scholarly journals Effects of Conventional Uric Acid–Lowering Therapy on Monosodium Urate Crystal Deposits

2019 ◽  
Vol 72 (1) ◽  
pp. 150-156 ◽  
Author(s):  
Hanna Ellmann ◽  
Sara Bayat ◽  
Elizabeth Araujo ◽  
Bernhard Manger ◽  
Arnd Kleyer ◽  
...  
Keyword(s):  
Uric Acid ◽  
Monosodium Urate ◽  
Lowering Therapy ◽  
Urate Crystal

scholarly journals Soluble Uric Acid Is an Intrinsic Negative Regulator of Monocyte Activation in Monosodium Urate Crystal–Induced Tissue Inflammation

2020 ◽  
Vol 205 (3) ◽  
pp. 789-800 ◽  
Author(s):  
Qiuyue Ma ◽  
Mohsen Honarpisheh ◽  
Chenyu Li ◽  
Markus Sellmayr ◽  
Maja Lindenmeyer ◽  
...  
Keyword(s):  
Uric Acid ◽  
Negative Regulator ◽  
Monosodium Urate ◽  
Monocyte Activation ◽  
Tissue Inflammation ◽  
Urate Crystal

scholarly journals HIPERURISEMIA DAN RESPONS IMUN

2013 ◽  
Vol 3 (2) ◽  
Author(s):  
Aaltje E. Manampiring
Keyword(s):  
Uric Acid ◽  
Essential Role ◽  
Adult Population ◽  
Monosodium Urate ◽  
Metabolic Disturbances ◽  
Monosodium Urate Crystals ◽  
Cytokines And Chemokines ◽  
Urate Crystal ◽  
Urate Crystals

Abstract: Hyperuricemia, a highly prevalent condition in adult population, is associated with hemodynamic and metabolic disturbances. Albeit, pathophysiological aspects of hyperuricemia are still not clearly understood. Uric acid plays an essential role in immunity by induction of some cytokines and chemokines, such as TNFα, Il-1β, IL-6, CXCL8 (IL-8), and CXCL1 (growth-related oncogene α). Deposits of monosodium urate crystals in joint cavities and periarticular tissues  are related to an autoinflammatory disturbance, namely gout. Keywords: hyperuricemia, monosodium urate crystal, immune responsse.   Abstrak: Hiperurisemia merupakan suatu keadaan yang umum dijumpai pada populasi dewasa dan berhubungan dengan kelainan metabolik dan hemodinamik. Aspek patofisiologik dari hiperurisemia belum sepenuhnya dipahami dengan jelas. Asam urat berperan penting dalam imunitas dengan menginduksi berbagai sitokin dan kemokin, antara lain TNFα, Il-1β, IL-6, CXCL8 (IL-8) dan CXCL1 (growth-related oncogene α). Deposit kristal monosodium urat di dalam rongga sendi dan jaringan periartikuler berkaitan dengan gangguan autoinflamasi yang dikenal sebagai gout. Kata kunci: hiperurisemia, kristal monosodium urat, respons imun.

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.

Natural Products and Extracts as Xantine Oxidase Inhibitors – A Hope for Gout Disease?

2020 ◽  
Vol 26 ◽  
Author(s):  
Ilkay Erdogan Orhan ◽  
Fatma Sezer Senol Deniz
Keyword(s):  
Natural Products ◽  
Uric Acid ◽  
Waste Product ◽  
Acid Synthesis ◽  
Intermediate Compound ◽  
Living System ◽  
Ginsenoside Rd ◽  
Drug Classes ◽  
Urate Crystal ◽  
High Concentrations

: Xanthine oxidase (EC 1.17.3.2) (XO) is one of the main enzymatic sources that create reactive oxygen species (ROS) in the living system. It is a dehydrogenase enzyme that performs electron transfer to nicotinamide adenine dinucleotide (NAD+ ), while oxidizing hypoxanthin, which is an intermediate compound in purine catabolism, first to xanthine and then to uric acid. XO turns into an oxidant enzyme that oxidizes thiol groups under certain stress conditions in the tissue. The last metabolic step, in which hypoxanthin turns into uric acid, is catalyzed by XO. Uric acid, considered a waste product, can cause kidney stones and gouty-type arthritis as it is crystallized, when present in high concentrations. Thus, XO inhibitors are one of the drug classes used against gout, a purine metabolism disease that causes urate crystal storage in the joint and its surroundings caused by hyperuricemia. Urate-lowering therapy include XO inhibitors that reduce uric acid production as well as uricosuric drugs that increase urea excretion. Current drugs that obstruct uric acid synthesis through XO inhibition are allopurinol, febuxostat, and uricase. However, since the side effects, safety and tolerability problems of some current gout medications still exist; intensive research is ongoing to look for new, effective, and safer XO inhibitors of natural or synthetic origins for the treatment of the disease. In the present review, we aimed to assess in detail XO inhibitory capacities of pure natural compounds along with the extracts from plants and other natural sources via screening Pubmed, Web of Science (WoS), Scopus, and Google Academic. The data pointed out to the fact that natural products, particularly phenolics such as flavonoids (quercetin, apigenin, and scutellarein), tannins (agrimoniin and ellagitannin), chalcones (melanoxethin), triterpenes (ginsenoside Rd and ursolic acid), stilbenes (resveratrol and piceatannol), alkaloids (berberin and palmatin) have a great potential for new XO inhibitors capable of use against gout disease. In addition, not only plants but other biological sources such as microfungi, macrofungi, lichens, insects (silk worms, ants, etc) seem to be the promising sources of novel XO inhibitors.

Can Serum Uric Acid Lowering Therapy Contribute to the Prevention or Treatment of Nonalcoholic Fatty Liver Disease?

2018 ◽  
Vol 16 (3) ◽  
pp. 269-275 ◽  
Author(s):  
Paschalis Paschos ◽  
Vasilios G. Athyros ◽  
Achilleas Tsimperidis ◽  
Anastasia Katsoula ◽  
Nikolaos Grammatikos ◽  
...  
Keyword(s):  
Uric Acid ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Serum Uric Acid ◽  
Fatty Liver Disease ◽  
Nonalcoholic Fatty Liver ◽  
Lowering Therapy

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 Uric Acid and Hypertension: Prognostic Role and Guide for Treatment

2021 ◽  
Vol 10 (3) ◽  
pp. 448
Author(s):  
Federica Piani ◽  
Arrigo F. G. Cicero ◽  
Claudio Borghi
Keyword(s):  
Clinical Trials ◽  
Uric Acid ◽  
Mendelian Randomization ◽  
Strong Association ◽  
Epidemiological Studies ◽  
Hypertensive Disease ◽  
Genetic Studies ◽  
Lowering Therapy ◽  
The Relationship

The relationship between serum uric acid (SUA) and hypertension has been a subject of increasing interest since the 1870 discovery by Frederick Akbar Mahomed. Several epidemiological studies have shown a strong association between high SUA levels and the presence or the development of hypertension. Genetic analyses have found that xanthine oxidoreductase (XOR) genetic polymorphisms are associated with hypertension. However, genetic studies on urate transporters and Mendelian randomization studies failed to demonstrate a causal relationship between SUA and hypertension. Results from clinical trials on the role of urate-lowering therapy in the management of patients with hypertension are not uniform. Our study sought to analyze the prognostic and therapeutic role of SUA in the hypertensive disease, from uric acid (UA) biology to clinical trials on urate-lowering therapies.

Sign in / Sign up

Export Citation Format

Share Document