Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “URIC ACID”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 667 records · Page 37Linked to original sources

Automated analysis of flour extracts for uric acid and its correlation with degree of insect defilement.

An automated method is described for quantitating uric acid in a sodium acetate extract of flour. The difference in color intensity developed in a flour extract treated with the enzyme uricase and one that is not treated is measured spectrophotometrically. A mean recovery of 97.1% was obtained for 50 g flour samples spiked with 1 mg uric acid. The method can measure as little as 50 micrograms uric acid in 50 g flour and is used to establish a correlation between the uric acid in the flour and the number of insect fragments and excreta pellets present. A 42-data point least squares straight line having a slope of 1.62 and a correlation coefficient of 0.750 (99.9-100% valid) is used to establish the relationship of uric acid to insect defilement.

Animals↗

[The effect of phototherapy on serum uric acid (author's transl)].

20 newborn infants treated wih phototherapy for icterus neonatorum had analyzed their glutathione reductase activity in the erythrocytes, serum uric acid concentration and the urinary content of uric acid, xanthine and hypoxanthine before and after phototherapy. The activity of glutathione reductase is a sensitive indicator for the availability of riboflavine. There was a significant decrease of serum riboflavine and of serum uric acid during light therapy. The decrease of serum uric acid concentration is discussed as effect of direct photodecomposition on one hand and an inhibitory effect of riboflavine deficiency on uric acid formation on the other.

Erythrocytes↗

Changes in serum uric acid concentrations during normal pregnancy.

Serial changes in serum uric acid concentrations have been studied in a group of healthy women before conception, at regular intervals throughout pregnancy and finally 12 weeks after delivery. Compared with pre-pregnancy values uric acid concentrations decreased significantly by 8 weeks gestation and this reduced level was maintained until about 24 weeks. Thereafter the concentrations increased such that by term they were greater than the pre-pregnancy values in the majority of patients and remained elevated until at least 12 weeks after delivery. If clinical management during the second half of pregnancy is to be based on increases in serum uric acid concentrations then such increases will have to be carefully interpreted against the background of rising concentrations which occur as part of the physiological response to normal pregnancy.

Adult↗

Short- and long-term association between uric acid and a natural disaster.

OBJECTIVE: This paper analyzes the longitudinal relationship between serum uric acid level and a natural disaster. METHODS: The sample consists of factory workers who were participating in a longitudinal epidemiological study of coronary heart disease risk factors. Participants were seen in 1975 (baseline), 1980 (5 year follow-up), and 1987 (12 year follow-up). The 5 year (1980) follow-up examination was interrupted by a major earthquake and resumed 2 weeks after the quake. At this examination, participants seen after the quake had, on the average, significantly lower serum uric acid than those seen before the earthquake. In 1987 (7 years after the quake), participants were questioned whether or not (in their own perception) they were still suffering from damages due to the 1980 earthquake. RESULTS: At the examination in 1987, participants who reported suffering from damage due to the 1980 quake showed on the average significantly increased serum uric acid compared with participants who reported not suffering from damages due to the 1980 quake. The analyses of the data of 578 individuals who participated in all three examinations confirmed these findings and showed that they were independent from levels of uric acid measured prior to the disaster. CONCLUSIONS: The reason for this apparent different association with uric acid and acute and long-term exposure to the quake remains to be clarified but these findings are consistent with the existence of diverse patterns of physiologic response to different stressors.

Adaptation, Psychological↗

[Effects of some drugs on plasma uric acid in rats--actions of catecholamines and beta-blocking agents].

Effects of catecholamines on plasma uric acid and allantoin levels were studied in oxonate-treated rats and non-treated rats. 1) In non-treated rats, epinephrine, isoproterenol and phenylephrine, which were injected intravenously, clearly increased plasma uric acid and allantoin, and norepinephrine had only a slight effect. The orders of potency to increase plasma uric acid and allantoin were epinephrine greater than isoproterenol greater than phenylephrine greater than norepinephrine. Beta-adrenoceptor agonists also increased plasma uric acid and allantoin in non-treated rats. The order of potency to increase plasma uric acid was isoproterenol salbutamol trimetoquinol greater than terbutaline, and that of potency to increase plasma allantoin was isoproterenol salbutamol greater than or equal to trimetoquinol greater than terbutaline. 2) In oxonate-treated rats, the four beta-adrenoceptor agonists (50 micrograms/kg, i.v.) markedly potentiated the hyperuricemic effect of oxonate. These effects of beta-adrenoceptor agonists were inhibited by propranolol (2.0 mg/kg. i.v.). In addition, the effect of isoproterenol was inhibited by butoxamine (1.0 mg/kg, i.v.), but not by atenolol (1.0 mg/kg, i.v.). These results suggest that hyperuricemia induced by catecholamines is closely related to beta 2-adrenoceptor action.

Adrenergic beta-Antagonists↗

Voltammetric peak separation of dopamine from uric acid in the presence of ascorbic acid at greater than ambient solution temperatures.

Peak overlap in voltammetry poses challenges for the quantitative analysis of electroactive species. Dopamine and uric acid are typically challenging to determine voltammetrically because of their very similar oxidation peak potentials. We report preliminary results of the use of a screen-printed carbon electrode for the determination of dopamine and uric acid in an electrolyte solution maintained above ambient temperatures. Higher temperatures resulted in dramatic shifting of the dopamine oxidation peak toward lower potentials, while the uric acid peak was essentially stationary. Ascorbic acid, an interference in voltammetric uric acid determinations, is effectively suppressed at higher temperatures. This resulted in a greater peak separation of dopamine from uric acid at higher temperatures, which is desirable for better peak integration. In addition, greater current responses for both species were recorded at higher temperatures. The cause for such an increase in peak current is unraveled using ac impedance measurements. Presented are preliminary results for determining dopamine and uric acid at temperatures higher than ambient. Much improved voltammetric peak separation and sensitivity is obtained at these higher temperatures compared to ambient.

Ascorbic Acid↗

The clinical utility of serum uric acid measurements in pre-eclampsia and transient hypertension in pregnancy.

BACKGROUND: Our purpose was to evaluate the clinical utility of serum uric acid measurements in the hypertension diseases of pregnancy. METHODS: We identified 286 women and categorized them into three diagnostic groups according to definitions of hypertensive diseases in pregnancy published by the National Working Group on Hypertension in Pregnancy: pre-eclampsia (94), transient hypertension (102) and normal (90). We compared the median uric acid concentration for each group and calculated the sensitivities and the specificities in diagnosing pre-eclampsia. The results were analyzed by the Mann-Whitney test. RESULTS: Median serum uric acid values in the pre-eclamptic group, in the transient hypertension group and in the control group were 375 (262-536) mumol/L, 309 (214-387) mumol/L, 259 (143-339) mumol/L, respectively. Compared with normal, the median serum uric acid levels in women with pre-eclampsia or transient hypertension were significantly elevated. Differences in median serum uric acid concentrations between women with preeclampsia and with transient hypertension were statistically significant too. The prevalence of IUGR in the pre-eclamptic group and transient hypertension group was 65.9% and 29.4%, respectively. Sensitivity for serum uric acid levels of 339 mumol/L was 77.3% in the pre-eclamptic group and 32.3% in the transient hypertension group; the difference was statistically significant. Specificity was exactly the same in both groups (92%). CONCLUSIONS: Our data, in accordance with international literature, confirm the clinical utility of serum uric acid as a marker of pre-eclampsia, but not of transient hypertension. Furthermore its high predictive value makes it possible to select a group of pre-eclamptic women with high risk for intrauterine growth retardation.

Biomarkers↗

[Effects of uric acid on the B cell in the isolated perfused rat pancreas (author's transl)].

Methylxanthines, such as caffeine and theophylline, show effects increasing the secretion of insulin. Perfusion experiments were intended to find out whether insulin secretion is influenced by uric acid, which is chemically closely related. Besides, it was to be demonstrated that uric acid causes no damages to islet cell structures for it is well established that alloxan, which is chemically related to uric acid, produces necroses in B cells. Isolated rat pancreata were stimulated by glucose at concentrations of 100 mg/100 ml and 300 mg/100 ml. In part of the experiments uric acid was added to the perfusion medium at a concentration of 12 mg/100 ml. We found that uric acid has no influence on insulin secretion if it is stimulated by glucose at a concentration of 100 mg/100 ml. However, if B cells are stimulated by glucose at a concentration of 300 mg/100 ml insulin secretion is enhanced by the addition of uric acid by more than 100%. This indicates that this substance exhibits a glucose-potentiating effect. The characteristic dynamics of insulin secretion demonstrate together with light- and electron-microscopic investigations that uric acid causes a real additional secretion and no leaking of intracellular insulin as a result of destruction of islet cell structures by an effect of uric acid similar to that of alloxan.

Animals↗

Uric acid concentrations in early pregnancy among preeclamptic women with gestational hyperuricemia at delivery.

OBJECTIVE: We investigated changes in serum uric acid across pregnancy in women with gestational hyperuricemia at delivery, with and without preeclampsia, compared with normal pregnant and women with preeclampsia without gestational hyperuricemia. STUDY DESIGN: This was a nested case-control study of 116 controls, 27 women with preeclampsia with predelivery hyperuricemia, 37 women with preeclampsia without predelivery hyperuricemia, and 35 women with gestational hypertension with hyperuricemia at delivery but without proteinuria. Serum uric acid and creatinine was measured across pregnancy. RESULTS: Women with predelivery hyperuricemia, with and without preeclampsia, had increased uric acid concentrations across pregnancy compared with controls, after 25 weeks' gestation compared with women with preeclampsia without predelivery hyperuricemia. Adjusting for differences in glomerular filtration by serum creatinine accounted for part but not all of the increase in serum uric acid among women with preeclampsia and predelivery hyperuricemia. CONCLUSIONS: Among women with hyperuricemia at delivery, elevations in uric acid occur early. Multiple mechanisms may contribute to increased uric acid including changes in renal function.

Adult↗

Nitrosation of uric acid by peroxynitrite. Formation of a vasoactive nitric oxide donor.

Peroxynitrite (ONOO-), formed by the reaction between nitric oxide (. NO) and superoxide, has been implicated in the etiology of numerous disease processes. Low molecular weight antioxidants, including uric acid, may minimize ONOO---mediated damage to tissues. The tissue-sparing effects of uric acid are typically attributed to oxidant scavenging; however, little attention has been paid to the biology of the reaction products. In this study, a previously unidentified uric acid derivative was detected in ONOO--treated human plasma. The product of the uric acid/ONOO- reaction resulted in endothelium-independent vasorelaxation of rat thoracic aorta, with an EC50 value in the range of 0.03-0.3 microM. Oxyhemoglobin, a .NO scavenger, completely attenuated detectable .NO release and vascular relaxation. Uric acid plus decomposed ONOO- neither released .NO nor altered vascular reactivity. Electrochemical quantification of .NO confirmed that the uric acid/ONOO- reaction resulted in spontaneous (thiol-independent) and protracted (t1/2 approximately 125 min) release of .NO. Mass spectroscopic analysis indicated that the product was a nitrated uric acid derivative. The uric acid nitration/nitrosation product may play a pivotal role in human pathophysiology by releasing .NO, which could decrease vascular tone, increase tissue blood flow, and thereby constitute a role for uric acid not previously described.

Animals↗

Uric acid is a risk factor for myocardial infarction and stroke: the Rotterdam study.

BACKGROUND AND PURPOSE: The role of uric acid as a risk factor for myocardial infarction is controversial, and little is known about its role as a risk factor for stroke. Recent evidence suggests that uric acid may be an important causal agent in cardiovascular disease, for example, by inducing renal disease and hence hypertension. We investigated the association between serum uric acid and coronary heart disease and stroke in a large prospective population-based study. METHODS: The study was based on 4385 participants of the Rotterdam Study who, at baseline (1990 to 1993), were > or =55 years of age, free from stroke and coronary heart disease, and had blood taken. Follow-up for incident stroke and myocardial infarction was complete until January 1, 2002. Data were analyzed with Cox proportional hazards models with adjustment for relevant confounders. RESULTS: Average follow-up was 8.4 years. High serum uric acid levels were associated with risk of myocardial infarction and stroke; age- and sex-adjusted hazard ratios (95% CIs) for highest versus lowest quintile of uric acid were 1.68 (1.24 to 2.27) for cardiovascular disease (515 cases), 1.87 (1.12 to 3.13) for myocardial infarction (194 cases), 1.57 (1.11 to 2.22) for stroke (381 cases), 1.77 (1.10 to 2.83) for ischemic stroke (205 cases), and 1.68 (0.68 to 4.15) for hemorrhagic stroke (46 cases). Adjustment for other vascular risk factors only slightly attenuated these associations. Associations were stronger in persons without hypertension than in those with hypertension. CONCLUSIONS: Uric acid is a strong risk factor for myocardial infarction and stroke.

Aged↗

Uric Acid and renal disease.

The interrelationship between uric acid and renal disease is reviewed in a historical context. Four phases can be distinguished--the descriptions of uric acid stones and gravel in the eighteenth century, of chronically scarred kidneys containing urate crystals in the nineteenth, the appearance of the syndrome of acute urate nephropathy following tumour lysis in the mid twentieth century, and finally the realization that soluble urate affects both systemic and glomerular blood vessels, and may play a role in both hypertension and chronic renal damage.

Humans↗

Identification of products from oxidation of uric acid induced by hydroxyl radicals.

The aim of the present study was to separate and characterise products formed by oxidation of uric acid by hydroxyl radicals with a view to probing for these products in vivo in clinical contexts. Aerated solutions of 200 microM uric acid, or its oxidation products, allantoin or parabanic acid, were exposed to gamma radiolysis, (52.0 Gy/min), as a source of HO. radicals, at pH 3.4 and 7.4. Aliquots were taken every 5 minutes for 20 minutes and oxidation products were separated by HPLC and analysed with a diode array detector. Identities of oxidation products were confirmed on the basis of similarity of retention times and absorbance spectra and peak purity parameters of known standards. Hydroperoxides were measured by tri-iodide formation in the 20 minute sample. Exposure of uric acid to such HO.fluxes produced a net loss of the parent compound with formation of a complex mixture of products with allantoin and parabanic acid being the predominant products at pH 3.4. The rate of uric acid degradation at physiological pH was slower and the distribution of oxidation products was different. A small but significant amount of uric acid hydroperoxide was detected at both pHs. A mechanism for uric acid oxidation under these conditions is presented.

Chromatography, High Pressure Liquid↗

The kinetics of formation and dissolution of uric acid crystals.

The kinetics of crystallization and dissolution of uric acid have been studied at temperatures from 15 to 45 C, using a highly reproducbile seeding technique. The rates of reaction have been followed by a precision conductometric method. The mineralization rate follows an equation second-order in relative supersaturation and the experimental evidence points to a surface controlled crystal growth. In contrast, the rapid dissolution of seed crystals into undersaturated uric acid solutions seems to be controlled by diffusion of electrolyte through the hydrodynamic boundary layer at the crystal surface. The activation energy for dissolution, 13.1 +/- 2.6 kJ/mole, is close to that expected for bulk diffusion. Values are reported for the solubility product and dissociation constant for uric acid from 15 to 45 C.

Crystallization↗

Renal transport of oxalate: effects of diuretics, uric acid, and calcium.

Clearance experiments were performed in the rat to examine the effects of diuretics on the renal transport of oxalate. In addition, the effect of infusing either uric acid or calcium on the renal transport of oxalate was examined. During control periods, the fractional excretion of oxalate (FEOx) averaged 118.0 +/- 2.1%. Acute administration of either chlorothiazide, furosemide, or indanyl-oxyacetic acid (MK-196), a new uricosuric diuretic, resulted in a significant decrease in the FEOx in all groups to 104.8 +/- 2.4%, 111.3 +/- 2.1%, and 108.6 +/- 2.7%, respectively. Infusion of uric acid increased urinary uric acid excretion from 2.41 +/- 0.28 to 4.26 +/- 0.03 micrograms/min/g kidney wt (P less than 0.001) and decreased FEOx to 104.0 +/- 2.4% (P less than 0.001 compared to control). Infusion of calcium chloride increased urinary calcium excretion from 0.10 +/- 0.04 to 0.44 +/- 0.06 micrograms/min/g kidney wt (P less than 0.001) but had no effect on the FEOx which averaged 118.3 +/- 8.3% (P = NS compared to control). These studies show that the acute administration of chlorothiazide, furosemide, or MK-196, as well as increasing urinary uric acid excretion by uric acid infusion, are all associated with a decrease in the FEOx. Acutely increasing urinary calcium excretion, however, had no effect on oxalate transport.

Animals↗

Serum triglycerides and serum uric acid in untreated and thiazide-treated patients with mild hypertension. The Oslo study.

Levels of serum lipids, uric acid and body weight are reported from a controlled trial of drug treatment of middle-aged men with uncomplicated mild hypertension. The results come from 300 men after three years of follow up; 150 men in the treatment group and 150 men in the control group. The treatment has been standardized starting with hydrochlorothiazide alone and adding alpha methyldopa when necessary. In case of side effects, alpha methyldopa was replaced with propranolol. Pretreatment results demonstrated a strong covariation among body weight, uric acid and triglycerides. In the entire treatment group, there was no significant change in triglycerides after three years (increase from 1.85 to 2.02 mM/liter, P greater than 0.05). Cholesterol was also unchanged. Further analysis showed that certain patients reacted with an increase in triglycerides during treatment: those prone to a distinct increase in uric acid and those gaining weight. Those who needed combination therapy (having the highest pretreatment blood pressure) showed most of the increase in triglyceride and uric acid. In the group treated with hydrochlorothiazide alone, the triglycerides were unchanged. However, those selected from this group with a distinct increase in uric acid also showed an increase in triglycerides. The treatment increased the pretreatment positive correlation between uric acid and triglycerides.

Adult↗

[Oral purine loading test for latent metabolic disorders of uric acid in patients with calcium containing upper urinary calculi].

For the detection of metabolic disorders of uric acid in upper urolithiasis, an oral purine loading test was performed in 78 patients with calcium-containing calculi, 5 patients with uric acid calculi, and 34 stone free subjects. From the results of the normal subject group, the criteria of hyperuricemia, latent hyperuricemia, hyperuricosuria and latent hyperuricosuria were proposed. In calcium-containing stone formers, 6 male patients showed hyperuricosuria, 18 male patients and 4 female patients showed latent hyperuricemia or latent hyperuricosuria. In uric acid urinary stone formers, all cases showed latent hyperuricemia or latent hyperuricosuria. These findings indicated that the metabolic disorders of uric acid might be one of the risk factors for the formation of calcium containing urinary stones, as well as uric acid urinary stones.

Administration, Oral↗

Social class gradients and serum uric acid in males and females.

The relation between serum uric acid and social class is examined by sex among 910 persons in Wensleydale, Yorkshire, 321 persons in Watford, Hertfordshire, and 1,213 persons in New Haven, Connecticut, all of whom were drawn from the general population. Among the men of Wensleydale there is a tendency of marginal significance at the 5% level for serum uric acid to increase with decreasing social class; in the New Haven women this same trend is significant at the 2.5% level; no trend was found among any of the other four sex-specific groups. Age did not account for the patterns observed. The difference between these findings and those of several studies from the United States is consistent with the view that both serum uric acid levels and gout are under multifactorial control.

Adult↗