scholarly journals SAT0442 CALCIUM PYROPHOSPHATE CRYSTAL ARTHRITIS DURING HOSPITALIZATIONS: A PROSPECTIVE, CRYSTAL-PROVEN CASE SERIES

Author(s):  
Laura Ranieri ◽  
Francisca Sivera ◽  
Mariano Andrés
2019 ◽  
Vol 4 (1) ◽  
pp. 20-26 ◽  
Author(s):  
Merit P. George ◽  
Floranne C. Ernste ◽  
Aaron Tande ◽  
Douglas Osmon ◽  
Tad Mabry ◽  
...  

Abstract. Introduction: Calcium pyrophosphate deposition disease (CPPD), or pseudogout, is rare in prosthetic joints, but can mimic prosthetic joint infection (PJI) according to case reports. The purpose of this case series is to describe the demographics, presentation, management, and outcomes of a cohort of these patients seen at our academic medical center.Methods: Patients with post-implant pseudogout, who were evaluated at our medical center between January 1, 2000 and June 30, 2016, were identified from our EHR. Data pertaining to demographics, presentation, management, and outcomes were abstracted, and patients were categorized into two groups based on presence of concomitant infection along with positive CPDD findings in synovial fluid.Results: 22 patients were included. 90.9% of cases involved a TKA. The most common indication for arthroplasty was degenerative joint disease. Only four patients had a history of previous gout or pseudogout, three of which belonged to the group with no evidence of concomitant joint infection. Clinical features for patients without concomitant infection included pain (100%), swelling at the joint (88.9%), redness (33.3%), fever (22.2%), and decreased range of motion (100%). 45.5% of patients received antibiotics prior to joint aspiration (44.4% of patients with negative synovial fluid cultures, 46.2% of patients with concomitant infection).Conclusion: Our study suggests similar clinical presentation between post-implant pseudogout and PJI. Among patients with pseudogout as well as in those with PJI, the first dose of antibiotics should not be given before sampling for synovial culture. Unfortunately, many patients receive antibiotics prior to culture ascertainment, which raises concern for antibiotic overuse.


2019 ◽  
Author(s):  
N Lawrence Edwards

The destructive potential of intracellular crystals has been recognized for over a century. The mechanisms by which crystals induce inflammation and bone and cartilage destruction have been elucidated over the past decade. The three most common crystal-induced arthropathies are caused by precipitation of monosodium urate monohydrate, calcium pyrophosphate dihydrate (CPP) and basic calcium phosphate. The definition, epidemiology, pathogenesis and etiology, diagnosis, and treatment of gout and CPP crystal deposition are reviewed, as well as the clinical stages of gout (i.e., acute gouty arthritis, intercritical gout, advanced gout, nonclassic presentations of gout, and other conditions associated with gout). Also reviewed are the clinical manifestations of calcium pyrophosphate dihydrate deposition disease (CPPD), such as asymptomatic CPPD, osteoarthritis with CPPD, acute CPP crystal arthritis, and chronic CPP crystal inflammatory arthritis. Figures illustrate renal transport of urate, monosodium urate crystals, acute gouty flare, advanced gouty arthritis, gouty synovial fluid, radiographic changes of advanced gout, ultrasound appearance of the femoral intercondylar cartilage, pharmacologic management of gout, the effect of gender and age on knee chondrocalcinosis, radiographs of chondrocalcinosis, and compensated polarized microscopy of CPPD. Tables present the major factors responsible for hyperuricemia, characteristics of classic gouty flares, antiinflammatory therapy for gout, and urate-lowering therapy. This chapter contains 90 references. This review contains 11 figures, 12 tables, and 88 references. Keywords: acute gouty arthritis, intercritical gout, advanced gout, asymptomatic CPPD, osteoarthritis with CPPD, acute CPP crystal arthritis, chronic CPP crystal inflammatory arthritis


Author(s):  
Michael Doherty

Three main crystals associate with arthritis: monosodium urate (MSU); calcium pyrophosphate, the usual cause of cartilage calcification (chondrocalcinosis); and basic calcium phosphates (BCP), including hydroxyapatite. Gout is a true crystal deposition disease caused by MSU. Calcium pyrophosphate crystal deposition (CPPD) is the umbrella term for calcium pyrophosphate deposition. Calcium pyrophosphate crystals cause inflammation in acute calcium pyrophosphate crystal arthritis and chronic calcium pyrophosphate crystal inflammatory arthritis. However, osteoarthritis (OA) commonly associates with calcium pyrophosphate (OA with CPPD) and BCP crystals and, in this context, it is unclear if the crystals are pathogenic.


2015 ◽  
Vol 2015 ◽  
pp. 1-5 ◽  
Author(s):  
Marco Di Carlo ◽  
Antonella Draghessi ◽  
Marina Carotti ◽  
Fausto Salaffi

A 71-year-old man with osteoarthritis and chondrocalcinosis came to our observation developing a swelling in the groin region after a recent left colectomy for adenocarcinoma. The imaging techniques revealed the presence of an iliopsoas bursitis in connection with the hip. The synovial fluid analysis detected the presence of calcium pyrophosphate (CPP) crystals and allowed the final and unusual diagnosis of iliopsoas bursitis related to acute CPP crystal hip arthritis.


Author(s):  
Abhishek Abhishek ◽  
Michael Doherty

The treatment of calcium pyrophosphate crystal deposition (CPPD) is mainly symptomatic. Acute calcium pyrophosphate (CPP) crystal synovitis should be treated with rest, local application of ice packs, joint aspiration, and/or intra-articular corticosteroid injection (once joint sepsis has been excluded). Oral colchicine or prednisolone may be used if joint aspiration and/or injection are not feasible. Anti-inflammatory agents (with proton pump inhibitors) may be used but in general these should be avoided as most patients with acute CPP crystal arthritis are elderly, and at a high risk of gastrointestinal and renal complication of non-steroidal anti-inflammatory drug (NSAIDs). Principles of management of CPPD with osteoarthritis (OA) are identical to those for isolated OA. However, patients may have more inflammatory signs and symptoms and periodic joint aspiration and corticosteroid injection may be required more often than in isolated OA. Oral NSAIDs (with gastro-protection), colchicine, low-dose corticosteroids, hydroxychloroquine, and radiosynovectomy have been suggested as options for the treatment of chronic CPP crystal arthritis. There is growing interest in use of anti-interleukin-1 agents for acute or chronic CPP crystal arthritis but the efficacy of these agents has not been formally studied, and their use should be considered on an individual basis.


Rheumatology ◽  
2019 ◽  
Vol 59 (4) ◽  
pp. 900-903 ◽  
Author(s):  
Sara K Tedeschi ◽  
Daniel H Solomon ◽  
Kazuki Yoshida ◽  
Kathleen Vanni ◽  
Dong Hyun Suh ◽  
...  

2019 ◽  
Author(s):  
N Lawrence Edwards

The destructive potential of intracellular crystals has been recognized for over a century. The mechanisms by which crystals induce inflammation and bone and cartilage destruction have been elucidated over the past decade. The three most common crystal-induced arthropathies are caused by precipitation of monosodium urate monohydrate, calcium pyrophosphate dihydrate (CPP) and basic calcium phosphate. The definition, epidemiology, pathogenesis and etiology, diagnosis, and treatment of gout and CPP crystal deposition are reviewed, as well as the clinical stages of gout (i.e., acute gouty arthritis, intercritical gout, advanced gout, nonclassic presentations of gout, and other conditions associated with gout). Also reviewed are the clinical manifestations of calcium pyrophosphate dihydrate deposition disease (CPPD), such as asymptomatic CPPD, osteoarthritis with CPPD, acute CPP crystal arthritis, and chronic CPP crystal inflammatory arthritis. Figures illustrate renal transport of urate, monosodium urate crystals, acute gouty flare, advanced gouty arthritis, gouty synovial fluid, radiographic changes of advanced gout, ultrasound appearance of the femoral intercondylar cartilage, pharmacologic management of gout, the effect of gender and age on knee chondrocalcinosis, radiographs of chondrocalcinosis, and compensated polarized microscopy of CPPD. Tables present the major factors responsible for hyperuricemia, characteristics of classic gouty flares, antiinflammatory therapy for gout, and urate-lowering therapy. This chapter contains 90 references. This review contains 11 figures, 12 tables, and 88 references. Keywords: acute gouty arthritis, intercritical gout, advanced gout, asymptomatic CPPD, osteoarthritis with CPPD, acute CPP crystal arthritis, chronic CPP crystal inflammatory arthritis


Sign in / Sign up

Export Citation Format

Share Document