Journal articles: 'Uric acid increases'

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Menon, R. K., D. P. Mikhailidis, J. L. Bell, P. B. Kernoff, and P. Dandona. "Warfarin administration increases uric acid concentrations in plasma." Clinical Chemistry 32, no. 8 (August 1, 1986): 1557–59. http://dx.doi.org/10.1093/clinchem/32.8.1557.

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Abstract The effect of warfarin administration on plasma uric acid was investigated. A representative sample of patients on long-term warfarin treatment had a significantly higher concentration of uric acid in plasma than did age-matched patients with comparable plasma urea concentrations who were not taking warfarin. In women, this association was observed only in patients with normal values for plasma urea, not in those with high values. In contrast, in men this association was present in both groups (normal and high plasma urea). In a longitudinal study involving patients, their plasma uric acid significantly increased after warfarin administration. There was no significant change in the renal clearance of uric acid after a single dose of warfarin in normal, healthy volunteers; this contrasts with the increase observed with other coumarin anticoagulants. Our findings suggest that the increase in plasma uric acid noted with warfarin administration is probably due to an increase in uric acid production and may predispose to gout those patients who are on long-term therapy with warfarin.

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Kakutani-Hatayama, Miki, Manabu Kadoya, Hirokazu Okazaki, Masafumi Kurajoh, Takuhito Shoji, Hidenori Koyama, Zenta Tsutsumi, Yuji Moriwaki, Mitsuyoshi Namba, and Tetsuya Yamamoto. "Nonpharmacological Management of Gout and Hyperuricemia: Hints for Better Lifestyle." American Journal of Lifestyle Medicine 11, no. 4 (September 2, 2015): 321–29. http://dx.doi.org/10.1177/1559827615601973.

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We reviewed lifestyle factors that influence serum uric acid levels and risk of gout flare, and how to improve their deleterious effects. Since obesity increases uric acid and weight gain increases gout risk, weight reduction by daily exercise and limiting intake of excess calories is recommended. However, strenuous exercise, which causes adenine nucleotide degradation; starvation, which decreases uric acid excretion; and dehydration may raise the level of uric acid in serum and trigger gout. Increased intake of purine-rich foods, such as meat and seafood, raise the level of uric acid in serum and is associated with increased risk of gout, whereas dairy products, especially low-fat types, are associated with a lower risk of gout. Also, heavy alcohol drinking raises the uric acid level and increases the risk of gout through adenine nucleotide degradation and lactate production. Sweet fruits and soft drinks containing fructose should be moderated, since fructose may raise uric acid and increase gout risk through uric acid production and/or decreased excretion. On the other hand, the Mediterranean diet is recommended for gout patients, since it may also help prevent hyperuricemia. Furthermore, coffee and vitamin C supplementation could be considered as preventive measures, as those can lower serum uric acid levels as well as the risk of gout.

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Masuda, Akira, Takehisa Asahi, Midori Sakamaki, Katsuhito Nakamaru, Koki Hirota, and Yusuke Ito. "Uric Acid Excretion Increases During Propofol Anesthesia." Anesthesia & Analgesia 85, no. 1 (July 1997): 144–48. http://dx.doi.org/10.1097/00000539-199707000-00026.

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Masuda, Akira, Takehisa Asahi, Midori Sakamaki, Katsuhito Nakamaru, Koki Hirota, and Yusuke Ito. "Uric Acid Excretion Increases During Propofol Anesthesia." Anesthesia & Analgesia 85, no. 1 (July 1997): 144–48. http://dx.doi.org/10.1213/00000539-199707000-00026.

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Balasubramanian, T. "Uric Acid or 1-Methyl Uric Acid in the Urinary Bladder Increases Serum Glucose, Insulin, True Triglyceride, and Total Cholesterol Levels in Wistar Rats." Scientific World JOURNAL 3 (2003): 930–36. http://dx.doi.org/10.1100/tsw.2003.90.

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In animals deprived of food for a long period, a drop in the fat mass below 5% of the total body mass results in an increase in blood glucocorticoids and uric acid levels, followed by foraging activity. Since the glucocorticoids increase the uric acid excretion, an increase in the level of uric acid in the bladder urine could be the signal for this feeding behaviour and subsequent fat storage. Accumulation of fat is associated with hyperglycaemia, hyperinsulinaemia, hyperlipidaemia, and hypercholesterolaemia as seen in the metabolic syndrome or hibernation. It is hypothesized that uric acid or its structurally related compound, 1-methyl uric acid (one of the metabolites of the methyl xanthines namely caffeine, theophylline, and theobromine present in coffee, tea, cocoa, and some drugs), can act on the urinary bladder mucosa and increases the blood glucose, insulin, triglyceride, and cholesterol levels. In rats, perfusion of the urinary bladder with saturated aqueous solution of uric acid or 1-methyl uric acid results in a significant increase in the serum levels of glucose, insulin, true triglyceride, and total cholesterol in comparison with perfusion of the bladder with distilled water at 20, 40, and 80 min. The uric acid or the 1-methyl uric acid acts on the urinary bladder mucosa and increases the serum glucose, insulin, true triglyceride, and total cholesterol levels.

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Sayfutdinova, L. N., and M. A. Derkho. "BLOOD PROTEINS AND THEIR INFORMATIVENESS IN ASSESSING THE ADAPTIVE RESOURCES OF CHICKENS UNDER TECHNOLOGICAL STRESS." Scientific Notes Kazan Bauman State Academy of Veterinary Medicine 245, no. 1 (March 1, 2021): 169–76. http://dx.doi.org/10.31588/2413-4201-1883-245-1-169-176.

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In the body of chickens, when exposed to the technological factor (the density of birds in the cage), a stress reaction developed as a result of activation of the hypathalamic-pituitary-adrenal system. The response and state of the neuroendocrine pathway is associated with the magnitude of the technological stress factor. When it is increased by 1.50 times, the maximum changes in the body of chickens are detected 4 hours after the start of the experiment. At the same time, the level of corticosterone and cortisol in the blood of birds increases by 3.42 and 2.99 times, increasing the rate of catabolic reactions in protein metabolism. Therefore, the amount of total protein in the blood-stream of chickens increases by 34.32 %, albumins by 26.74 %, urea and uric acid by 2.07 and 2.29 times, and the activity of AsAT and AlAT increases by 2.15 and 4.53 times (p<0.05). The catabolic processes involve mainly blood albumins, whose nitrogen is used for the synthesis of uric acid. This is evidenced by a decrease in the value of Alb/uric acid by 42.74 % (p<0.05). With an increase in the density of birds in the cage by 2 times, the reaction of the GGNS more pronounced and long-lasting. Although the maximum changes are registered 2 hours after the initiation of stress, they per-sist throughout the study period. At the same time, the level of corticosterone and cortisol in the blood of chickens increases by 4.17 and 3.67 times, the concentration of total protein by 39.44 %, both due to albumins (by 41.78 %) and globulins (by 37.82 %); the increase in the amount of urea and uric acid is 2.18 and 2.45 times. Both albumins and blood globulins are subjected to oxidative decomposition, which determines the decrease in the ratio TP/Urea, Alb/urea at, TP/uric acid and Alb/uric acid at 35.72-43.18 %. At the same time, the activity of AlAT increases by 7.56 times and AsAT by 2.21 times, determining the predominant use of carbon residues of free amino acids in the processes of gluconeogenesis (AlAT/AsAT increased by 3.75 times).

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Mass, Baba, Brea Nance, and Saroja Voruganti. "Fructose Increases the Expression of Uric Acid-Induced Oxidative Stress Genes, NOX4 and FOXO3, in Cultured HepG2 Cells." Current Developments in Nutrition 4, Supplement_2 (May 29, 2020): 1266. http://dx.doi.org/10.1093/cdn/nzaa058_024.

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Abstract Objectives Uric acid is the final product of purine metabolism. The role of uric acid in oxidative stress is not clear. Studies have shown uric acid as antioxidant as well as pro-oxidant. High fructose sugar consumption increases uric acid levels by ATP depletion and the subsequent formation AMP which is a uric acid precursor. In our study, we investigated the effect of dose dependent treatments of fructose, uric acid, or a combination of both uric acid and fructose on expression of oxidative stress-related genes, mainly NADPH oxidase 4 (NOX4), superoxide dismutase 3 (SOD3), Forkhead Box O3 (FOXO3) and xanthine dehydrogenase (XDH) in cultured Hep G2 cells. Methods Human hepatocellular carcinoma [HEPG2] (ATCC HB8065) cells were treated with serum-free medium containing either 10 mM fructose, soluble uric acid (0.25 mM, 0.5 mM, or 0.75 mM), or a combination of fructose and uric acid. The cells were collected at the end of each incubation period (30 min, 2 and 24 hours) to extract total RNA. cDNA was synthesized from the extracted RNA. TaqMan assays were designed for use on real-rime PCR platform (QuantStudio 12 K Flex). TaqMan open array primers were custom-made by Thermo Fisher Scientific. Target quantification values were normalized against GAPDH levels and a combination of students’ t-test and ANOVA were applied. Results Soluble uric acid, either by itself or in conjunction with fructose, did not change the expression of the tested genes at 30 minutes or 2 hours. However, after 24 hours of incubation, uric acid increased the expression of NOX4 by 2 and FOXO3 by 1.5-fold (p < 0.05) whereas uric acid plus fructose-containing media increased the expression of NOX4 by 3.5 and FOXO3 by 2-fold (p < 0.05) after 24 hours of incubation as compared to control. No treatment differences were observed in the expression of SOD3. Conclusions These findings demonstrate that fructose increases the expression of uric acid-induced oxidative stress related genes. Funding Sources None.

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Karwur, Ferry Fredy, and Dwi Rahayu Pujiastuti. "Review Article: URIC ACID HOMEOSTASIS AND DISTURBANCES." Folia Medica Indonesiana 53, no. 4 (December 28, 2017): 292. http://dx.doi.org/10.20473/fmi.v53i4.7164.

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This review examined the homeostasis of uric acid in human body and analyzed recent studies of the affecting major variables. Normal uric acid concentration in male is 3.5-7.2 mg/dL and in female is 2.6-6 mg/dL. Daily turnover of normal uric acid ranges from 498-1392 mg/day, miscible pool is 767-1650 mg, reabsorption is 8064 mg/day, renal excretion is 262-620 mg/day and intestine 186-313 mg/day. The dynamics of uric acid is influenced by factors of food, drink, age, history of disease, and genetic. High purine dietary consumption increases blood uric acid by 1-2 mg/dL, 213-290 g/day fructose drinks increases 0.52-1.7 mg/dL, 1.5 g/kgBW sucrose increases 0.61 mg/dL, and 10-20 ml/kgBW beer increases 0.50-0.92 mg/dL. The ABCG2 gene plays a role in bringing uric acid out of the body by 114.31-162.73 mg/dL, SLC2A9 of 5.43-20.17 mg/dL, and SLC22A12 of 5.77-6.71 mg/dL. The data described the homeostasis of uric acid and the magnitude of the impact of environmental (consumption of food, beverages, and lifestyle) and genetic factors. Understanding uric acid homeostasis and its disturbances is important in managing diseases as a consequence of hyperuricemia and hypouryscemia

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Pandey, Rachana, Sanjaya Humagain, Prabodh Risal, Rahul Kumar Yadav, and Buddhi Raj Pokhrel. "Association between Serum Uric Acid and Blood Glucose Level in Diabetic and Non-diabetic Patients." Nepal Medical College Journal 24, no. 4 (December 23, 2022): 271–75. http://dx.doi.org/10.3126/nmcj.v24i4.50576.

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Uric acid increases insulin resistance; likewise, hyperinsulinemia increases uric acid concentration, and both are global health problems. This study is conducted to find the association between serum uric acid and blood glucose level. This was a cross-sectional study conducted in the Department of Biochemistry and Internal Medicine at Dhulikhel Hospital, Nepal, for a duration of six months (September 2021 - February 2022). A total of 130 diabetic patients who consented were compared with 130 non-diabetics by using non-probability convenient sampling technique. Ethical clearance was taken from the Institutional Review Committee-Kathmandu University School of Medical Sciences. Venous blood was collected and fasting blood glucose, post-prandial blood glucose, and serum uric acid were measured. Data were analyzed in the Statistical Package for Social version 16.0. Analytical data were compared using Mann Whitney U test, and Spearman correlation was performed to correlate numerical parameters. Statistical significance was defined as a two-sided p-value of less than 0.05. The median of serum uric acid level was significantly higher in diabetics than non-diabetics; the level of fasting and post-prandial blood glucose positively correlated with serum uric acid (p<0.05). Hyperuricemia was more in diabetics than non-diabetics (p<0.05). Serum uric acid level increased with the increase in age and duration of diabetes.

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Liu, S., and J. N. Miner. "THU0534 Skipping Breakfast Increases Serum Uric Acid Levels." Annals of the Rheumatic Diseases 75, Suppl 2 (June 2016): 385.1–385. http://dx.doi.org/10.1136/annrheumdis-2016-eular.1792.

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Sodhi, Komal, Jordan Hilgefort, George Banks, Chelsea Gilliam, Sarah Stevens, Hayden A. Ansinelli, Morghan Getty, Nader G. Abraham, Joseph I. Shapiro, and Zeid Khitan. "Uric Acid-Induced Adipocyte Dysfunction Is Attenuated by HO-1 Upregulation: Potential Role of Antioxidant Therapy to Target Obesity." Stem Cells International 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/8197325.

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Increased uric acid levels have been implicated in the pathogenesis of metabolic syndrome. To examine the mechanisms by which this occurs, we hypothesized that an increase in heme oxygenase 1, a potent antioxidant gene, will decrease uric acid levels and adipocyte dysfunction via suppression of ROS and xanthine oxidase (XO) levels. We examined the effect of uric acid on adipogenesis in human mesenchymal stem cells (MSCs) in the presence and absence of cobalt protoporphyrin (CoPP), an HO-1 inducer, and tin mesoporphyrin (SnMP), an HO activity inhibitor. Uric acid increased adipogenesis by increasing NADPH oxidase expression and elevation in the adipogenesis markers C/EBPα, PPARγ, and Mest, while decreasing small lipid droplets and Wnt10b levels. We treated MSCs with fructose, a fuel source that increases uric acid levels. Our results showed that fructose increased XO expression as compared to the control and concomitant treatment with CoPP significantly decreased XO expression and uric acid levels. These beneficial effects of CoPP were reversed by SnMP, supporting a role for HO activity in mediating these effects. These findings demonstrate that increased levels of HO-1 appear crucial in modulating the phenotype of adipocytes exposed to uric acid and in downregulating XO and NADPH oxidase levels.

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Yang, Zhou, Wang Xiaohua, Jiang Lei, Tan Ruoyun, Xiong Mingxia, He Weichun, Fang Li, Wen Ping, and Yang Junwei. "Uric acid increases fibronectin synthesis through upregulation of lysyl oxidase expression in rat renal tubular epithelial cells." American Journal of Physiology-Renal Physiology 299, no. 2 (August 2010): F336—F346. http://dx.doi.org/10.1152/ajprenal.00053.2010.

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Urate is produced as the major end product of purine metabolism. In the last decade, the incidence of hyperuricemia increased markedly, and similar trends in the epidemiology of metabolic syndrome have been observed. Hyperuricemia is associated with renal disease, and recent studies have reported that mild hyperuricemia results in hypertension, intrarenal vascular disease, and renal injury. This has led to the hypothesis that uric acid may contribute to renal fibrosis and progressive renal disease. Our purpose was to investigate the relationship between uric acid and renal tubular injury. We applied the method of intraperitoneal injection of uric acid to generate the hyperuricemic mouse model. Compared with the saline injection group, the expression of lysyl oxidase (LOX) and fibronectin in kidneys was increased significantly in hyperuricemic groups. In vitro, uric acid significantly induced NRK-52E cells to express the ECM marker fibronectin, as well as LOX, which plays a pivotal role in ECM maturation, in a time- and dose-dependent manner. Upregulation of the urate transporter URAT1, which is located in the apical membrane of proximal tubules, sensitized the uric acid-induced fibronectin and LOX induction, while both knocking down URAT1 expression in tubular epithelial cells by RNA interference and inhibiting URAT1 function pharmacologically attenuated LOX and fibronectin expression. Furthermore, knockdown of LOX expression by a small interfering RNA strategy led to a decrease in fibronectin abundance induced by uric acid treatment. In addition, evidence of a uric acid-induced activation of the NF-κB signaling cascade was observed. Our findings highlight a need for carefully reevaluating our previous view on the pathological roles of hyperuricemia in the kidney and nephropathy induced by uric acid in clinical practice.

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Atıl, Avcı, and Avcı Deniz. "Could be serum uric acid a risk factor for thrombosis and/or uveitis in Behcet’s disease?" Vascular 26, no. 4 (January 23, 2018): 378–86. http://dx.doi.org/10.1177/1708538117742831.

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Introduction Serum uric acid level increases in many inflammatory conditions. Uric acid triggers the vascular inflammation and artery damage, which causes to an increased risk of endothelial dysfunction and atherosclerosis. It is not clear in the literature whether uric acid contributes to uveitis by similar mechanisms. We investigated whether uric acid level increases in Behcet’s disease patients with thrombosis or anterior uveitis. Patients and methods We reviewed the medical records of 914 Behcet’s disease. After screening for exclusion criteria, there were 50 Behcet’s disease patients with thrombotic complication and as the control group 202 BD patients without any vascular complication were included to the study. In the Anterior uveitis group, there were 53 Behcet’s disease patients. The Control group consisted of 39 Behçet’s disease patients without eye findings. Results Mean uric acid value was 4.96 ± 1.06 mg/dl in Behcet’s disease patients with thrombosis whereas 4.08 ± 0.94 mg/dl in controls, indicating a significant difference ( p < 0.001). There was no significant difference between the mean ages of the patients in both groups. The mean age of the BD group without eye findings was 39.31 ± 10.47 years and that of the Behcet’s disease with Anterior Uveitis group was 37.72 ± 9.65 years ( p = 0.453). The mean serum UA in the BD group without eye findings was 4.21 ± 1.21 mg/dl, while in the BD with Anterior Uveitis group it was 4.57 ± 1.37 mg/dl ( p = 0.201). Conclusion The extent of increase in uric acid level was greater in Behcet’s disease patients that have a thrombotic complication compared to those without thrombotic complication. Uric acid seems to play a role in the pathogenesis of thrombosis. It is concluded that the elevation of serum uric acid level in patients with anterior uveitis with Behcet’s disease is not statistically significant.

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K. McMullen, Michael. "Fructose Increases Uric Acid Contributing to Metabolic Syndrome - Herbal, Nutritional and Dietary Strategies to Reduce Uric Acid." OBM Integrative and Complementary Medicine 3, no. 3 (September 28, 2018): 1. http://dx.doi.org/10.21926/obm.icm.1803022.

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Ma, Zhao, Li-hui Long, Jing Liu, and Yong-xiao Cao. "Montmorillonite adsorbs uric acid and increases the excretion of uric acid from the intestinal tract in mice." Journal of Pharmacy and Pharmacology 61, no. 11 (November 2009): 1499–504. http://dx.doi.org/10.1211/jpp.61.11.0009.

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Ma, Zhao, Li-hui Long, Jing Liu, and Yong-xiao Cao. "Montmorillonite adsorbs uric acid and increases the excretion of uric acid from the intestinal tract in mice." Journal of Pharmacy and Pharmacology 61, no. 11 (November 1, 2009): 1499–504. http://dx.doi.org/10.1211/jpp/61.11.0009.

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Mizuno, Shoichi, Masako Tomita, and Takashi Murayama. "Serum uric acid increases after smoking cessation (Longitudinal study)." Gout and Nucleic Acid Metabolism 30, no. 2 (2006): 217–23. http://dx.doi.org/10.6032/gnam1999.30.2_217.

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Sloop, Gregory D., Jessica K. Bialczak, Joseph J. Weidman, and J. A. St. Cyr. "Uric acid increases erythrocyte aggregation: Implications for cardiovascular disease." Clinical Hemorheology and Microcirculation 63, no. 4 (October 5, 2016): 349–59. http://dx.doi.org/10.3233/ch-152023.

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Obermayr, Rudolf P., Christian Temml, Georg Gutjahr, Maarten Knechtelsdorfer, Rainer Oberbauer, and Renate Klauser-Braun. "Elevated Uric Acid Increases the Risk for Kidney Disease." Journal of the American Society of Nephrology 19, no. 12 (September 17, 2008): 2407–13. http://dx.doi.org/10.1681/asn.2008010080.

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Elena, Irene Maria, Marshell Tendean, El Nissi, and Guntur Darmawan. "Hyperuricemia of The Pregnancy and Gestasional Diabetes." Jurnal Kedokteran Meditek 25, no. 3 (December 19, 2019): 118–21. http://dx.doi.org/10.36452/jkdoktmeditek.v25i3.1776.

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This review aims to determine the metabolic effect of hyperuricemia in pregnant woman, especially those with gestational diabetes mellitus (GDM). In women, the serum uric acid level is lower compared to men of similar age. The value is related to higher estrogen concentration to increase uric acid clearance. Hyperuricemia already established as independent risk factors for metabolic syndrome and cardiovascular disease (CVD) as well as type 2 Diabetes Mellitus (DM). Asymptomatic hyperuricemia in non-pregnant adult women will increase insulin resistance due to oxidative stress, and production of inflammatory cytokine (tumor necrosis factor-a), which inevitably increases blood sugar level. Uric acid level and serum creatinine is lower in normal pregnancy due to increased renal clearance and the uricosuric effect of estrogen. Hyperuricemia is one of the contributing factors associated with insulin resistance among pregnancy instead direct effect of placental hormones. Earlier in the first trimester of pregnancy, the risk for GDM is increased. However, the causal effect of uric acid levels on DM still requires further study .

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Clark, M. G., S. M. Richards, M. Hettiarachchi, J. M. Ye, G. J. Appleby, S. Rattigan, and E. Q. Colquhoun. "Release of purine and pyrimidine nucleosides and their catabolites from the perfused rat hindlimb in response to noradrenaline, vasopressin, angiotensin II and sciatic-nerve stimulation." Biochemical Journal 266, no. 3 (March 15, 1990): 765–70. http://dx.doi.org/10.1042/bj2660765.

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Uric acid and uracil were released at constant rates (0.95 and 0.4 nmol/min per g respectively) by the perfused rat hindlimb. Noradrenaline, vasopressin or angiotensin II further increased the release of these substances 2-5-fold, coinciding with increases in both perfusion pressure (vasoconstriction) and O2 uptake. The hindlimb also released, but in lesser amounts, uridine, hypoxanthine, xanthine, inosine and guanosine, and all but hypoxanthine and guanosine were increased during intense vasoconstriction. Uric acid and uracil releases were increased by noradrenaline in a dose-dependent manner. However, the release of these substances did not fully correspond with the dose-dependent increase in O2 uptake and perfusion pressure, where changes in the latter occurred at lower doses of noradrenaline. Sciatic-nerve stimulation (skeletal-muscle contraction) did not increase the release of uracil, uric acid or uridine, but instead increased the release of inosine (7-fold) and hypoxanthine (2-fold). Since the UTP content as well as the UTP/ATP ratio are higher in smooth muscle than in skeletal muscle, it is proposed that release of uric acid and uracil arises from increased metabolism of the respective adenosine and uridine nucleotides during intense constriction of smooth muscle.

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Sofiana, Liena, Arfiani Nur Khusna, and Righa Pradana. "Blood glucose and uric acid increases the risk of hypertension in elderly." International Journal Of Community Medicine And Public Health 6, no. 11 (October 24, 2019): 4706. http://dx.doi.org/10.18203/2394-6040.ijcmph20195043.

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Background: Hypertension is still a big challenge in Indonesia. Survey data shows that Yogyakarta province is included in the top five provinces with the most cases of hypertension with a number of 35.8% above the average of all Indonesia, which is 31.7%. Life style changes such as dietary changes lead to ready-to-eat dishes that contain lots of fat, high protein and salt but are low in dietary fiber, bringing consequences as one of the factors developing degenerative diseases such as hypertension. The purpose of this study was to determine the relationship between blood glucose and uric acid with the incidence of hypertension in the elderly at Posyandu Lansia Kauman Yogyakarta.Methods: The study was observational analytic with cross-sectional design. The population in this study were all elderly people living in the Posyandu Lansia Kauman Yogyakarta with a total of 33 people. The instrument used was a checklist sheet and the instrument used was a tensimeter, glucometer and uric acid test. The data analysis technique used is the Fisher's test.Results: There was a significant relationship between blood glucose (p=0.023) and uric acid (p=0.036) with an increased risk of hypertension in the elderly in the Posyandu Elderly Kauman Yogyakarta.Conclusions: There is a relationship between blood glucose and uric acid levels with an increased risk of hypertension in the elderly at the Posyandu Lansia Kauman, Yogyakarta.

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Hasan, Rashedul, Projesh Kumar Roy, and Masudur Rahman Khan. "Relation Of Serum Uric Acid Concentrations With Etiology And Severity In Patients With Cirrhosis Of Liver." Gastroenterology Pancreatology and Hepatobilary Disorders 5, no. 2 (June 2, 2021): 01–06. http://dx.doi.org/10.31579/2641-5194/019.

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Background: Hyperuricemia is now an established factor to cause oxidative stress, insulin resistance and systemic inflammation. So it is likely that hyperuricemia might be involved in hepatic necro-inflammation and destruction which are the common underlying pathophysiology of cirrhosis. On the other hand, as uric acid is the end product of cellular degradation, increased hepatocyte destruction due to any etiology increases the level of serum uric acid which might further aggravate hepatic necro-inflammation, cirrhosis & complications. Objectives: To assess serum uric acid concentrations in patients of cirrhosis of liver and its relation with cirrhosis of different etiology, disease severity and liver enzymes. Materials and Methods: This cross sectional observational study was carried out in the Department of Gastroenterology, BSMMU, Bangladesh during the period of September 2015 to October 2016. A total of 220 diagnosed cases of cirrhosis of liver due to any cause from inpatient & outpatient Department of Gastroenterology of Banghabandhu Sheikh Mujib Medical University were enrolled as the study population. Serum uric acid level was measured in each patient and its relationship with different etiology of cirrhosis, severity of cirrhosis and liver enzymes were assessed. Results: The mean age was found to be 47.8 ± 14.6 years and male: female ratio was 1.9:1. Majority patients (52.3%) belonged to CTP Class C. The mean (±SD) value of serum uric acid was 6.19 (±3.25mg/dl) and hyperuricemia (>7 mg/dl) was detected in 27.73% patients. Among all etiologies of CLD, the higher mean (±SD) level of serum uric acid was found in NAFLD (19.54 ±2.20 mg/dl). There was positive correlation of serum uric acid with liver enzymes. Conclusion: Mean serum uric acid level increased gradually as the cirrhotic patients progressed to higher CTP classes & there was positive correlation of serum uric acid with liver enzymes. It requires further large scale multicenter studies with increased sample size & prolong follow-up to establish serum uric acid as a risk factor of CLD.

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Okui, Daisuke, Tomomitsu Sasaki, Masahiko Fushimi, and Tetsuo Ohashi. "The effect for hyperuricemia inpatient of uric acid overproduction type or in combination with topiroxostat on the pharmacokinetics, pharmacodynamics and safety of dotinurad, a selective urate reabsorption inhibitor." Clinical and Experimental Nephrology 24, S1 (November 16, 2019): 92–102. http://dx.doi.org/10.1007/s10157-019-01817-3.

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Abstract Background Dotinurad, a novel selective urate reabsorption inhibitor (SURI), increases urinary uric acid excretion. The aim of this study is to examine the pharmacokinetics, pharmacodynamics, and safety of dotinurad according to the type of hyperuricemia, with or without concomitant use of xanthine oxidase inhibitor, in uric acid “overproduction type” patients. Methods This open-label clinical pharmacology study was conducted in a hospital. Dotinurad 1 mg was administered for 7 days to hyperuricemic patients with uric acid “overproduction type” (overproduction group, n = 6; and combination group, n = 6) and uric acid “underexcretion type” (underexcretion group, n = 6). In the combination group, topiroxostat 80 mg was used concomitantly. Results No significant differences were observed in pharmacokinetics and safety between overproduction group and underexcretion group, and the percent change in serum uric acid level and the amount of urinary uric acid excretion after administration were comparable. In “overproduction type” patients of combination group, the percent change in serum uric acid level significantly increased and the amount of urinary uric acid excretion significantly decreased compared to those of overproduction group. No clinically meaningful differences were observed in safety between the overproduction group and the combination group. Conclusion In inpatients, differences in hyperuricemic type did not significantly influence the pharmacokinetics, pharmacodynamics, and safety of dotinurad. Moreover, in “overproduction type”, the coadministration of dotinurad and topiroxostat had an add-on serum uric acid lowering effect and suppressed urinary uric acid excretion. Trial registration ClinicalTrials.gov Identifier: NCT02837198.

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Coelho, Mariana O. C., Alistair J. Monteyne, Ishara D. Kamalanathan, Vesna Najdanovic-Visak, Tim J. A. Finnigan, Francis B. Stephens, and Benjamin T. Wall. "Short-Communication: Ingestion of a Nucleotide-Rich Mixed Meal Increases Serum Uric Acid Concentrations but Does Not Affect Postprandial Blood Glucose or Serum Insulin Responses in Young Adults." Nutrients 12, no. 4 (April 17, 2020): 1115. http://dx.doi.org/10.3390/nu12041115.

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Circulating uric acid concentrations have been linked to various metabolic diseases. Consumption of large boluses of nucleotides increases serum uric acid concentrations. We investigated the effect of a nucleotide-rich mixed meal on postprandial circulating uric acid, glucose, and insulin responses. Ten healthy adults participated in a randomised, controlled, double-blind, crossover trial in which they consumed a mixed-meal containing either nucleotide-depleted mycoprotein (L-NU) or high-nucleotide mycoprotein (H-NU) on two separate visits. Blood samples were collected in the postabsorptive state and throughout a 24 h postprandial period, and were used to determine circulating uric acid, glucose, and insulin concentrations. Mixed meal ingestion had divergent effects on serum uric acid concentrations across conditions (time x condition interaction; P < 0.001), with L-NU decreasing transiently (from 45 to 240 min postprandially) by ~7% (from 279 ± 16 to 257 ± 14 µmol·L−1) and H-NU resulting in a ~12% increase (from 284 ± 13 to 319 ± 12 µmol·L−1 after 210 min), remaining elevated for 12 h and returning to baseline concentrations after 24 h. There were no differences between conditions in blood glucose or serum insulin responses, nor in indices of insulin sensitivity. The ingestion of a nucleotide-rich mixed-meal increases serum uric acid concentrations for ~12 h, but does not influence postprandial blood glucose or serum insulin concentrations.

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Ogura, Jiro, Kaori Kuwayama, Atsushi Takaya, Yusuke Terada, Takashi Tsujimoto, Takahiro Koizumi, Hajime Maruyama, et al. "Intestinal Ischemia-Reperfusion Increases Efflux for Uric Acid Via Paracellular Route in the Intestine, but Decreases that Via Transcellular Route Mediated by BCRP." Journal of Pharmacy & Pharmaceutical Sciences 15, no. 2 (April 26, 2012): 295. http://dx.doi.org/10.18433/j3w896.

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Purpose. Uric acid is thought to be one of the most important antioxidants in human biological fluids. Intestinal ischemia-reperfusion (I/R) is an important factor associated with high rates of morbidity and mortality. Reactive oxygen species (ROS) are responsible for intestinal I/R injury. The aim of this study was to clarify the efflux for uric acid from the intestine after intestinal I/R. Methods. We used intestinal ischemia-reperfusion (I/R) model rats. Serosal to mucosal flux for [14C]-uric acid was assessed by using Ussing-type diffusion chambers. BCRP/Bcrp expression was assessed by Western blot analysis. Caco-2 cells were used for a model of the intestinal epithelium, and rotenone was used as a mitochondrial dysfunction inducer. Results. Serosal to mucosal flux for uric acid was increased after intestinal I/R, and that for mannitol was also increased. Ko143, which is a BCRP inhibitor, did not affect the uric acid transport. The decreasing uric acid transport mediated by Bcrp was caused by decrease in the level of Bcrp homodimer, bridged by an S-S bond. The suppression of Bcrp S-S bond formation was associated with mitochondrial dysfunction. Moreover, BCRP S-S bond formation activity was decreased by rotenone in Caco-2 cells. Conclusions. Serosal to mucosal flux for uric acid is significantly increased via the paracelluler route, but that via the transcellular route mediated by Bcrp is decreased after intestinal I/R. The decreasing uric acid flux mediated by Bcrp is caused by suppression of Bcrp S-S bond formation. This suppression of Bcrp S-S bond formation may be related to mitochondrial dysfunction. This article is open to POST-PUBLICATION REVIEW. Registered readers (see “For Readers”) may comment by clicking on ABSTRACT on the issue’s contents page.

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Prosiannikov, Michail Y., Nikolay V. Anokhin, Sergey A. Golovanov, Olga V. Konstantinova, Andrey V. Sivkov, and Oleg I. Apolihin. "Urine stones of different chemical composition occurrence depending on the level of uricuria." Urology reports (St. - Petersburg) 10, no. 2 (July 24, 2020): 107–13. http://dx.doi.org/10.17816/uroved102107-113.

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Introduction. According to modern concepts one of the key links in the pathogenesis of urolithiasis is metabolic lithogenic disturbances. The study of the complex effect of many factors on the metabolism of urolithiasis patient is the basis of modern scientific research. We studied the frequency of various chemical urinary stones occurrence depending on various levels of uricuria. Materials and methods. Data from of 708 urolithiasis patients (303 men and 405 women) were analized. The results of blood and urine biochemical analysis and chemical composition of urinary stone were studied. The degree of uricuria was ranked by 10 intervals: from 0.4 to 14.8 mmol/day to assess the occurrence of different stones at various levels of uricuria. Results. The incidence of calculi consisting of uric acid also increases with increasing levels of uric acid in the urine. An increase in the level of uricuria above 3.11 mmol/day is observed to increase calcium-oxalate stones occurrence. Decrease in the prevalence of carbonatapatite and struvite stones observed at an increase of urine uric acid excretion. At high levels of uric acid excretion, we found uric acid and calcium oxalate stones most often. Conclusion. Control over the level of urinary acid excretion in urine is important in case of calcium-oxalate and uric acid urolithiasis.

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Crane, John K., Jacqueline E. Broome, and Agnieszka Lis. "Biological Activities of Uric Acid in Infection Due to Enteropathogenic and Shiga-Toxigenic Escherichia coli." Infection and Immunity 84, no. 4 (January 19, 2016): 976–88. http://dx.doi.org/10.1128/iai.01389-15.

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In previous work, we identified xanthine oxidase (XO) as an important enzyme in the interaction between the host and enteropathogenicEscherichia coli(EPEC) and Shiga-toxigenicE. coli(STEC). Many of the biological effects of XO were due to the hydrogen peroxide produced by the enzyme. We wondered, however, if uric acid generated by XO also had biological effects in the gastrointestinal tract. Uric acid triggered inflammatory responses in the gut, including increased submucosal edema and release of extracellular DNA from host cells. While uric acid alone was unable to trigger a chloride secretory response in intestinal monolayers, it did potentiate the secretory response to cyclic AMP agonists. Uric acid crystals were formedin vivoin the lumen of the gut in response to EPEC and STEC infections. While trying to visualize uric acid crystals formed during EPEC and STEC infections, we noticed that uric acid crystals became enmeshed in the neutrophilic extracellular traps (NETs) produced from host cells in response to bacteria in cultured cell systems and in the intestinein vivo. Uric acid levels in the gut lumen increased in response to exogenous DNA, and these increases were enhanced by the actions of DNase I. Interestingly, addition of DNase I reduced the numbers of EPEC bacteria recovered after a 20-h infection and protected against EPEC-induced histologic damage.

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Sundaram, Pradeep Raj Meenakshi, Ravin Devasir Sathyaseelan, and Srisanthanakrishnan V. "Hyperuricemia among hypertensive and normotensive individuals: a case control study." International Journal of Advances in Medicine 7, no. 2 (January 23, 2020): 206. http://dx.doi.org/10.18203/2349-3933.ijam20200066.

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Background: The depth of association between hypertension and serum uric acid remains a mystery. In order to know the exact association between hypertension and serum uric acid, authors intended to investigate the serum uric acid levels among hypertensive and non-hypertensive patients and, authors assessed whether hyperuricemia increases with increasing duration of hypertension and severity of hypertension.Methods: This case control study was conducted among hypertensive (Cases) and non-hypertensive patients (Controls) attending outpatient and inpatient department of general medicine in Sri Muthukumaran Medical College and Research Institute during January 2019 to March 2019. A total of hundred patients were included in this study with fifty cases and control each. Data was conducted using a proforma, covering particulars related to hypertension and the levels of serum uric acid were also noted in the same. Data analysis was done using SPSS.Results: Hyperuricemia among cases and control was found to be statistically significant association with odds ratio of 3.7. Also, the study showed that the serum uric acid levels were significantly increased in patients with Stage 2 hypertension compared to stage 1 hypertension. Also, cases with longer duration of hypertension had significantly raised serum uric acid levels compared to cases with lesser duration of hypertension.Conclusion: Assessment of serum uric acid may be recommended for all the hypertensive cases.

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Daudon, Michel, Olivier Traxer, Pierre Conort, Bernard Lacour, and Paul Jungers. "Type 2 Diabetes Increases the Risk for Uric Acid Stones." Journal of the American Society of Nephrology 17, no. 7 (June 14, 2006): 2026–33. http://dx.doi.org/10.1681/asn.2006030262.

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Lapsia, Vijay, Richard J. Johnson, Bhagwan Dass, Michiko Shimada, Ganesh Kambhampati, Noel I. Ejaz, Amir A. Arif, and A. Ahsan Ejaz. "Elevated Uric Acid Increases the Risk for Acute Kidney Injury." American Journal of Medicine 125, no. 3 (March 2012): 302.e9–302.e17. http://dx.doi.org/10.1016/j.amjmed.2011.06.021.

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Singhal, Gaurav, Shilpa Bhardwaj, Ashok Kumar Ahirwar, and Harish C. Sharma. "Hyperuricemia as a risk factor for increase severity of coronary vessel occlusion disease: a cross-sectional study in North Indian population." International Journal of Research in Medical Sciences 8, no. 6 (May 26, 2020): 1989. http://dx.doi.org/10.18203/2320-6012.ijrms20202082.

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Background: Cardiovascular disease (CVD) is the most common cause of death worldwide. The present study was conducted to study uric acid as a potential biomarker in predicting the severity of CVD in terms of vessel involvement.Methods: A cross-sectional study, conducted at Rajiv Gandhi Super Speciality Hospital, Tahirpur, Delhi. A total of 52 consecutive male and female patients age between 30 to 70 years was included in this study. Written informed consent was obtained from all the enrolled patients. Automated analysers were used for the analysis of blood glucose, lipid profile and serum uric acid level. IBM SPSS Statistics (Version 20.0, IBM SPSS, IL, USA) was used for the statistical analyses.Results: In this study, a total of 52 consecutive patients were divided into three groups; single-vessel disease (n=19), double vessel disease (n=19) and triple vessel disease (n=14). Biochemical profile of all the groups was calculated. A group of triple vessel disease patients showing higher amount (164±42 mg/dl) of cholesterol level as compared to the other two groups (157±34 mg/dl). The mean level of serum uric acid levels significantly differed and its mean levels increases as the severity of vessel diseases increases. The receiver operating characteristic curve shows the uric level has 71% sensitivity and 52.5% specificity for detecting the severity of coronary vessel disease.Conclusions: This study demonstrated an increased serum uric acid levels were associated with increased severity of vessel disease, and serum uric acid is an independent risk factor for coronary artery disease.

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V., Padma, and Amogh Banupriya. "Serum uric acid levels in acute myocardial infarction." International Journal of Advances in Medicine 4, no. 4 (July 20, 2017): 1010. http://dx.doi.org/10.18203/2349-3933.ijam20173222.

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Background: Higher uric acid is a negative prognostic factor in patients with mild to severe heart failure. Studies have shown that there is a close correlation between serum uric acid concentration and Killip classification in patients of acute myocardial infarction and uric acid levels are higher in patients with higher Killips class.Methods: We studied 100 patients with acute myocardial infarction and compared with 100 controls. Serum uric acid level was measured on day 0, 3 and 7 of MI and results were analysed.Results: Average uric acid level in male cases was 5.6 and female cases was 5.2, male controls were 4.2 and female controls was 3.6. Females had a higher mortality when compared with male patients. One female died due to MI on day 0, one male and two females died on day 3 and four males and four females died on day 7. All patients who died had higher uric acid levels.Conclusions: Serum uric acid levels are higher in patients of acute myocardial infarction as compared to normal healthy persons. Serum uric levels increases in patients with higher Killip class. Combination of Killip class and serum uric acid level after acute myocardial infarction is a good predictor of mortality after acute myocardial infarction.

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Hasan, Rashedul, Projesh Kumar Roy, Md Masudur Rahman Khan, Farid Ahmed, Md Razibul Alam, and Gobinda Gain. "Relation of Serum Uric Acid Concentrations with Etiology and Severity in Patients with Cirrhosis of Liver." Bangladesh Medical Journal 50, no. 1 (January 31, 2021): 46–51. http://dx.doi.org/10.3329/bmj.v50i1.58253.

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Hyperuricaemia is now an established factor to cause oxidative stress, insulin resistance and systemic inflammation. So it is likely that hyperuricemia might be involved in hepatic necroinflammation and destruction which are the common underlying pathophysiology of cirrhosis. On the other hand, as uric acid is the end product of cellular degradation, increased hepatocyte destruction due to any etiology increases the level of serum uric acid which might further aggravate hepatic necroinflammation, cirrhosis and complications. The aim of this study is to assess serum uric acid concentrations in patients of cirrhosis of liver and its relation with cirrhosis of different etiology, disease severity and liver enzymes. This cross sectional observational study was carried out in the Department of Gastroenterology, Banghabandhu Sheikh Mujib Medical University, Bangladesh during the period of September 2015 to October 2016. A total of 220 diagnosed cases of cirrhosis of liver due to any cause from inpatient and outpatient Department of Gastroenterology were enrolled as the study population. Serum uric acid level was measured in each patient and its relationship with different etiology of cirrhosis, severity of cirrhosis and liver enzymes were assessed. The mean age was found to be 47.8 ± 14.6 years and male: female ratio was 1.9:1. Majority patients (52.3%) belonged to Child-Turcotte-Pugh Class C. The mean (±SD) value of serum uric acid was 6.19 (±3.25mg/dl) and hyperuricemia (>7 mg/dl) was detected in 27.73% patients. Among all etiologies of cirrhosis, the higher mean (±SD) level of serum uric acid was found in Non-alcoholic Fatty Liver Disease (19.54 ±2.20 mg/dl). There was positive correlation of serum uric acid with liver enzymes. Mean serum uric acid level increased gradually as the cirrhotic patients progressed to higher CTP classes and there was positive correlation of serum uric acid with liver enzymes. It requires further large scale multicenter studies with increased sample size & prolong follow-up to establish serum uric acid as a risk factor of cirrhosis of liver. Bangladesh Med J. 2021 January; 50(1) : 46-51

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Goldhammer, David S., Frederick M. Stephen, and Timothy D. Paine. "Average radial growth rate and chlamydospore production of Ceratocystis minor, Ceratocystis minor var. barrasii, and SJB 122 in culture." Canadian Journal of Botany 67, no. 12 (December 1, 1989): 3498–505. http://dx.doi.org/10.1139/b89-429.

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Two symbiotic fungi (SJB 122, an unidentified basidiomycete, and Ceratocystis minor (Hedgecock) Hunt variety barrasii Taylor) and one pathogenic phoretic fungus (C. minor (Hedgecock) Hunt variety minor) of the southern pine beetle, Dendroctonus frontalis Zimmermann, were inoculated onto six different concentrations of D. frontalis frass, loblolly pine (Pinus taeda L.) phloem, and uric acid media to observe radial growth rates and chlamydospore production. The average radial growth rate per day of C. minor var. barrasii increased significantly from the control on all three media, but growth was faster at increased concentrations of added phloem compared with the other supplemented media. Significant increases in chlamydospores produced by C. minor var. barrasii from the control occurred only on frass media, with more chlamydospores being produced at higher concentrations. The average radial growth rate per day of SJB 122 fungus increased significantly from the control on only one concentration of phloem and two concentrations of uric acid, but decreased significantly on low concentrations of frass media. SJB 122 chlamydospore production increased with increasing concentration on frass, was not different from the control on phloem, and increased significantly at intermediate concentrations on uric acid. Ceratocystis minor var. minor average radial growth rate per day increased with increasing concentration on both frass and phloem media but on uric acid decreased significantly at higher concentrations, following an initial signficant increase as compared with the controls.

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Nurcahyani, Endang, Novita Herliani, and M. Kanedi M Kanedi. "Antihyperuricemia Activity of Vanilla (Vanilla planifolia Andrews) Fruits Ethanol Extract to Male Mice (Mus musculus L.)." Biomedical and Pharmacology Journal 15, no. 3 (September 29, 2022): 1583–88. http://dx.doi.org/10.13005/bpj/2496.

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Hyperuricemia is a disease caused by an increase in uric acid levels in the blood over the normal level. Increased uric acid levels happen because the levels of purines in the body are quite high, so that the breakdown of purines into uric acid increases. This study used dried vanilla fruit extract using 60% ethanol solvent. The test animals used were 24 mice which were divided into 6 groups namely group Kn (standard feed), group K- (induced with suspension of chicken liver), group K + (induced by suspension of chicken liver and given allopurinol 10 mg / kgBB), group treatments P1, P2, and P3 were induced by suspension of chicken liver and vanilla fruit extract with doses of 50 mg / kgBB, 100 mg / kgBB, and 200 mg / kgBB respectively. Statistical data analysis using ANOVA (Analysis of Variance) through the SPSS 15.0 program with a level of α = 5% and continued with Duncan test at the level of α = 5%. The results of this study showed that vanilla fruit extract treatment P1, P2, and P3 had potential activity of antihyperuricemia, because it can reduce blood uric acid levels in mice induced by the chicken liver. The antihyperuricemia activity of vanilla fruit extract is comparable to the standard allopurinol chemical drug in reducing blood uric acid levels in mice statistically.

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Onwubuya, Emmanuel Ikechukwu, Nkiruka Rose Ukibe, Ofia Anya Kalu, Solomon Nwabueze Ukibe, and Obinwanne Chikamnario Osuagwu. "ASSESSMENT OF SERUM AND URINE URIC ACID LEVEL IN RELATION WITH ANTHROPOMETRIC INDICES IN OVERWEIGHT AND OBESE UNIVERSITY UNDERGRADUATE STUDENTS." Asian Journal of Pharmaceutical and Clinical Research 11, no. 9 (September 7, 2018): 443. http://dx.doi.org/10.22159/ajpcr.2018.v11i9.27995.

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Objectives: Elevated uric acid level is related to a variety of adverse metabolic conditions including gout, obesity, and risk factor for cardiovascular diseases. This prospective study designed to assess the serum and urine uric acid level in relation with anthropometric indices in overweight and obese undergraduate students at NAU, Nnewi, Nigeria.Methods: A total of 302 undergraduate students aged between 18 and 40 years were randomly recruited for the present study. They were grouped based on their body mass index (BMI) as overweight, obese, and control participants. 132 participants were males, of which 21 were obese, 34 were overweight while 77 were normal (control) males. 170 participants were females, of which 56 were obese, 62 were overweight while the remaining 52 were normal (control) females. Fasting blood and 24 h urine sample were aseptically collected from all the participants for determination of serum and urine uric acid.Results: The study observed significantly higher serum uric acid level in obese and overweight males than female and control counterparts (p=0.000, respectively). Urine uric acid level was significantly higher in obese males and females than in their overweight and control counterparts (p=0.000). This shows increase production and accumulation of monosodium urate with decreased uric acid excretion which may result in hyperuricemia and hyperuricosuria which may result in gout. Serum and urine uric acid levels were significantly higher among age range (26–32) and (33–40) years compared with those among age range (18–25) (p<0.05) signifying that uric acid level increases with age. Serum and urine uric acid were significantly positively correlated with BMI, waist circumference, and waist hip ratio (p<0.05).Conclusions: High serum uric acid is a prerequisite for gout and also associated with the metabolic syndrome and risk factors for cardiovascular disease. Proper awareness of the implication of hyperuricemia among undergraduate students is necessary.

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P., Amudha, Nithya D., Pradeeba S., and Manochithra B. "Correlation between first trimester uric acid level and subsequent development of gestational diabetes mellitus." International Journal of Reproduction, Contraception, Obstetrics and Gynecology 6, no. 2 (January 31, 2017): 606. http://dx.doi.org/10.18203/2320-1770.ijrcog20170391.

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Background: The aim of the study was to correlate between first trimester uric acid level and its association with subsequent development of gestational diabetes mellitus.Methods: This is a prospective study conducted at Govt. Raja Mirasudar Hospital attached to Thanjavur Medical College, Thanjavur over a period of one year from September 2015. A total of one hundred and eighty seven ante natal women less than 14 weeks of gestational age who attended the outpatient antenatal department were included in this study. Serum uric acid estimation was done in women with <14 weeks of gestation and they were subsequently screened for GDM between 24 to 28 weeks by oral glucose tolerance test (OGTT) with 75 gms glucose according to IADPSG criteria.Results: In our study, among 178 antenatal pregnant women 13 with uric acid >3.6 mg/dl and 2 with serum uric acid <3.6 mg/dl developed GDM. This shows development of GDM increases with increase in uric acid concentration.Conclusions: Though our study results suggest that serum uric acid level estimation in first trimester can be used as a marker to predict GDM in pregnant women, large scale studies are required before it can be recommended as a routine first trimester screening test for prediction of gestational diabetes mellitus.

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Hill, C. E., and M. S. Olson. "Stimulation of uric acid release from the perfused rat liver by platelet activating factor or potassium." Biochemical Journal 247, no. 1 (October 1, 1987): 207–14. http://dx.doi.org/10.1042/bj2470207.

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The stimulation of hepatic glycogenolysis by platelet activating factor (AGEPC) or increased perfusate potassium concentration ([K+]o), but not phenylephrine, causes a transient increase in uric acid release into the effluent perfusate of perfused rat livers. Uric acid was identified in chromatograms of perfusate samples using reversed-phase h.p.l.c., which show a peak which co-elutes with authentic uric acid, and by the fact that the A293 of perfusate samples decreases in the presence of uricase. Uric acid release is dose-dependent with respect to both AGEPC and [K+]o, and is blocked completely by prior exposure of the perfused liver to 5 mM-allopurinol, a specific inhibitor of xanthine oxidase (XOD). Allopurinol inhibits the increase in portal vein pressure induced by AGEPC, increased [K+]o or phenylephrine; the inhibitory effect increases with increasing concentrations of the agents. Also, allopurinol inhibits the second phase of O2 uptake and glucose release characteristic of concentrations of AGEPC or increased [K+]o equal to or greater than their reported half-maximal concentration for glucose release. The ratio of xanthine dehydrogenase (XDH) to XOD activity in extracts of freeze-clamped perfused livers is not affected by treatment of the livers with AGEPC or increased [K+]o. The results suggest that uric acid production may be an indicator of ischaemia within localized hepatic sinusoids, and that allopurinol partially protects the hepatocyte from the effects of AGEPC or increased [K+]o by inhibiting XOD-dependent superoxide production. We propose that the second phase of the glycogenolytic response to these agents results from ischaemia and subsequent reperfusion. Activation of XOD in vivo and hence O2-derived free radical production may be involved in the response of the liver to vasoactive agonists under a variety of pathophysiological conditions.

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Lee, Seung Yun, Won Park, Young Ju Suh, Mie Jin Lim, Seong-Ryul Kwon, Joo-Hyun Lee, Young Bin Joo, Youn-Kyung Oh, and Kyong-Hee Jung. "Association of Serum Uric Acid with Cardiovascular Disease Risk Scores in Koreans." International Journal of Environmental Research and Public Health 16, no. 23 (November 21, 2019): 4632. http://dx.doi.org/10.3390/ijerph16234632.

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As the prevalence of gout and hyperuricemia increases, the comorbidities of gout and hyperuricemia have become a public health burden. In particular, risks of cardiovascular disease (CVD)-related complications are increasing. However, a few guidelines exist for the management of hyperuricemia. This cross-sectional study aimed to investigate the association of serum uric acid with CVD risk in the general population of Korean adults. We examined cross-sectional data from the first and second years of the seventh Korea National Health and Nutrition Examination Survey 2016–2017. Among 16,277 participants, 8781 were analyzed. We estimated the CVD risk using a 10-year CVD risk score prediction formula. There was a significant association of serum uric acid with 10-year CVD risk scores after adjusting for physical activity, body mass index, serum creatinine, and alcohol consumption in both sexes (p < 0.001). In the fitted fractional polynomial model, an approximate U-shaped association between serum uric acid levels and 10-year CVD risk scores was found in men. At the serum uric acid level of 6.9 mg/dL, the CVD risk was lowest. An approximate J-shaped association between serum uric acid levels and 10-year CVD risk scores was found in women. Our study showed that hyperuricemia was associated with an increased CVD risk. Hypouricemia was also associated with an increased CVD risk in men. We, therefore, recommend proper management of uric acid levels in the general population to reduce CVD risks.

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Stabouli, Stella, Katerina Chrysaidou, Athanasia Chainoglou, Dimos Gidaris, Vasilios Kotsis, and Dimitrios Zafeiriou. "Uric Acid Associates With Executive Function in Children and Adolescents With Hypertension." Hypertension 77, no. 5 (May 2021): 1737–44. http://dx.doi.org/10.1161/hypertensionaha.120.16761.

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Observational studies show that serum uric acid levels associate with cardiometabolic risk factors and subclinical target organ damage. The aim of the present study is to investigate the association of traditional cardiometabolic risk factors and uric acid with the executive performance in children and adolescents. Ninety-nine children and adolescents aged 5 to 18 years referred for assessment of primary hypertension were included. Traditional cardiometabolic risk factors, uric acid, and ambulatory blood pressure parameters were assessed. Executive performance was assessed by the validated Behavior Rating Inventory of Executive Function parent questionnaire. Serum uric acid correlated with cardiometabolic parameters, daytime and nighttime systolic blood pressure. High uric acid levels and ambulatory hypertension were associated with behavior regulation independently of other cardiometabolic risk factors or presence of metabolic syndrome. Participants with combined hypertension and high uric acid levels presented the lowest behavior regulation performance. Children with high uric acid had worse behavior regulation indices T scores with estimated marginal means 56.47 (95% CI, 51.68–61.27) compared with 49.22 (95% CI, 45.91–52.53) in those with low uric acid levels ( P =0.023, adjusted for age, sex, nighttime systolic blood pressure, daytime and nighttime heart rate). Mediation analysis showed that part of the effect of high uric acid levels on behavior regulation was mediated by nighttime systolic blood pressure. In conclusion, we found a positive association of serum uric acid with worse executive performance in children at risk for primary hypertension. Extending these cross-sectional findings with longitudinal studies may determine whether high uric acid levels increases the risk of cognitive decline in youth.

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Haen, Sebastian P., Vicky Eyb, Nora Roth, Christoph Faul, Hans-Georg Rammensee, Lothar Kanz, and Wolfgang A. Bethge. "Serum Uric Acid Levels Can Serve As a Sensitive Biomarker for Immunologic Activity in Patients Undergoing Hematopoietic Cell Transplantation." Blood 118, no. 21 (November 18, 2011): 4558. http://dx.doi.org/10.1182/blood.v118.21.4558.4558.

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Abstract Abstract 4558 Background: Both, autologous and allogeneic hematopoietic cell transplantation (HCT) are important treatment options for patients with hematologic malignancies. During transplantation multiple humoral danger signals, chemokines and cytokines modulate immune reconstitution and post-regeneration immune responses. Uric acid crystals have been identified to act as strong endogenous danger signals. Local high concentrations of uric acid without crystal formation have immunoactivating properties which are reflected by only slight changes in uric acid serum levels. We here extended our previous studies (Haen et al, Blood 2010 (ASH Annual Meeting Abstracts), 116: 4701) and analyzed uric acid serum levels in patients during HCT and a control group during induction chemotherapy for acute leukemia to test the applicability of uric acid as a sensitive biomarker for immunological activity. Patients and Methods: We retrospectively analyzed daily serum levels of uric acid, creatinine and peripheral blood counts of 150 consecutive patients (mean age 47 years, range 18–74 years) with different hematologic malignancies after 202 interventions: In the evaluation group 50 patients after allogeneic HCT (53 transplantations; mean age 48 years, range 19–73 years) and 50 patients after autologous HCT (61 transplantations; mean age 51 years, range 20–69 years) were included. In the control group 50 patients after induction chemotherapy for acute myeloid leukemia (AML, n = 25; 39 chemotherapy cycles; mean age 51 years, range 18–74 years) and acute lymphoblastic leukemia (ALL, n = 25; 49 chemotherapy cycles; mean age 31 years, range 19–61 years) were included. In the transplantation group, indications for treatment were AML (n = 29), ALL (n = 7), multiple myeloma (n = 12), lymphoma (n = 28), myelodysplastic syndromes (n = 7), myeloproliferative disease (n = 3), chronic lymphatic leukemia (n = 2), chronic myeloid leukemia (n = 1), germinal cell cancer (n = 9), and Ewing-sarkoma (n = 2). Results: All patients presented with a significant decrease of uric acid serum levels during conditioning or induction therapy and subsequent aplasia (p < 0.001) with all but 5 patients (97%) developing hypouricemic serum levels (< 3.4 mg/dl, p < 0.001) occurring independently from allopurinol application. Post-treatment serum levels recovered to pre-treatment values (p = 0.08). In all patients the nadir of uric acid serum levels was observed significantly earlier than the detection of first increasing leukocytes (day 11 vs. day 13, p < 0.001; detection limit 50 cells/μl). Most patients undergoing allogeneic or autologous HCT only had one re-increase of uric acid during aplasia (mean 1 and 1.4 re-increases after allogeneic and autologous HCT, respectively). In allogeneic HCT patients this re-increase started earlier than detection of > 50/μl leukocytes (day 9.1 versus day 11.5, p < 0.001), while in autologous HCT the re-increase occurred concomitantly with increasing leukocytes (day 6.6 versus day 6.3, p = 0.26). In contrast, most patients treated with induction chemotherapy presented with more than one re-increase of uric acid serum levels between chemotherapy and hematopoietic regeneration (mean 2.7 and 2.9 re-increases in AML and ALL patients, respectively). Hence, a re-increase of uric acid was indicative for incipient immunologic activity and leukocyte recovery out of aplasia after HCT but not in the control group. Moreover, we observed a drop of uric acid levels in patients with transplant rejection (n = 3) and one patient with bone marrow failure after induction chemotherapy three to four days before vanishing of leukocytes. Conclusion: Uric acid serum levels can indicate early immunologic activity in patients undergoing HCT. A re-increase of uric acid after allogeneic HCT is indicative for immanent leukocyte recovery before > 50 leukocytes/μL can be detected in peripheral blood, while after autologous HCT this increase was observed concomitantly with leukocyte recovery. In contrast, uric acid serum levels did not indicate incipient leukocytic regeneration in patients undergoing induction chemotherapy for AML or ALL, possibly reflecting residual immunologic activity. Of note, a drop of leukocytes shortly after a decrease of serum uric acid may be a hallmark of graft failure or rejection. Disclosures: No relevant conflicts of interest to declare.

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Wahyuni, Yulia, Umi Kholifah, and Idrus Jus'at. "MACRONUTRIENT INTAKE, VITAMIN C, PURINE INTAKE, BODY MASS INDEX AND URIC ACID LEVELS IN MAN (AGED 26-45 YEARS OLD) IN RW 05 SUB-DISTRICT BUKIT DURI JAKARTA." Jurnal Kesehatan 12, no. 2 (January 3, 2020): 73–80. http://dx.doi.org/10.23917/jk.v12i2.9763.

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Hyperurisemia is a condition that uric acid levels in blood above the normal value. Uric acid levels are influenced by consumption of purines, carbohydrate intake, protein, fat, vitamin C and Body Mass Indeks (BMI). The purpose of study was to describe correlation of consumption of purine, carbohydrate intake, protein, fat, vitamin C, BMI and uric acid level in man (aged 26-45 years old) in RW 05 sub-district Bukit Duri Jakarta, 2017. This study was used a cross sectional design with sample of 56 man aged 26-45 years old. Data of carbohydrate , protein, fat,vitamin C and purine intake were collected from Food Frequency Questionaire semi quantitative used food phothograph. BMI was measured by is a person’s weight in kilograms divided by the square of height in meters. Uric acid levels was measured by GCU Easy Touch. Data was analyzed by Pearson’s test and One-Way ANOVA test. There are 56 respondents, as many as 57.1% had normal uric acid levels. While 37.5% respondents have high uric acid levels. Based on statistical Pearson’s test showed there are significant relation between consumption of purine (0,001), protein intake (0,001), fat intake (0,001), vitamin C (0,008) and uric acid levels. There is not relation between carbohidrat intake (0,259), IMT (0,117). Another One-Way ANOVA test founded that there are differences consumption of purine, carbohydrate intake, protein, fat, vitamin C based on uric acid levels (p<0,020). The higher intake of the purin, protein and fat increases uric acid levels. The higher intake of the vitamin C can reduce uric acid levels

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W. Waring, Stephen, David J. Webb, and Simon R. J. Maxwell. "Systemic Uric Acid Administration Increases Serum Antioxidant Capacity in Healthy Volunteers." Journal of Cardiovascular Pharmacology 38, no. 3 (September 2001): 365–71. http://dx.doi.org/10.1097/00005344-200109000-00005.

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Ward, V. L., J. F. McGinty, and W. H. Church. "Iron(III) chloride injection increases nigral uric acid in guinea-pig." NeuroReport 4, no. 6 (June 1993): 787–90. http://dx.doi.org/10.1097/00001756-199306000-00048.

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Manowitz, P., L. F. Amorosa, H. S. Goldstein, and P. L. Carlton. "Uric acid level increases in humanswho are gambling: A preliminary report." Biological Psychiatry 35, no. 9 (May 1994): 698. http://dx.doi.org/10.1016/0006-3223(94)90956-3.

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Takada, Tappei, Kimiyoshi Ichida, Hirotaka Matsuo, Akiyoshi Nakayama, Keizo Murakami, Yoshihide Yamanashi, Hiroshi Kasuga, Nariyoshi Shinomiya, and Hiroshi Suzuki. "ABCG2 Dysfunction Increases Serum Uric Acid by Decreased Intestinal Urate Excretion." Nucleosides, Nucleotides and Nucleic Acids 33, no. 4-6 (April 4, 2014): 275–81. http://dx.doi.org/10.1080/15257770.2013.854902.

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Tayag, Emilio C., Somnath N. Nair, Samina Wahhab, Christos D. Katsetos, James W. Lighthall, and John C. Lehmann. "Cerebral uric acid increases following experimental traumatic brain injury in rat." Brain Research 733, no. 2 (September 1996): 287–91. http://dx.doi.org/10.1016/0006-8993(96)00669-5.

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Ayoub-Charette, Sabrina, Laura Chiavaroli, Qi Liu, Tauseef Ahmad Khan, Andreea Zurbau, Fei Au-Yeung, Annette Cheung, et al. "Different Food Sources of Fructose-Containing Sugars and Fasting Blood Uric Acid Levels: A Systematic Review and Meta-Analysis of Controlled Feeding Trials." Journal of Nutrition 151, no. 8 (June 4, 2021): 2409–21. http://dx.doi.org/10.1093/jn/nxab144.

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ABSTRACT Background Although fructose as a source of excess calories increases uric acid, the effect of the food matrix is unclear. Objectives To assess the effects of fructose-containing sugars by food source at different levels of energy control on uric acid, we conducted a systematic review and meta-analysis of controlled trials. Methods MEDLINE, Embase, and the Cochrane Library were searched (through 11 January 2021) for trials ≥ 7 days. We prespecified 4 trial designs by energy control: substitution (energy-matched replacement of sugars in diets); addition (excess energy from sugars added to diets); subtraction (energy from sugars subtracted from diets); and ad libitum (energy from sugars freely replaced in diets) designs. Independent reviewers (≥2) extracted data and assessed the risk of bias. Grading of Recommendations, Assessment, Development, and Evaluation was used to assess the certainty of evidence. Results We included 47 trials (85 comparisons; N = 2763) assessing 9 food sources [sugar-sweetened beverages (SSBs), sweetened dairy, fruit drinks, 100% fruit juice, fruit, dried fruit, sweets and desserts, added nutritive sweetener, and mixed sources] across 4 energy control levels in predominantly healthy, mixed-weight adults. Total fructose-containing sugars increased uric acid levels in substitution trials (mean difference, 0.16 mg/dL; 95% CI: 0.06–0.27 mg/dL; P = 0.003), with no effect across the other energy control levels. There was evidence of an interaction by food source: SSBs and sweets and desserts increased uric acid levels in the substitution design, while SSBs increased and 100% fruit juice decreased uric acid levels in addition trials. The certainty of evidence was high for the increasing effect of SSBs in substitution and addition trials and the decreasing effect of 100% fruit juice in addition trials and was moderate to very low for all other comparisons. Conclusions Food source more than energy control appears to mediate the effects of fructose-containing sugars on uric acid. The available evidence provides reliable indications that SSBs increase and 100% fruit juice decreases uric acid levels. More high-quality trials of different food sources are needed. This trial was registered at clinicaltrials.gov as NCT02716870.

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Svarchevska, Oksana, and Nataliia Ohorodnyk. "THE INFLUENCE OF DIETARY BASIC LIMITING AMINO ACIDS AND METABOLIC ENERGY LEVELS ON PROTEIN METABOLISM INDICATORS AND PRODUCTIVITY OF PIGLETS." Scientific and Technical Bulletin of the Institute of Animal Science NAAS of Ukraine, no. 124 (2020): 170–77. http://dx.doi.org/10.32900/2312-8402-2020-124-170-177.

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Data about the influence of most limiting essential amino acids (lysine, methionine, threonine) and metabolic energy (ME), provided that their level in the diet increases on the growth and content of total protein, urea and uric acid in the blood plasma of piglets are presented in the article. The stimulatory influence of these additions to the piglets' diet on the growth and protein metabolism in their body was shown. The positive effect of the introduction of essential amino acids (lysine, methionine and threonine) and sunflower oil to the diet on the taste of the mixed feed, the intensity of its eating and the growth of piglets was shown in the conducted research. The greatest gains in piglets of the 4th experimental group, where the level of ME in the diet was 13.72 MJ, lysine - 13.8 g / kg, methionine and threonine - 9.2 g / kg of the mixed feed were observed. At the same time, the safety of piglets was directly proportional to their average daily gain. The highest it was in piglets of the 4th experimental group (96.7%), and the lowest in the control group (89.7%). The increase of the content of lysine, methionine, threonine and fat in the piglets' diet led to an increase in the blood plasma of proteins level and a decrease of urea and uric acid. A clear tendency to increased total protein concentration in blood, when increasing the intensity of pre-starter mixed feed intake by piglets with the additional introduction of lysine, methionine, threonine and sunflower oil was observed. It follows from these data that if the level of the most limiting essential amino acids (lysine, methionine and threonine) increases in the diet, the synthesis of blood plasma proteins in the liver of piglets increases and this process is stimulated by the addition of fat. At the same time, feeding young piglets with amino acid and fat additions contributed to a decrease in the content of urea and uric acid in blood plasma. A significant influence of the investigated factors on the use of amino acids and metabolic energy in energy processes in the animal body indicated.

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Journal articles on the topic 'Uric acid increases'

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