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Gout
Published in Charles Theisler, Adjuvant Medical Care, 2023
Gout, or acute gouty arthritis, typically presents as an excruciating attack of pain, usually in a single joint of the foot or ankle. Gout is the most common inflammatory arthritis of men and is increasing in prevalence.1 Gout is associated with an overproduction (10% of patients) or decreased renal excretion (90% of patients) of purines. Because the end product of purine metabolism is uric acid, gout is characterized by elevated blood uric acid levels.2 Needle-like uric acid crystals form in joint spaces resulting in episodes of sudden excruciating pain, swelling, redness, warmth, and tenderness. Chronic inflammation and clumps of crystals (tophi) can lead to permanent joint damage, deformity, and stiffness. Tophi can also form in white chalky nodules on the helix of the ear. These tophi typically become painful before or during gout attacks.
Paper 4
Published in Aalia Khan, Ramsey Jabbour, Almas Rehman, nMRCGP Applied Knowledge Test Study Guide, 2021
Aalia Khan, Ramsey Jabbour, Almas Rehman
Other drugs which may induce hyperuricaemia include: cytotoxics, pyrazinamide and ethambutol. Characterised but not always defined by hyperuricaemia, gout results from a disorder of purine metabolism, which causes urate crystal deposition and painful synovitis. Cartilage damage may occur and large urate deposits are known as tophi. Acute attacks are treated by rest, fluids, stopping any causative drugs and administering NSAIDs, e.g. diclofenac; however, steroids may be necessary. Maintenance treatment includes lifestyle modification, e.g. reducing alcohol intake and making dietary changes, and uricosuric drugs, e.g. allopurinol, which are not effective acutely.
Structural Organization of the Liver
Published in Robert G. Meeks, Steadman D. Harrison, Richard J. Bull, Hepatotoxicology, 2020
Functionally, peroxisomes are specialized for performing oxidative reactions using molecular oxygen. As stated above, they generate hydrogen peroxide, which they both use and destroy by means of the catalase they contain. They are involved in detoxifying various molecules; for example, oxidation of ethanol and acetaldehyde. It is estimated that peroxisomes normally account for about 10% of the total oxygen uptake of the liver. In addition to detoxification, peroxisomes catalize the (3-oxidation of fatty acid to acetyl CoA which can be utilized by the mitochondria (to feed the citric acid cycle) or by biosynthetic reactions elsewhere. Peroxisomes are also thought to be involved in purine metabolism. (deDuve and Baudhuin, 1966; Lazarow, 1988).
Advances in pharmacotherapies for hyperuricemia
Published in Expert Opinion on Pharmacotherapy, 2023
Federica Piani, Davide Agnoletti, Claudio Borghi
Uric acid is the end product of endogenous and exogenous purine metabolism. It is both metabolized and excreted, although humans have lost the capacity to metabolize uric acid into 5-hydroxyisourate and allantoin by uricase or urate oxidase. Two-thirds of serum uric acid is excreted by the kidneys and 1/3 by the gut, with the normal renal fractional excretion being about 10% [1]. Although the causality of the association between uric acid and cardiovascular disease remains partially unconfirmed, epidemiological, and genetic studies have shown an independent role of uric acid in the pathogenesis and progression of cardiovascular risk factors and cardiovascular diseases [2,3]. Several mechanisms have been proposed to explain this association, including oxidative stress, systemic inflammation, endothelial dysfunction, and insulin resistance [3,4].
Development of quantitative assay for simultaneous measurement of purine metabolites and creatinine in biobanked urine by liquid chromatography-tandem mass spectrometry
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2022
Dmitri Svistounov, Marit D. Solbu, Trond G. Jenssen, Ulla Dorte Mathisen, Terkel Hansen, Katja Benedikte Prestø Elgstøen, Svetlana N. Zykova
Purine metabolism is essential for all known terran creatures defined as living (within the current materialistic life science paradigm) [1], which also includes non-cellular forms, such as viruses and viroids, but excludes prions. Therefore an assay determining several key metabolites in purine pathway could find an application in many areas of biology, particularly medicine. Uric acid (UA) is the break-down product of purines from DNA, RNA and nucleotides, such as GTP, cGMP, ATP, cAMP, NADH and coenzyme A. During purine catabolism, adenosine, inosine and guanine are converted to UA via precursors xanthine and hypoxanthine (Figure 1). UA can be further hydrolyzed by the enzyme uricase to a highly soluble excretory product allantoin in all mammals except humans and higher apes. Allantoin can still be measured in the circulation of humans where it is believed to represent a non-enzymatic oxidation product of UA which renders it a marker of oxidative stress and ageing [2].
Purine metabolites can indicate diabetes progression
Published in Archives of Physiology and Biochemistry, 2022
Yogaraje Gowda C. Varadaiah, Senthilkumar Sivanesan, Shivananda B. Nayak, Kashinath R. Thirumalarao
Purines are fundamental parts of nucleotides and nucleic acids, playing numerous important roles in human physiology, disturbing tissue function, cell integrity and oxidation. Purine metabolism comprises of synthesis and degradation of purine nucleotides and regulates the level of the adenylate and guanylate pool (Dudzinska et al. 2010). In this way, it is responsible for the complete concentrations of intracellular ATP and GTP. In purine catabolism, their monophosphate forms are transformed to inosine and guanosine; purine nucleoside phosphorylase changes them to hypoxanthine and guanine, respectively (Figure 1). Xanthine oxidase (XO) and guanine deaminase are the enzymes that convert them to xanthine which is oxidized by XO to uric acid (Maiuolo et al. 2016). Serum uric acid, an end product of purine metabolism, has been shown to be associated with an increased risk of hypertension, cardiovascular disease, and chronic kidney disease. Hyperuricemia raises the risk of peripheral arterial disease, insulin resistance, and components of the metabolic syndrome (Ekpenyong and Akpan 2014). In diabetes, hyperuricemia has been associated with both micro and macrovascular complications. It is well known that purine metabolic pathway may be strongly linked with the development of diabetic microvascular complications (Xia et al. 2014).