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Calcium pyrophosphate (CPP) deposition disease (CPPD) is a prevalent condition characterised by the presence of CPP crystals in articular tissues, especially hyaline cartilage and fibrocartilage. It is most frequently idiopathic, but CPPD may also be associated with other metabolic disorders, such as primary hyperparathyroidism, hereditary hemochromatosis or hypomagnesemia (eg, in a context of Gitelman’s disease).1 Some mutations, such as in ANKH, have also been described in familial forms of the disease.2
CPPD is a cause of acute or chronic inflammatory arthritis. The management of CPP crystal–induced arthritis has been extrapolated from that of gout flares and includes colchicine, non-steroidal anti-inflammatory drugs (NSAIDs) or corticosteroids.1 In cases of failure of or contraindications to these drugs, case series suggested that the interleukin 1 (IL-1) inhibitor anakinra was an alternative, especially in acute CPP arthritis.3 However, IL-1 inhibitors may be ineffective or induce …
Handling editor Josef S Smolen
Contributors Conception of the work: AL, H-KE, AF, FL, TB, PR. Acquisition, analysis or interpretation of data: all authors. Drafting the work or revising it critically for important intellectual content: all authors. Final approval of the version submitted: all authors.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.
Patient consent for publication Not required.
Provenance and peer review Not commissioned; externally peer reviewed.
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