Calcium Pyrophosphate Deposition Disease Treatment & Management

Updated: Jan 23, 2018
  • Author: Constantine K Saadeh, MD; Chief Editor: Herbert S Diamond, MD  more...
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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. [29]

Studies have suggested that the inflammasome complex plays a pivotal role for interleukin-1 (IL-1) in pseudogout attacks, which means that the IL-1 receptor antagonist anakinra (Kineret) is a potential alternative for treating patients with calcium pyrophosphate disease. [30] This was initially 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. [30]

In a study of anakinra for treatment of CPPD when conventional therapies are contraindicated or ineffective, 14 of 16 patients demonstrated beneficial responses; 10 had good responses and four had partial responses. These researchers concluded that anakinra may have a role in helping to control flares of CPPD in such patients. [31] In a similar study, four of five patients showed rapid clinical and biological responses at a mean of 3 days after treatment with anakinra. [32]

Surgical care

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


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.