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.

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

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.

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 Could MicroRNAs be Regulators of Gout Pathogenesis?

2015 ◽  
Vol 36 (6) ◽  
pp. 2085-2092 ◽  
Author(s):  
Yangang Wang ◽  
Donghua Xu ◽  
Bin Wang ◽  
Xu Hou
Keyword(s):  
Inflammatory Arthritis ◽  
Inflammatory Diseases ◽  
Gouty Arthritis ◽  
Noncoding Rnas ◽  
Monosodium Urate ◽  
Regulate Gene Expression ◽  
Acute Gouty Arthritis ◽  
Monosodium Urate Crystals ◽  
Urate Crystals

MicroRNAs (miRNAs) are a class of noncoding RNAs that mainly negatively regulate gene expression. miRNAs have important roles in many diseases, including inflammatory diseases. Gout is a common arthritis caused by deposition of monosodium urate crystals within joints. Recent studies suggested that miRNAs may be involved in the development of inflammatory arthritis, including acute gouty arthritis. In the present review, we systemically discuss relevant publications in order to provide a better understanding on the possible role of miRNAs in gout. miRNAs may act as regulators of gout pathogenesis via several pathways. Targeting miRNAs may be a promisingstrategy in the treatment of gout.

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.

Biostatistical Analysis and Possible Forecasting of Relationship Between Uric Acid and Specific Laboratory Tests in Cases of Gouty Arthritis

2017 ◽  
Vol 68 (6) ◽  
pp. 1234-1241
Author(s):  
Adina Octavia Duse ◽  
Delia Berceanu Vaduva ◽  
Mirela Nicolov ◽  
Cristina Trandafirescu ◽  
Marcel Berceanu Vaduva ◽  
...  
Keyword(s):  
Uric Acid ◽  
Laboratory Tests ◽  
Gouty Arthritis ◽  
Main Diagnosis ◽  
Monosodium Urate ◽  
Glutamate Pyruvate ◽  
Metatarsophalangeal Joints ◽  
The Relationship ◽  
Biostatistical Analysis ◽  
Urate Crystals

Acute gouty arthritis represents an inflammatory response to microcrystals of monosodium urate that precipitate in joint tissues from supersaturated body fluids or are shed from preexisting articular deposits [1]. Gout is a metabolic disease characterized by recurrent episodes of arthritis associated with the presence of monosodium urate crystals in the tissue or synovial fluid during the attack.These forms of crystal-induced arthritis usually affect peripheral joints, including knee, ankle, wrist, and metacarpophalangeal and metatarsophalangeal joints. All of them may be associated with other inflammatory, endocrine diseases [2]. The present study was done to highlight the relationship between increased levels of uric acid and specific laboratory tests in order to possible forecast development of further disease in patients with gouty arthrithis.The present study was done on 34 patients hospitalized in Felix Hospital of Rehabilitation in 2015-2016, with age between 44 and 74, having the main diagnosis of gouty arthritis.We studied the following laboratory tests:urea and other related analysis, like uric acid, creatinine, cholesterol, glutamate pyruvate transaminase and glutamate oxalate transaminase.

scholarly journals Application of a Novel Diagnostic Rule in the Differential Diagnosis between Acute Gouty Arthritis and Septic Arthritis

2015 ◽  
Vol 30 (6) ◽  
pp. 700 ◽  
Author(s):  
Kwang-Hoon Lee ◽  
Sang-Tae Choi ◽  
Soo-Kyung Lee ◽  
Joo-Hyun Lee ◽  
Bo-Young Yoon
Keyword(s):  
Differential Diagnosis ◽  
Septic Arthritis ◽  
Gouty Arthritis ◽  
Acute Gouty Arthritis
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