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Crystalline Arthritis
Published in Jason Liebowitz, Philip Seo, David Hellmann, Michael Zeide, Clinical Innovation in Rheumatology, 2023
Hyperuricemia is primarily due to inadequate uric acid excretion in the kidneys. Several well-studied urate transporters, predominantly in the kidney (but also the gut), are responsible for uric acid handling. Genome-wide association studies (GWAS) identified SLC2A9 (encoding GLUT9), SLC22A12 (encoding URAT1), SLC17A1 (encoding NPT1), and ABCG2 as key genes. A heritability analysis of a large twin cohort reported the concordance of hyperuricemia to be 53% in monozygotic twins and 24% in dizygotic twins.5
Rheumatic Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Treatment of gout is aimed at relieving the acute synovitis with anti-inflammatory medication and preventing further crystal formation. Dietary advice for patients with hyperuricaemia is listed in Table 4.15.
Rheumatology
Published in Kaji Sritharan, Jonathan Rohrer, Alexandra C Rankin, Sachi Sivananthan, Essential Notes for Medical and Surgical Finals, 2021
Kaji Sritharan, Jonathan Rohrer, Alexandra C Rankin, Sachi Sivananthan
Causes of hyperuricaemia: decreased uric acid excretion – idiopathic (majority of cases), drugs (e.g. thiazides, ciclosporin), renal failure, alcoholincreased uric acid production – rare genetic disorders (e.g. Lesch-Nyhan syndrome) or any cause of high cell turnover (e.g. myelo- and lymphoproliferative disorders, psoriasis).
The effects of cardiometabolic factors on the association between serum uric acid and risk of all-cause mortality in adults with congestive heart failure
Published in Postgraduate Medicine, 2023
Tao Liu, Jia Song, Ronghua Zuo, Lifang Sun, Zhijian Zhu, Bing Wang, Zhigang Lu, Yesheng Pan
Furthermore, the results of the present study also found that the U-shaped relationship between SUA and all-cause mortality also exists in different age and sex subgroups. It is well known that the possible optimal level of SUA in different age groups and sexes remains unknown. The results of the present study found that the possible optimal levels of SUA in the high-age group and the low-age group were 360 umol/L and 356 umol/L, respectively, and the probable optimal levels of SUA in males and females are 378 umol/L and 360 umol/L, respectively. The optimal levels of SUA varied by age and gender. In addition, the risk of all-cause mortality among CHF populations varies by age or sex. The findings presented above might serve as a clinical reference for the primary prevention of hyperuricemia. However, study participants are all from the United States. Thus, the generalizability of the results remains to be verified in other populations. This might also be one of the limitations of the present study.
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
Hyperuricemia is characterized by the accumulation of excess amount of uric acid in the blood. Imbalance in the rate of production and excretion of uric acid results in the occurrence of numerous associated diseases such as gout, cardiovascular complications, diabetes, chronic kidney diseases, etc. [1,2]. Uric acid is the end product of purine degradation pathway, which is produced by the oxidation of hypoxanthine to xanthine and subsequently into uric acid [3]. Xanthine oxidase (XO) is the key enzyme accountable for the catalysis of uric acid production. Mitigation of hyperuricemic condition may gain a reasonable therapeutic significance in the treatment of hyperuricemia and its associated diseases. This can be achieved through inhibiting the activity of XO [4]. Allopurinol and febuxostat are the common medications used to alleviate the hyperuricemia. Unfortunately, these XO inhibitors exert severe side effects such as gastrointestinal intolerance, nausea, rash, hypersensitivity, undesirable liver, and cardiovascular function [5,6]. Hence, the search for a novel XO inhibitor with respectable efficacy and least side effect will get a great acceptance.
Limosilactobacillus fermentum JL-3 isolated from “Jiangshui” ameliorates hyperuricemia by degrading uric acid
Published in Gut Microbes, 2021
Ying Wu, Ze Ye, Pengya Feng, Rong Li, Xiao Chen, Xiaozhu Tian, Rong Han, Apurva Kakade, Pu Liu, Xiangkai Li
High levels of UA in plasma have long been associated with hyperuricemia.12 There are two ways of UA accumulation in humans. First is an endogenous buildup caused by enzyme deficiencies in the purine metabolism pathway. This deficiency in major purine metabolism enzymes leads to an increased rate of nucleic acid decomposition and UA production, which is under the control of a mechanism whereby an end product control itself by inhibiting the enzyme producing it.13 Another route of UA accumulation is through the intake and exogenous absorption of purine rich foods. A recent study showed that the intake of meat increases the risk of gout by 21%, while sea food intake increases its risk by just 7%.14 Hyperuricemia can be alleviated effectively by external interventions.15 In general, it can also be managed through the excretion of UA in large amounts by the kidneys, while only 30% of the total UA is degraded by the action of intestinal flora burden per time.13,16,17 However, the effectiveness of the intestinal flora can be greatly influenced by purine-rich foods, which may disturb the purine metabolism process, thereby elevating serum UA levels.18,19 It is thus necessary to control UA from external sources to prevent hyperuricemia.3