Uric acid and OA_Ma 2017.pdf (original) (raw)
Related papers
Molecular basis of oxidative stress in gouty arthropathy
Clinical Rheumatology, 2015
Gout is a disorder of urate metabolism in which persistent high urate levels in the extracellular fluids result in the deposition of monosodium urate (MSU) crystal in joints and periarticular tissues. In recent years, this disease represents an increasingly common health problem, so the pace of investigation in the field has accelerated tremendously. New research advances in the pathogenesis of hyperuricemia and in the understanding of how MSU crystals induce an acute gouty attack have been focused in this review on the processes of inflammation and involvement of the innate immune response; in addition, we discuss new knowledge about the role of the reactive oxygen species in establishing oxidative stress in MSU crystalinduced arthritis.
The Role of Uric Acid and Other Crystals in Osteoarthritis
Current Rheumatology Reports, 2010
Clinicians have long assumed that an association exists between crystal arthropathies and the presence of osteoarthritis (OA). However, studies establishing an independent association between calcium pyrophosphate or uric acid crystal disease and OA are sparse. Even less is known about a possible pathogenic relationship. Whereas some studies suggest that the relationships between crystals and OA may not be incidental and that crystal deposition may contribute to the onset and/or acceleration of OA joint damage, other authors have challenged this assertion. In this review, we provide an overview of past and current research elucidating the role of crystal deposition, including monosodium urate, calcium pyrophosphate, and other crystals, in OA. Given the clinical frequency of gout and that agents exist to modulate serum UA levels, special attention is given to the role of monosodium urate crystals.
New insights into the epidemiology of gout
Gout is a true crystal deposition disease caused by formation of monosodium urate crystals in joints and other tissues. It is a common inflammatory arthritis that has increased in prevalence in recent decades. Gout normally results from the interaction of genetic, constitutional and environmental risk factors. It is more common in men and strongly age related. A major determinant is the degree of elevation of uric acid levels above the saturation point for urate crystal formation, principally caused by inefficient renal urate excretion. Local joint tissue factors may influence the topography and extent of crystal deposition. Recent studies have provided information on dietary risk factors for gout: higher intakes of red meat, fructose and beer are independently associated with increased risk, whereas higher intakes of coffee, low-fat dairy products and vitamin C are associated with lower risk. Several renal urate transporters have been identified including URAT1 and SLC2A9 (GLUT9) and polymorphisms in these genes are associated with an increased risk of hyperuricaemia and gout. Many drugs influence serum uric acid levels through an effect on renal urate transport. Comorbidities, including the metabolic syndrome and impaired renal function are common in gout patients. The usual initial presentation of gout is with rapidly developing acute inflammatory monoarthritis, typically affecting the first MTP joint. If left untreated it may progress with recurrent acute attacks and eventual development of chronic symptoms and joint damage. New knowledge of the modifiable risk factors for gout can be integrated into the management strategy to optimize long-term patient outcomes.
Revista de Chimie
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, havin...
Both gout and osteoarthritis (OA) are common forms of arthritis that inflict a huge burden to an aging population with the increasing prevalence of obesity. Clinicians have long observed the link between these two conditions. In this review, we summarize the evidence from epidemiologic and immunological studies that described the possible relationship between the two conditions. The recent new understanding on monosodium uric acid crystal-induced inflammation has given insight into probable shared pathogenesis pathways for both conditions. We describe the potential therapeutic implications, particularly regarding the possibility of repurposing traditional gout medications for use in OA.
Gout: Joints and beyond, epidemiology, clinical features, treatment and co-morbidities
Maturitas, 2014
Gout is a common inflammatory arthritis precipitated by an inflammatory reaction to urate crystals in the joint. Gout is increasingly being recognised as a disease primarily of urate overload with arthritis being a consequence of this pathological accumulation. It is associated with a number of important co-morbidities including chronic kidney disease, obesity, diabetes and cardiovascular disease.
Treating to target: a strategy to cure gout
2009
Acute gout attacks and the long-term complications of gout are associated with the deposition of monosodium urate (MSU) monohydrate crystals in the joints and soft tissues, causing acute and chronic inflammation. The aim of long-term treatment is to reduce the serum urate (sUA) level to 6 mg/dl (4360 mol/l), below the saturation point of MSU, so that new crystals cannot form and existing crystals are dissolved. Serial joint aspiration studies confirmed the disappearance of crystals with effective urate-lowering therapy. There is good evidence that achieving sUA <6 mg/dl (360 mol/l) results in freedom from acute gout attacks, and shrinkage and eventual disappearance of tophi. Gout patients must be informed about their diagnosis and educated about gout management including the importance of compliance with long-term treatment. Patients starting urate-lowering therapy need to understand the importance of prophylactic therapy with colchicine or NSAIDs to reduce the risk of 'mobilization flares' in the first few months. In the long term, reduction in the sUA below the target level will result in gout being effectively cured.