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Rheumatic Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
The mean serum urate level in healthy individuals is approximately 300 µmol/L in males and 240 µmol/L in females, while the saturation value of serum urate is approximately 400 µmol/L. The risk of gouty arthritis and/or renal stones increases with increasing serum urate level and with duration of hyperuricaemia.
Crystalline Arthritis
Published in Jason Liebowitz, Philip Seo, David Hellmann, Michael Zeide, Clinical Innovation in Rheumatology, 2023
In 2020, the American College of Rheumatology updated guidelines for the treatment of gout.28 The 2020 guidelines differ from earlier ones in considering costs of care and including the input of gout patients themselves. Highlights include a strong recommendation for a treat-to-target strategy. The 2020 guidelines conditionally recommend continuing ULT indefinitely, pointing to observational data that most patients will experience recurrent flares when ULT is discontinued. Additionally, the guidelines no longer specify a urate goal of less than 5 mg/dL for those with more severe disease, owing to a lack of high-quality evidence. Research supports more rapid dissolution of tophi at lower serum urates; however, the risk-benefit ratio of targeting a lower goal has not been substantiated. Dose titration, per 2020 ACR guidelines, should be on the scope of “weeks to months, not years.” This is an example of how the 2020 guidelines are less prescriptive and promote shared decision-making between patients and providers compared with prior guidelines.29
Selected topics
Published in Henry J. Woodford, Essential Geriatrics, 2022
Gout is more common in younger men than women, but affects women more frequently in older age.28 In older age it is frequently associated with diuretic use. It can also be precipitated by declining renal function or myeloproliferative disorders, and is associated with obesity and hypertension. A diet high in red meat, seafood and alcohol (especially beer) make gout more likely. Acute gout produces severe pain, reaching maximal intensity within 12 hours, with overlying erythema.29 Symptoms affecting the first tarsometaphalagneal joint are highly likely to be due to gout. Serum urate levels are not useful for confirming or excluding acute gout. After a first attack of gout the majority of people will have a further attack within one year if untreated. Chronic gout is associated with the formation of tophi (collections of monosodium urate crystals usually on the fingers, toes or elbows). Serum urate levels are often, but not always, elevated.
Lifestyle factors and comorbidities in gout patients compared to the general population in Western Sweden: results from a questionnaire study
Published in Scandinavian Journal of Rheumatology, 2022
M Dehlin, LEJM Scheepers, AJ Landgren, L Josefsson, K Svensson, LTH Jacobsson
Gout is the most common inflammatory arthritis and much is known concerning its pathogenesis (1). Hyperuricaemia, i.e. increased levels of urate in the blood, is by far the strongest risk factor for the disease. To a large extent, the risk factors for gout coincide with those for hyperuricaemia (2). Non-modifiable risk factors are increasing age, male gender, and genes. However, only 15–20% of males and females with hyperuricaemia develop gout over 30 years of follow-up (3, 4). Well-known modifiable risk factors for both gout and hyperuricaemia are obesity, physical inactivity, and dietary factors, such as excessive intake of meat, seafood, alcohol, and sugar-sweetened drinks. These risk factors are highlighted in the European League Against Rheumatism (EULAR) guidelines for the management of gout from 2016 (5), where it is stated that every person with gout should receive advice on weight loss, if appropriate, avoidance of alcohol, and regular exercise. Furthermore, smoking has been shown to decrease levels of serum urate and the risk of developing gout in men (6). A proposed mechanism that links smoking with a decreased risk of developing gout is that free radical components of cigarette smoke exert a rapid oxidative effect in the blood, which may lead to a depletion of antioxidants, including urate (6).
Inosine supplements only reach the CNS in molybdenum deficient humans and may cause astrocyte degeneration and bulbar–respiratory disease
Published in Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 2022
A 12-week pilot trial of oral inosine in ALS patients was published after the ALS untangled review (5). The rationale for the trial was that oxidative stress is implicated in the pathogenesis of ALS and inosine is metabolized to urate, and urate is a potent antioxidant. The 25 participants had a baseline serum urate level of 4.1 mg/dL. Oral inosine loading, up to 3000 mg per day, lifted this to 7–8 mg/dL over 6 weeks. These figures are consistent with only partial metabolization of inosine to urate, the remaining inosine would have reached the CNS. Three biomarkers of oxidative stress were measured, 3-nitrotyrosine, ferric-reducing antioxidant power, and glutathione. Plasma levels for the first two changed in a predictable manner in response to the urate increase, CSF levels were not determined. More significantly, urate did not trigger an increase in plasma or brain glutathione, almost as though some other factor was preventing this, for example, concurrent sulfite oxidase deficiency. SO is a Mo-dependent enzyme.
In vitro enzyme inhibition and in vivo anti-hyperuricemic potential of eugenol: an experimental approach
Published in Drug Development and Industrial Pharmacy, 2021
V. Vijeesh, A. Vysakh, Ninan Jisha, M. S. Latha
The global index of the hyperuricemia incidence has reached 1.13 billion in 2015 [16]. The incidence of hyperuricemia and its associated diseases were increased in many countries during the last decades [17]. When the serum urate levels exceed the normal threshold, it leads to the hyperuricemia [18]. Exogenous purine intake, a source of uric acid production ranges from 100 to 200 mg per day, with the majority of serum uric acid coming from endogenous sources such as nucleic acid breakdown and de novo purine production [19]. That is why the elevated levels of uric acid in an individual with preoperative condition are considered as a potential risk factor for the development of postoperative hyperuricemia linked complications [20]. Hyperuricemia is one of the signs of tumor lysis syndrome [21]. The frequent consumption of organ meat, seafood, alcohol, etc. also increases the risk of hyperuricemia condition [22]. The recent studies proposed that the fructose metabolism, high intracellular glucose and excess fat storage are positively correlated with high level of uric acid production [23–25]. Xanthine oxidase is a therapeutic target in humans because it catalyzes the conversion of purines to uric acid. The hyperuricemia condition can be induced in rat model by inhibiting the uricase enzyme. PO is a well-known uricase inhibiting agent commonly used to induce hyperuricemia condition.