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SP0008 MANAGEMENT OF CPPD DISEASE

Background: Calcium pyrophosphate deposition (CPPD) is a common cause of arthritis. Its’ prevalence increases with ageing, and it manifests with asymptomatic chondrocalcinosis, acute crystal synovitis, and chronic arthritis. Objectives: The objectives of this talk are to summarize the treatment options for the management of CPPD, and, to review the evidence base supporting them. Methods: A systematic literature search was performed to identify all studies published in the English language, and, reporting on the treatment of acute and chronic manifestations of CPPD. All published studies were included with the exception of case reports and conference abstracts. Similarly, a literature search was performed to identify the metabolic and hereditary risk-factors of CPPD. The findings of the systematic literature search are described in a narrative manner. Interventions for which there is no published data are recommended based on clinical experience and expert opinion. Results: Based on clinical experience, oral or intra-articular corticosteroids are recommended for the management of CPPD. Colchicine and interleukin-1 antagonists are effective and recommended for the management of acute CPP crystal arthritis. Interleukin-1 antagonists should be reserved for use in refractory cases. Oral NSAIDs should be avoided as people with CPPD are frequently elderly. Low-dose oral colchicine and hydroxychloroquine can be used in the management of recurrent acute CPP crystal arthritis to prevent recurrent flares. Based on current evidence, methotrexate cannot be recommended for the management of CPPD. However, there are anecdotal reports of beneficial effects of methotrexate in the management of chronic CPP crystal inflammatory arthritis, and, this agent holds promise for a role in the management of chronic CPP crystal arthritis which requires investigation in future studies. Radiosynovectomy may be effective in joints with chronic synovitis and CPPD. Individuals with young-onset CPPD, or polyarticular CPPD should be screened for inherited disorders such as ANKH gene mutations, Gitelman”s syndrome; and for metabolic conditions such as hyperparathyroidism, haemochromatosis, hypomagnesemia and hypophosphatasia. When present, the underlying metabolic abnormality should be treated appropriately. In joints with end-stage osteoarthritis, the presence of CPPD does not adversely affect the outcomes of total joint replacement. There are anecdotal case-reports of radiographic articular chondrocalcinosis due to hyperparathyroidism or hypomagnesemia resolving after parathyroidectomy, or magnesium supplementation, to date, it has not been possible to dissolve CPPD in vivo with targeted drug therapy. Several candidate pharmaceutical agents that have the potential of dissolving CPPD have been identified, but, their clinical trial is generally precluded by the risk of systemic toxicity. Conclusion: Although the pathogenesis of CPPD and CPP crystal mediated inflammation are well understood, its’ management remains symptomatic. Expedited drug development programs and high quality randomised controlled trials are needed to advance the management of people with this disorder. Disclosure of Interests: Abhishek Abhishek Grant/research support from: AstraZeneca and OxfordImmunotech, Grant/research support from: AstraZeneca and Oxford Immunotech, Speakers bureau: Menarini pharmaceuticals, Speakers bureau: Menarini pharmaceuticals