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.

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.

scholarly journals Tu-Teng-Cao Extract Alleviates Monosodium Urate-Induced Acute Gouty Arthritis in Rats by Inhibiting Uric Acid and Inflammation

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Rongmei Yao ◽  
Zihan Geng ◽  
Xin Mao ◽  
Yanyan Bao ◽  
Shanshan Guo ◽  
...  
Keyword(s):  
Uric Acid ◽  
Gouty Arthritis ◽  
Histological Evaluation ◽  
Therapeutic Effects ◽  
Monosodium Urate ◽  
Cell Degeneration ◽  
Acute Gouty Arthritis ◽  
Monosodium Urate Crystals ◽  
Potassium Oxonate ◽  
Urate Crystals

Gouty arthritis is an inflammatory joint disease closely related to hyperuricemia. It is characterized by deposition of monosodium urate crystals in the joints, resulting in an intense inflammatory process and pain. Control of hyperuricemia and anti-inflammation treatments are the main therapeutic approaches. However, the commonly used drugs for inhibiting uric acid and acute gouty arthritis have obvious gastrointestinal and renal toxicity; thus, there is an urgency to develop new alternative therapeutic drugs. An extract of Tu-Teng-Cao (TTC), a compound drug used in traditional Chinese medicine, has been widely applied to the clinical treatment of arthritis. In this study, we investigated the therapeutic effects of TTC on gouty arthritis. In this study, an animal model of acute gouty arthritis with hyperuricemia was established using potassium oxonate and monosodium urate crystals. After treatment with TTC, the results showed obvious therapeutic effects on the rat model of acute gouty arthritis. The treatment significantly attenuated the degree of ankle swelling, inflammation, and dysfunction index, and the levels of proinflammatory cytokines. In addition, TTC has significant antihyperuricemia activity in rats with hyperuricemia induced by potassium oxonate. Histological evaluation showed that TTC relieved pathological damage in rats with acute gouty arthritis induced by monosodium urate crystals. All the groups treated with TTC showed improvement in cartilage degeneration, cell degeneration, synovial hyperplasia, and inflammatory cell invasion in the ankle joint of rats. TTC significantly alleviated swelling, inflammation, and bleeding of the renal corpuscle and convoluted tubules of rats. The results of this study suggest that TTC is capable of treating gouty arthritis and decreasing ankle injury through the control of uric acid and inflammation.

scholarly journals Citrobacter koseri causing osteomyelitis in a diabetic foot with concomitant acute gouty arthritis successfully treated with ertapenem

2019 ◽  
Vol 12 (7) ◽  
pp. e230432
Author(s):  
Dillon Tinevez ◽  
Nebojsa Nick Knezevic
Keyword(s):  
Septic Arthritis ◽  
Gouty Arthritis ◽  
Acute Gout ◽  
Monosodium Urate ◽  
Acute Gouty Arthritis ◽  
Monosodium Urate Crystals ◽  
X Ray ◽  
Fluid Analysis ◽  
Wound Culture ◽  
Urate Crystals

We present an elderly diabetic man with left hallux pain and drainage who was initially diagnosed with acute gouty arthritis using the diagnostic rule for acute gout and monosodium urate crystals presented on synovial fluid analysis. Further investigation with surgical debridement, plain X-ray, MRI and wound culture revealed concomitant Citrobacter koseri septic arthritis with osteomyelitis. C. koseri is considered an opportunistic infection that rarely causes musculoskeletal infections. Acute gouty arthritis and septic arthritis are rarely seen occurring concomitantly in the same joint and are often difficult to differentiate due to similar findings on exam and imaging. The present case illustrates that osteomyelitis with an opportunistic organism can present concomitantly with acute gouty arthritis, and the diagnosis of one should not exclude the other.

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

Role of miR-146a in regulation of the acute inflammatory response to monosodium urate crystals

2015 ◽  
Vol 74 (4) ◽  
pp. 786-790 ◽  
Author(s):  
Nicola Dalbeth ◽  
Bregina Pool ◽  
Odette M Shaw ◽  
Jacquie L Harper ◽  
Paul Tan ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Acute Inflammatory Response ◽  
Monosodium Urate ◽  
Monosodium Urate Crystals ◽  
Urate Crystals

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 Role of S100A8 and S100A9 in neutrophil recruitment in response to monosodium urate monohydrate crystals in the air-pouch model of acute gouty arthritis

2003 ◽  
Vol 48 (8) ◽  
pp. 2310-2320 ◽  
Author(s):  
Carle Ryckman ◽  
Shaun R. McColl ◽  
Karen Vandal ◽  
Rinaldo de Médicis ◽  
André Lussier ◽  
...  
Keyword(s):  
Gouty Arthritis ◽  
Neutrophil Recruitment ◽  
Monosodium Urate ◽  
Air Pouch ◽  
Acute Gouty Arthritis ◽  
Air Pouch Model

SAT0528 Role of Micrornas in Regulation of the Acute Inflammatory Response to Monosodium Urate Crystals

2014 ◽  
Vol 73 (Suppl 2) ◽  
pp. 782.2-782
Author(s):  
N. Dalbeth ◽  
B. Pool ◽  
C. Franklin ◽  
M.E. House ◽  
J. Cornish ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Acute Inflammatory Response ◽  
Monosodium Urate ◽  
Monosodium Urate Crystals ◽  
Urate Crystals
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