Crystal arthropathy

2018 ◽  
Author(s):  
Michael Doherty
Keyword(s):  
Inflammatory Arthritis ◽  
Calcium Phosphates ◽  
Calcium Pyrophosphate ◽  
Monosodium Urate ◽  
Crystal Deposition ◽  
Cartilage Calcification ◽  
Crystal Deposition Disease ◽  
Deposition Disease ◽  
Crystal Arthritis

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.

Crystal-Induced Joint Disease

2019 ◽  
Author(s):  
N Lawrence Edwards
Keyword(s):  
Inflammatory Arthritis ◽  
Gouty Arthritis ◽  
Clinical Manifestations ◽  
Calcium Pyrophosphate ◽  
Calcium Pyrophosphate Dihydrate ◽  
Monosodium Urate ◽  
Crystal Deposition ◽  
Acute Gouty Arthritis ◽  
Crystal Arthritis ◽  
Pyrophosphate Dihydrate

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

Crystal-Induced Joint Disease

2019 ◽  
Author(s):  
N Lawrence Edwards
Keyword(s):  
Inflammatory Arthritis ◽  
Gouty Arthritis ◽  
Clinical Manifestations ◽  
Calcium Pyrophosphate ◽  
Calcium Pyrophosphate Dihydrate ◽  
Monosodium Urate ◽  
Crystal Deposition ◽  
Acute Gouty Arthritis ◽  
Crystal Arthritis ◽  
Pyrophosphate Dihydrate

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

Effect of colchicine, methotrexate, and hydroxychloroquine therapy on cardiovascular outcomes in patients with calcium pyrophosphate crystal deposition disease

2021 ◽  
Vol 15 (6) ◽  
pp. 76-83
Author(s):  
M. S. Eliseev ◽  
E. V. Cheremushkina ◽  
O. V. Zhelyabina ◽  
M. N. Chikina ◽  
A. A. Kapitonova ◽  
...  
Keyword(s):  
Cardiovascular Events ◽  
Serum Uric Acid Level ◽  
Calcium Pyrophosphate ◽  
Chronic Arthritis ◽  
Cardiovascular Outcomes ◽  
Crystal Deposition ◽  
Crystal Deposition Disease ◽  
Deposition Disease ◽  
History Of ◽  
Anti Inflammatory

Anti-inflammatory therapy, such as colchicine (COL), has been suggested to affect the incidence of cardiovascular events in patients with calcium pyrophosphate crystal deposition disease (CPPD).Objective: to study the effect of anti-inflammatory therapy with COL, hydroxychloroquine (HC), and methotrexate (MT) on cardiovascular outcomes in patients with CPPD.Patients and methods. The study included 305 patients with CPPD, the majority (62.30%) were women. The average follow-up period was 3.9±2.7 years. Among factors influencing cardiovascular outcome were considered: gender; age; smoking; alcohol intake >20 conventional doses per week; arterial hypertension; a history of cardiovascular diseases (CVD), in particular ischemic heart disease, acute myocardial infarction, acute cerebrovascular accident, chronic heart failure >III stage according to NYHA, as well as type 2 diabetes mellitus (DM); body mass index >25 kg/m2 and >30 kg/m2; cholesterol level (CHOL) >5.1 mmol/l; glomerular filtration rate (GFR) < 60 ml/min/1.73 m2; serum uric acid level >360 μmol/l; hypercalcemia (serum calcium level >2.62 mmol/L); CRP level >2 mg/l; the presence of hyperparathyroidism (parathyroid hormone level >65 pg/ml); CPPD phenotypes (asymptomatic, osteoarthritis with calcium pyrophosphate crystals, chronic arthritis, acute arthritis); intake of COL, HC, MT, glucocorticoids and non-steroidal anti-inflammatory drugs (NSAIDs).Results and discussion. 264 patients were under dynamic observation. Any of the studied cardiovascular events were registered in 79 (29.9%) patients. During the observation period, 46 (17.4%) patients died, in 76.1% of cases the cause of death was CVD. Death from other causes was diagnosed in 11 (23.9%) patients. Non-fatal cardiovascular events were reported in 44 (16.7%) cases. The risk of cardiovascular events was higher in patients over 65 years of age (odds ratio, OR 5.97; 95% confidence interval, CI 3.33–10.71), with serum cholesterol levels ≥5.1 mmol/L (OR 1,95; 95% CI 1.04–3.65), GFR <60 ml/min/1.73 m2 (OR 2.78; 95% CI 1.32–5.56), history of CVD (OR 2,32; 95% CI 1.22–4.44). COL therapy reduced the risk of cardiovascular events (OR 0.20; 95% CI 0.11–0.39).Conclusion. Poor CVD outcomes in CPPD are associated with age, hypercholesterolemia, chronic kidney disease, and a history of CVD. The use of COL, in contrast to MT and HC, was accompanied by a decrease in cardiovascular risk.

FLEXOR TENDON RUPTURE OF THE LITTLE FINGER CAUSED BY CALCIUM PYROPHOSPHATE DIHYDRATE CRYSTAL DEPOSITION DISEASE OF THE PISOTRIQUETRUM JOINT

Hand Surgery ◽  
2013 ◽  
Vol 18 (03) ◽  
pp. 413-415 ◽  
Author(s):  
Takuma Wakasugi ◽  
Ritsuro Shirasaka ◽  
Hiroaki Kimura ◽  
Yoshiaki Wakabayashi
Keyword(s):  
Flexor Tendon ◽  
Calcium Pyrophosphate ◽  
Calcium Pyrophosphate Dihydrate ◽  
Distal Stump ◽  
Crystal Deposition ◽  
Crystal Deposition Disease ◽  
Deposition Disease ◽  
Closed Rupture ◽  
Pyrophosphate Dihydrate ◽  
Little Finger

We report a case of closed rupture of the flexor tendons of the little finger caused by calcium pyrophosphate dihydrate crystal deposition disease of the pisotriquetrum joint. The patient could not flex the little finger and did not have wrist pain. Plain radiographs of the affected wrist joint showed severe arthritic changes of the pisotriquetrum joint and calcification around the joint. At operation, the pisotriquetrum joint capsule was ruptured and involved the flexor tendon of the little finger. The distal stump of the flexor tendon was transferred to the flexor tendon of the ring finger, and the pisiform was resected. Histological examination with polarized light microscopy revealed crystals showing weakly positive birefringence in the calcification.

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