Clinical features of calcium pyrophosphate crystal deposition

2016 ◽  
Author(s):  
Abhishek Abhishek ◽  
Michael Doherty
Keyword(s):  
Clinical Features ◽  
Inflammatory Arthritis ◽  
Clinical Manifestations ◽  
Signs And Symptoms ◽  
The Elderly ◽  
Rapid Onset ◽  
Calcium Pyrophosphate ◽  
Joint Involvement ◽  
Crystal Deposition ◽  
Crystal Arthritis

Calcium pyrophosphate deposition (CPPD) occurs in the elderly, and is commonly asymptomatic. However, it can cause acute calcium pyrophosphate (CPP) crystal arthritis, chronic CPP crystal inflammatory arthritis, and is frequently present in joints with osteoarthritis (OA). Acute CPP crystal arthritis presents with rapid onset of acute synovitis, which frequently affects the knees, wrists, shoulders, and elbows. It can mimic sepsis in the elderly, and may require hospital admission. Patients with CPPD plus OA may have more inflammatory signs and symptoms (e.g. joint swelling, stiffness) than those with OA alone. Additionally, patients with CPPD plus OA may also have intermittent attacks of acute CPP crystal arthritis. Some patients with CPPD may have more chronic inflammatory joint involvement and are classified as chronic CPP crystal inflammatory arthritis. This chapter describes the clinical features and differential diagnosis of common clinical manifestations of CPPD and outlines some of its rarer manifestations.

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

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.

Treatment of calcium pyrophosphate deposition

2016 ◽  
Author(s):  
Abhishek Abhishek ◽  
Michael Doherty
Keyword(s):  
Low Dose ◽  
Corticosteroid Injection ◽  
Interleukin 1 ◽  
Signs And Symptoms ◽  
Calcium Pyrophosphate ◽  
Crystal Deposition ◽  
Joint Aspiration ◽  
Renal Complication ◽  
Crystal Arthritis ◽  
Anti Inflammatory

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.

Calcium pyrophosphate crystal deposition (CPPD)

2013 ◽  
pp. 1211-1222
Author(s):  
Edward Roddy ◽  
Michael Doherty
Keyword(s):  
Inflammatory Arthritis ◽  
Low Dose ◽  
Joint Damage ◽  
Polarized Light ◽  
Treatment Strategies ◽  
Calcium Pyrophosphate ◽  
Related Phenomenon ◽  
Crystal Deposition ◽  
Crystal Arthritis ◽  
Novel Treatment Strategies

Calcium pyrophosphate crystal deposition (CPPD) in articular cartilage is a common age-related phenomenon. Recent important advances in our understanding of the pathophysiology of pyrophosphate metabolism include the identification of a mutation within the ANK gene which associates with familial CPPD, and elucidation of the interleukin-1β‎‎ (IL-1β‎‎)-dependent mechanisms by which crystals invoke an inflammatory response. Risk factors for CPPD include age, prior joint damage and osteoarthritis, genetic factors, and occasionally metabolic diseases (hyperparathyroidism, haemochromatosis, hypomagnesaemia, and hypophosphatasia). CPPD is commonly asymptomatic or may present as osteoarthritis with CPPD, acute calcium pyrophosphate (CPP) crystal arthritis, or chronic CPP crystal inflammatory arthritis. Although radiographic chondrocalcinosis is often taken to be synonymous with CPPD, other calcium crystals can also have this appearance and definitive diagnosis requires identification of CPP crystals by compensated polarized light microscopy of aspirated synovial fluid. Recently, the ultrasonographic appearances of CPPD have been described. Treatment of CPPD is targeted to the clinical presentation. Acute CPP crystal arthritis is treated by aspiration and injection of glucocorticosteroid, local ice packs, non-steroidal anti-inflammatory drugs (NSAIDS), low-dose colchicine, oral or parenteral glucocorticosteroids, or adrenocorticotrophic hormone (ACTH). Treatment of osteoarthritis with CPPD is very similar to the treatment of osteoarthritis alone. There is no specific therapy for chronic CPP crystal inflammatory arthritis: options include NSAID, low-dose colchicine, low-dose glucocorticosteroid, methotrexate, and hydroxychloroquine. Recommendations for the management of CPPD are derived from a small evidence base and largely based on clinical experience and extrapolation from gout. Further research into diagnosis and management including novel treatment strategies such as IL-1β‎‎ blockade is much needed.

Calcium pyrophosphate crystal deposition (CPPD)

2013 ◽  
Author(s):  
Edward Roddy ◽  
Michael Doherty
Keyword(s):  
Inflammatory Arthritis ◽  
Low Dose ◽  
Metabolic Diseases ◽  
Joint Damage ◽  
Polarized Light ◽  
Calcium Pyrophosphate ◽  
Related Phenomenon ◽  
Crystal Deposition ◽  
Age Related ◽  
Crystal Arthritis

Calcium pyrophosphate crystal deposition (CPPD) in articular cartilage is a common age-related phenomenon. Recent important advances in our understanding of the pathophysiology of pyrophosphate metabolism include the identification of a mutation within the ANK gene which associates with familial CPPD, and elucidation of the interleukin-1β‎ (IL-1β‎)-dependent mechanisms by which crystals invoke an inflammatory response. Risk factors for CPPD include age, prior joint damage and osteoarthritis, genetic factors, and occasionally metabolic diseases (hyperparathyroidism, haemochromatosis, hypomagnesaemia, and hypophosphatasia). CPPD is commonly asymptomatic or may present as osteoarthritis with CPPD, acute calcium pyrophosphate (CPP) crystal arthritis, or chronic CPP crystal inflammatory arthritis. Although radiographic chondrocalcinosis is often taken to be synonymous with CPPD, other calcium crystals can also have this appearance and definitive diagnosis requires identification of CPP crystals by compensated polarized light microscopy of aspirated synovial fluid. Recently, the ultrasonographic appearances of CPPD have been described. Treatment of CPPD is targeted to the clinical presentation. Acute CPP crystal arthritis is treated by aspiration and injection of glucocorticosteroid, local ice packs, non-steroidal anti-inflammatory drugs (NSAIDS), low-dose colchicine, oral or parenteral glucocorticosteroids, or adrenocorticotrophic hormone (ACTH). Treatment of osteoarthritis with CPPD is very similar to the treatment of osteoarthritis alone. There is no specific therapy for chronic CPP crystal inflammatory arthritis: options include NSAID, low-dose colchicine, low-dose glucocorticosteroid, methotrexate, and hydroxychloroquine. Recommendations for the management of CPPD are derived from a small evidence base and largely based on clinical experience and extrapolation from gout. Further research into diagnosis and management including novel treatment strategies such as IL-1β‎ blockade is much needed.

scholarly journals Clinical manifestations of chronic subdural hematoma in the elderly: Literature Review

2021 ◽  
Author(s):  
Gabriela Ferreira Kalkmann ◽  
Carlos Umberto Pereira ◽  
Francisco de Assis Pereira ◽  
Débora Moura da Paixão Oliveira ◽  
Nicollas Nunes Rabelo
Keyword(s):  
Early Diagnosis ◽  
Literature Review ◽  
Subdural Hematoma ◽  
Elderly Population ◽  
Clinical Presentation ◽  
Clinical Manifestations ◽  
Chronic Subdural Hematoma ◽  
Signs And Symptoms ◽  
The Elderly ◽  
Study Results

Introduction: The clinical manifestations of chronic subdural hematoma (CSDH) are often confused with other medical entities in the elderly, making their early diagnosis difficult or difficult. Early diagnosis is important, since its prognosis is directly associated with the preoperative neurological state, thus resulting in a worse vital and functional prognosis. Objectives: Report through a literature review the clinical manifestations of CSDH in the elderly population. Methods: Literature review, with the search terms: “Signs and Symptoms”, “Chronic Subdural Hematoma”, Aged, Diagnosis and Prognosis. In which PubMed, Lilacs, Scielo, Cochrane and TripDataBase data platforms were used. The inclusion criteria were: original studies published in any language. Articles in which full reading was prevented were excluded. With the application of the inclusion and exclusion criteria, 110 articles were included in the study. Results: Clinical presentation depends on the location, volume of the hematoma, rapid growth, the location of the CSDH, whether unilateral or bilateral, and the clinical conditions of the patient. Because the forms of clinical presentation of CSDH are variable, it is necessary that health professionals linked to the elderly (geriatrician, psychiatrist, general practitioner) have knowledge of this clinical entity. Conclusions: The recognition of classic forms as well as the identification of risk factors in the elderly favors the timely diagnosis and treatment of CSDH in the elderly population.

scholarly journals THE CLINICAL MANIFESTATIONS OF CALCIUM PYROPHOSPHATE CRYSTAL DEPOSITION DISEASE

2014 ◽  
Vol 0 (4) ◽  
pp. 405 ◽  
Author(s):  
F. M. Kudaeva ◽  
S. A. Vladimirov ◽  
M. S. Eliseev ◽  
A. V. Volkov ◽  
M. V. Severinova ◽  
...  
Keyword(s):  
Clinical Manifestations ◽  
Calcium Pyrophosphate ◽  
Crystal Deposition ◽  
Crystal Deposition Disease ◽  
Deposition Disease

Native Joint Septic Arthritis: Epidemiology, Clinical Features, and Microbiological Causes in a New Zealand Population

2015 ◽  
Vol 42 (12) ◽  
pp. 2392-2397 ◽  
Author(s):  
Nicholas Kennedy ◽  
Steven T. Chambers ◽  
Imogen Nolan ◽  
Kate Gallagher ◽  
Anja Werno ◽  
...  
Keyword(s):  
New Zealand ◽  
Septic Arthritis ◽  
Clinical Features ◽  
Inflammatory Arthritis ◽  
Clinical Characteristics ◽  
Calcium Pyrophosphate ◽  
Autoimmune Arthritis ◽  
Immunosuppressant Therapy ◽  
Yearly Incidence ◽  
Septic Polyarthritis

Objective.To determine the epidemiology, clinical features, and microbiology of adult native joint septic arthritis in Canterbury, New Zealand, over a 5-year period in individuals with and without an underlying rheumatic disorder.Methods.Patients with native joint septic arthritis were identified retrospectively and classified by Newman’s criteria. The clinical characteristics were described and comparisons made between those with and without underlying rheumatic disease.Results.Two hundred forty-eight cases of native joint septic arthritis (mean age 60, range 16–97 yrs) were identified with an overall incidence rate of 12.0/100,000/year (95% CI 10.6–13.6). Yearly incidence increased with age to a maximum of 73.4/100,000 in those > 90 years of age. Septic arthritis was iatrogenic in 16.9% of cases while 27% had an underlying inflammatory arthritis including gout (14.9%), calcium pyrophosphate disease (8.5%), and rheumatoid arthritis (4%). Few patients were taking immunosuppressant therapy, with just 1 taking a biological agent. Staphylococcus aureus was the most commonly identified organism. Those with underlying inflammatory arthritis were significantly older (73.6 yrs vs 55.6 yrs; p < 0.001), more likely to be female (55.2% vs 26.0%; p < 0.001), and to have septic polyarthritis (16.4% vs 4.4%; p = 0.002). The 30-day mortality was 2%, increasing to 6% at 90 days.Conclusion.The incidence of septic arthritis in Canterbury, New Zealand, is higher than in previous studies. Crystal arthropathy commonly coexisted with infection although autoimmune arthritis and immunosuppression was less of a factor than anticipated.

scholarly journals Infectious Endocarditis in the Elderly – Comparative Study of Clinical Features, Course and Outcomes

2020 ◽  
Vol 16 (2) ◽  
pp. 166-174
Author(s):  
N. S. Chipigina ◽  
N. Yu. Karpova ◽  
D. A. Anichkov ◽  
T. B. Kondratieva
Keyword(s):  
Cardiac Surgery ◽  
Hospital Mortality ◽  
Clinical Features ◽  
Odds Ratio ◽  
Drug Users ◽  
Clinical Manifestations ◽  
The Elderly ◽  
Comparative Assessment ◽  
Infectious Endocarditis ◽  
Oncological Diseases

In the context of the increased incidence of infectious endocarditis (IE) in the elderly, an assessment of clinical features of IE in elderly patients is still controversial.Aim. To study the clinical features and outcomes of IE in patients aged ≥65 years.Material and methods. А comparative assessment of risk factors, etiology, clinical manifestations, outcomes was performed in 75 IE patients ≥65 years old and in 356 IE patients <65 years old.Results. In patients ≥65 years old IE was more often associated with previous medical care (odds ratio [OR]=14.9; 95% confidence interval [95%CI] 8.6;25.9), infections and tumors of the genitourinary system or tumors of the gastrointestinal tract (OR=12.6; 95%CI 6.4;24.6); there were more concomitant oncological diseases (OR=66.2; 95%CI 19.3;226.8), diabetes mellitus (OR=9.9; 95%CI 4.5;22.1), chronic kidney disease (OR=27.0; 95%CI 13.6;53.3). In patients ≥65 years old compared with non-drug users IE patients <65 years old (n=266), the incidence of enterococcal IE was higher (OR=3.3; 95%CI 1.4;7.9); the timing of IE diagnosis was longer – 60 (37;152) vs 30 (20;110) days (p<0.05); cardiac surgery was performed less often (8% vs 24.8%; p<0.05); in-hospital mortality was almost two-fold higher. However, with the exclusion from the mortality rate assessment of postmortem diagnosed IE cases in-hospital mortality in patients ≥65 years old and patients <65 years old did not differ significantly (14.8% vs 12.2% in non-drug users <65 years old and 14.9% in drug-users IE).Conclusion. Late diagnosis of IE and comorbidity, which limits the possibility of cardiac surgery, are the most important prognostic unfavorable features of IE in the elderly.

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