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Crystalline Arthritis
Published in Jason Liebowitz, Philip Seo, David Hellmann, Michael Zeide, Clinical Innovation in Rheumatology, 2023
Uric acid is a human end product of purine degradation derived from exogenous intake, cell turnover, and de novo synthesis. The 2020 ACR gout treatment guidelines recommend limiting alcohol, purines, and high-fructose corn syrup intake as an adjuvant to ULT. However, new studies highlight the pitfalls of overly restricting individual macronutrients. Yokose et al. reason that excessively restricting purine-rich foods may lead to a compensatory increase in carbohydrate and fat intake.19 This, in turn, results in increased insulin resistance, elevated cholesterol levels, and hypertension, contributing to increased cardiovascular (CV) risk.
Nonalcoholic Fatty Liver Disease
Published in Nicole M. Farmer, Andres Victor Ardisson Korat, Cooking for Health and Disease Prevention, 2022
In addition to fructokinase, a second mechanism by which fructose may contribute to NAFLD is that fructose metabolism may raise uric acid levels (Lanaspa et al. 2012). Foods high in fructose can increase uric acid levels in the liver, increasing oxidative stress, which may lead to gout, kidney disease, and metabolic disease. Uric acid levels are a predictor of NAFLD. Reducing the amount of fructose has shown to reduce uric acid levels and the impact on the body (Jensen et al. 2018).
Lesch–Nyhan disease and variants
Published in William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop, Atlas of Inherited Metabolic Diseases, 2020
William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop
Allopurinol has been effective in reducing concentrations of uric acid and alleviating all of its direct clinical consequences. Doses of 200–400 mg/day lead promptly to normal plasma concentrations. Calculi and tophi are prevented or resorbed as concentrations of uric acid and in blood and urine fall. Nephropathy and arthritis are prevented. The total production of purine does not change; concentrations of xanthine and hypoxanthine increase. Some patients develop xanthine calculi. Determination of the levels of these oxypurines is very useful in providing the optimal dose of allopurinol. We aim to maximize the content of hypoxanthine without running the risk of oxypurinol lithiasis. It has become clear that doses required to accomplish this are highly individual and usually larger than employed in other diseases. An initial dose of 15–20 mg/kg is followed by assessment of concentrations of all of the oxypurines of the urine: uric acid; xanthine and hypoxanthine. Dosage is then modified, usually increased, to yield maximal concentrations of hypoxanthine which is soluble and minimal levels of xanthine, which causes the calculi in treated patients.
Appraisal of anti-gout potential of colchicine-loaded chitosan nanoparticle gel in uric acid-induced gout animal model
Published in Archives of Physiology and Biochemistry, 2022
Poonam Parashar, Ifrah Mazhar, Jovita Kanoujia, Abhishek Yadav, Pranesh Kumar, Shubhini A. Saraf, Sudipta Saha
Further, to prove the greater efficacy of CHNPgel over other treatments, estimation of the uric acid concentration in synovial fluid of gout induced animals was executed. The data presented in Figure 5, revealed similar results as observed with knee diameter. Treated groups showed significantly lower concentrations of uric acid at the end of study. Group IV (CHNPgel) exhibited normal uric acid levels at the end of study (45th day), likewise equivalent to Group I (normal control). However, uric acid level of group III (conventional gel treated) was found to be 2.28 ± 0.03 mg/dl, which was significantly higher than formulation treated group (1.79 ± 0.04 mg/dl), demonstrating the enhanced therapeutic efficacy of CHNPgel in treating gout and gout related symptoms. Nevertheless, a significant reduction in uric acid levels (p < .05) was observed in treated groups when compared with toxic control after the treatment period of 28 days, where also CHNPgel displayed it is a lead over conventional gel.
Inosine induces acute hyperuricaemia in rhesus monkey (Macaca mulatta) as a potential disease animal model
Published in Pharmaceutical Biology, 2021
Dong-hong Tang, Chen-yun Wang, Xi Huang, Hong-kun Yi, Zhe-li Li, Kai-li Ma, You-song Ye, Jian-wen Zhang
Hyperuricaemia (HUA) occurs because of purine metabolism aberrations and is typically characterized by increased uric acid formation or reduced uric acid excretion. HUA is defined as a serum urate concentration that allows urate saturation in bodily fluids (>7.0 mg/dL) (Roddy and Choi 2014). The incidence of HUA, which has currently increased (Roddy and Choi 2014), is approximately 13.3% (19.4% in men and 7.9% in women) in the Chinese population (Liu et al. 2015). Although the condition is more common in middle-aged or older men and postmenopausal women, the age at disease onset has been decreasing in recent years (Liu et al. 2015). Uric acid increases the risk of gout and cardiovascular disorders, nephrolithiasis, diabetes, obesity, dyslipidaemia (Feig 2014; Abeles 2015), chronic kidney diseases and metabolic syndromes (Feig 2014; Abeles 2015; Hahn et al. 2017). Therefore, a reliable animal model is urgently needed to screen drugs against HUA and investigate its pathophysiology (Zhu et al. 2017).
ABCG2 as a therapeutic target candidate for gout
Published in Expert Opinion on Therapeutic Targets, 2018
Kyoko Fujita, Kimiyoshi Ichida
Uric acid is the end product of purine metabolism in humans. In the mammalian lineage, there appears to have been concerted selection toward decreased function of uricase, the enzyme that metabolizes uric acid, culminating in the complete loss of uricase function in humans and other great apes. It has been suggested that the advantage of higher serum uric acid levels stems from the antioxidant activity of this compound [1,2]. However, an abnormally high concentration of uric acid in the serum, i.e. hyperuricemia which affects 43 million Americans, is the main risk factor for the onset of gout (almost 10 million in the U.S.A) [3–5]. Clinical hyperuricemia, causes gout and urolithiasis as a direct result of the precipitation of uric acid, in the form of monosodium urate crystals, in either synovial fluid (gouty arthritis) or the kidney tubule (kidney stones). Besides gout, hyperuricemia has also been linked to hypertension, chronic kidney disease, atherosclerosis, diabetes, and metabolic syndrome [6–9]. Although hyperuricemia is largely determined by environmental factors, such as alcohol consumption, diet, and lifestyle, it is also associated with genetic influences.