Introduction to gout

2016 ◽  
Author(s):  
Nicola Dalbeth
Keyword(s):  
Inflammatory Arthritis ◽  
Scientific Literature ◽  
Gouty Arthritis ◽  
Joint Damage ◽  
Monosodium Urate ◽  
Crystal Deposition ◽  
Treatment Targets ◽  
Urate Crystal ◽  
Practical Information ◽  
Low Levels

Gout is a chronic condition of monosodium urate crystal deposition. It is the most common form of inflammatory arthritis in adults, and leads to recurrent flares of severe joint damage and musculoskeletal disability. Although treatment targets are well defined, gout management is currently poor, with low levels of treatment targets achieved. The last decade has seen major advances in the understanding and treatment of gout. This handbook summarizes key scientific advances, including new insights into mechanisms of hyperuricaemia, acute gouty arthritis, and joint damage. Principles of gout diagnosis and management are discussed in detail, with practical information about use of well-established agents and also newer therapies. Gout-specific research tools are outlined to assist clinicians with interpretation of the latest scientific literature in gout. Future strategies for improved gout management are also discussed.

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

scholarly journals POS0132 IS THE INTERCRITICAL GOUT REALLY ASYMPTOMATIC? THE INFLAMMATORY ROLE OF THE SILENT URATE CRYSTAL DEPOSITION

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 277.1-278
Author(s):  
C. Diaz-Torne ◽  
M. A. Ortiz ◽  
S. Jeria Navarro ◽  
A. Garcia-Gullien ◽  
L. Sainz ◽  
...  
Keyword(s):  
Risk Factors ◽  
Whole Body ◽  
Subclinical Inflammation ◽  
Monosodium Urate ◽  
Crystal Deposition ◽  
Secretome Analysis ◽  
Healthy Donors ◽  
Cytokine Levels ◽  
Urate Crystal ◽  
Crystal Deposit

Background:Gout is the most prevalent inflammatory arthritis. Gout is chronic inflammatory deposition disease related to an increase of cardiovascular (CV) events and mortality. Subclinical chronic inflammation has been demonstrated in this patients but not its relation with the monosodium urate (MSU) crystal deposit size and the number of CV risk factors.Objectives:To study the subclinical inflammation in intercritical gout patients and its possible relation to the estimated size of the crystal deposition and the number of CV risk factors.Methods:To analyze subclinical inflammation we performed a secretome analysis and a cytokine and adiponektine plasma levels quantification (IL-1β, IL-18, IL-6, sIL-6R, TNFα, CXCL-5, RANTES, leptin, resistin and adiponectin) in a cohort of gout patients. As nowadays it is not feasible to determinate the whole body deposit of MSU crystals we created three different MSU crystal deposit size patient groups using an indirect clinical and analytical classification to estimate it. Then we compared cytokine levels between healthy donors and gout patients. We also compared cytokine levels between the different crystal size deposition groups and studied its association to the number of CV risk factors.Results:Ninety consecutive patients attending a Crystal Arthritis Unit were studied. Mean age was 68.27 (28-101) years. 81.1% were male. Clinical gout evolution was of 10.1±9.8 years. 77.5% were on urate lowering treatment. 24% had tophaceous gout. Mean uric acid was 6.3±2.1 mg/dl with 47.1% of them being on target. Hypertension was present in 68.9%, diabetes mellitus in 18.9%, dislipemia in 48.9%, BMI>30 in 32.9%, abdominal obesity in 50% and 16.1% suffered from ischemic heart disease. From the 102 molecules studied in the secretome analysis in 56 there was at least a 20% difference between donors group and any of the deposition groups. In 74% of them gout patients secreted lower levels. IL-18, sIL-6R, RANTES, leptin and adiponectin were higher in patients than in healthy donors. IL-18, sIL6-R, RANTES and CXCL5 levels were associated to the size of the crystal deposits. IL-18, sIL-6R, RANTES and leptin were higher in gout groups with CV risk factors. IL-18, sIL6-R, RANTES and leptin were higher in gout patients with no risk factors when compared to healthy donors with no risk factors. We found no differences when comparing urate lowering treated and non-treated patients.Conclusion:Our results demonstrate that some proinflammatory cytokines and metabolic proteins are raised in intercritical gout patients. Some of them are different from the flare/inflammasome expected ones. In some cytokines this elevation is related to the size of the monosodium urate crystal deposit and/or to the number of cardiovascular risk factors. This cytokine changes could help to explain the increase of the cardiovascular events in gout patients.Disclosure of Interests:Cesar Diaz-Torne Grant/research support from: Received a grant from Grünenthal, Maria Angels Ortiz: None declared, Sicylle Jeria Navarro: None declared, Andrea Garcia-Gullien: None declared, Lluis Sainz: None declared, Hector Corominas: None declared, Silvia Vidal: None declared

scholarly journals Autoinflammatory Features in Gouty Arthritis

2021 ◽  
Vol 10 (9) ◽  
pp. 1880
Author(s):  
Paola Galozzi ◽  
Sara Bindoli ◽  
Andrea Doria ◽  
Francesca Oliviero ◽  
Paolo Sfriso
Keyword(s):  
Differential Diagnosis ◽  
Inflammatory Arthritis ◽  
Important Implication ◽  
Gouty Arthritis ◽  
Molecular Genetic ◽  
Therapeutic Options ◽  
Monosodium Urate ◽  
Inflammatory Pathways ◽  
Genetic Contributions

In the panorama of inflammatory arthritis, gout is the most common and studied disease. It is known that hyperuricemia and monosodium urate (MSU) crystal-induced inflammation provoke crystal deposits in joints. However, since hyperuricemia alone is not sufficient to develop gout, molecular-genetic contributions are necessary to better clinically frame the disease. Herein, we review the autoinflammatory features of gout, from clinical challenges and differential diagnosis, to the autoinflammatory mechanisms, providing also emerging therapeutic options available for targeting the main inflammatory pathways involved in gout pathogenesis. This has important implication as treating the autoinflammatory aspects and not only the dysmetabolic side of gout may provide an effective and safer alternative for patients even in the prevention of possible gouty attacks.

scholarly journals Gout of feet and ankles in different disease durations: diagnostic value of single-source DECT and evaluation of urate deposition with a novel semi-quantitative DECT scoring system

2021 ◽  
Vol 61 (1) ◽  
Author(s):  
Jin Shang ◽  
Xiao-Hu Li ◽  
Shu-Qin Lu ◽  
Yi Shang ◽  
Lu-Lu Li ◽  
...  
Keyword(s):  
Scoring System ◽  
Diagnostic Performance ◽  
Disease Duration ◽  
Bone Erosion ◽  
Early Stage ◽  
Gouty Arthritis ◽  
Single Source ◽  
Crystal Deposition ◽  
Urate Crystal ◽  
Sensitivity Specificity

Abstract Objectives To investigate the diagnostic performance of single-source dual-energy computed tomography (DECT) based on gemstone spectral imaging technology (including Discovery CT750HD and Revolution CT) in patients with suspected feet/ankles gouty arthritis, and evaluate the urate deposition with a novel semi-quantitative DECT scoring system. Methods A total of 196 patients were consecutively included. Feet and ankles were evaluated in all patients by single-source DECT scan. The 2015 EULAR/ACR criteria were used as the reference for the diagnosis of gout. The sensitivity, specificity, and area under the receiver operating characteristic curve (AUC) of DECT for the diagnosis of gout in the early (≤1 year), middle (1–3 years), and late (> 3 years) disease durations were calculated. Besides, a novel semi-quantitative DECT scoring system was assessed for the measurement of urate deposition, and the correlation between the scores and the clinical and serological data were also evaluated. Moreover, the influences of artifacts on the diagnostic performance of DECT were also determined. Results The sensitivity, specificity, and AUC of DECT in 196 patients were 38.10, 96.43%, and 0.673 in the early-stage group; 62.96, 100.00%, and 0.815 in the middle-stage group; and 77.55, 87.50%, and 0.825 in the late-stage group, respectively. The overall diagnostic accuracies in the AUC of DECT (Discovery CT750HD and Revolution CT) in the middle and late stages of gout were higher than that in the early stage of gout. Besides, the monosodium urate crystals were deposited on the first metatarsophalangeal joints and ankles/midfeet. Age, the presence of tophus, bone erosion, and disease duration considerably affected the total urate score. No statistical difference in the positive detection of nail artifact, skin artifact, vascular calcification, and noise artifact was found between the case and control groups. Conclusion DECT (Discovery CT750HD and Revolution CT) showed promising diagnostic accuracy for the detection of urate crystal deposition in gout but had limited diagnostic sensitivity for short-stage gout. Longer disease duration, the presence of tophus, and bone erosion were associated with the urate crystal score system. The artifacts do not remarkably affect the diagnostic performance of DECT in gout.

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 acute gout

2016 ◽  
Author(s):  
Puja Khanna
Keyword(s):  
Inflammatory Arthritis ◽  
Adult Population ◽  
Gouty Arthritis ◽  
Acute Gout ◽  
Monosodium Urate ◽  
Epidemiological Evidence ◽  
Acute Gouty Arthritis ◽  
Over Time ◽  
Underlying Inflammation ◽  
Urate Crystals

Acute gout is a common inflammatory arthritis in the adult population. Epidemiological evidence suggests that the prevalence of gout is steadily on the rise due to longevity, coexisting comorbidities, and iatrogenic causes contributing to hyperuricaemia. Acute gout usually presents as a self-limiting flare of synovitis that occurs due to deposition of monosodium urate crystals. The frequency of flares generally increases over time in patients who continue to have hyperuricaemia and their risk factors for acute gout attacks have not been adequately addressed. Effective treatment of acute gouty arthritis is primary focused on pain which is the primary symptom but must target both the pain and underlying inflammation. Acute gout is frequently treated with non-steroidal anti-inflammatory agents, colchicine, and corticosteroids. This chapter reviews the available therapies for management of acute gout and ones that have shown promising results.

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