-articular corticosteroid injections—such as 40-80 mg (depending on the size of the joint) of methylprednisolone or triamcinolone—into the affected joint have the advantage of avoiding the adverse systemic effects of NSAIDs. Short courses of systemic corticosteroids may be used for polyarticular attacks of pseudogout.

The use of NSAIDs also can be considered, generally in higher doses during the acute attack and in lesser doses for prevention. Be aware of toxicity, which is common in elderly patients, including gastrointestinal and renal toxicities. Cyclooxygenase-2 (COX-2) ̶ selective NSAIDs (ie, COX-2 inhibitors) may be as effective as traditional NSAIDs but with less toxicity, although this has not been rigorously tested.

Oral colchicine, or even intravenous (IV) colchicine, can be considered for the treatment of acute pseudogout. Colchicine should be a treatment of last resort because of its poor therapeutic ratio.

Preventing acute attacks of pseudogout is difficult. The use of small doses of colchicine (0.6mg qd/bid) or NSAIDs have been tried, with variable success.

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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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  2. Tsui FW. Genetics and Mechanisms of Crystal Deposition in Calcium Pyrophosphate Deposition Disease. Curr Rheumatol Rep. Dec 24 2011;[Medline].

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  9. Ellabban AS, Kamel SR, Omar HA, El-Sherif AM, Abdel-Magied RA. Ultrasonographic diagnosis of articular chondrocalcinosis. Rheumatol Int. Dec 23 2011;[Medline].

  10. Ea HK, Liote F. Calcium pyrophosphate dihydrate and basic calcium phosphate crystal-induced arthropathies: update on pathogenesis, clinical features, and therapy. Curr Rheumatol Rep. Jun 2004;6(3):221-7. [Medline].

  11. Announ N, Palmer G, Guerne PA, Gabay C. Anakinra is a possible alternative in the treatment and prevention of acute attacks of pseudogout in end-stage renal failure. Joint Bone Spine. Jul 2009;76(4):424-6. [Medline].

  12. Doherty M. Calcium pyrophosphate deposition disease and other crystal deposition diseases. Curr Opin Rheumatol. Oct 1990;2(5):789-96. [Medline].

  13. Ea HK, Lioté F. Advances in understanding calcium-containing crystal disease. Curr Opin Rheumatol. Mar 2009;21(2):150-7. [Medline].

  14. Halverson PB, McCarty DJ. Patterns of radiographic abnormalities associated with basic calcium phosphate and calcium pyrophosphate dihydrate crystal deposition in the knee. Ann Rheum Dis. Jul 1986;45(7):603-5. [Medline].

  15. Pritzker KP. Calcium pyrophosphate dihydrate crystal deposition and other crystal deposition diseases. Curr Opin Rheumatol. Jul 1994;6(4):442-7. [Medline].

  16. Rachow JW, Ryan LM, McCarty DJ. Synovial fluid inorganic pyrophosphate concentration and nucleotide pyrophosphohydrolase activity in basic calcium phosphate deposition arthropathy and Milwaukee shoulder syndrome. Arthritis Rheum. Mar 1988;31(3):408-13. [Medline].

  17. Rothschild BM, Woods RJ. Osteoarthritis, calcium pyrophosphate deposition disease, and osseous infection in Old World primates. Am J Phys Anthropol. Mar 1992;87(3):341-7. [Medline].

  18. Ryan LM, Rachow JW, McCarty DJ. Synovial fluid ATP: a potential substrate for the production of inorganic pyrophosphate. J Rheumatol. May 1991;18(5):716-20. [Medline].

  19. Suan JC, Chhem RK, Gati JS, et al. 4 T MRI of chondrocalcinosis in combination with three-dimensional CT, radiography, and arthroscopy: a report of three cases. Skeletal Radiol. Nov 2005;34(11):714-21. [Medline].

  20. Yamazaki H, Uchiyama S, Kato H. Median nerve and ulnar nerve palsy caused by calcium pyrophosphate dihydrate crystal deposition disease: case report. J Hand Surg Am. Oct 2008;33(8):1325-8. [Medline].

 
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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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