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 451 records · Page 25Linked to original sources
PubMed1997

Maternal serum uric acid levels in preeclamptic women with multiple gestations.

Our study was designed to determine serum uric acid levels and establish clinically useful cutoff values for the diagnosis of preeclampsia in twin and triplet gestations. We reviewed the medical records of 129 multiple gestations with serum uric acid levels available. Fifty-five twin gestations were complicated by preeclampsia, 51 were not. Fifteen triplet gestations were complicated by preeclampsia, and 8 were not. Preeclampsia was defined as a persistent blood pressure > or =140/90 mmHg, and proteinuria, or elevated liver enzymes, thrombocytopenia, or eclamptic seizure. Receiver operating characteristic curves were generated for twin and triplet gestations. Serum uric acid levels at different stages of gestation in twin gestations were determined. Maternal serum uric acid levels in preeclamptic twin and triplet gestations were significantly higher than those in nonpreeclamptics. Serum uric acid levels at varying gestational ages were significantly higher in preeclamptic twin gestations than in nonpreeclamptics. Maternal serum uric acid levels of 6.3 mg/dL and 6.8 mg/dL were found to be the most useful cutoff values for the diagnosis of preeclampsia in twin and triplet gestations, respectively. We conclude that compared to nonpreeclamptics, preeclamptic women with multiple gestations had significantly higher serum uric acid levels. Mean serum uric acid levels based on gestational age should be justified for the diagnosis of preeclampsia in multiple gestations.

Adult↗
PubMed1976

The enzymatic spectrofluorimetric determination of uric acid in microsamples of plasma by using p-hydroxyphenylacetic acid as a fluorophor.

A sensitive spectrofluorimetric micromethod for the determination of uric acid is presented together with its application to human and rat plasma. The method is based on the reactions or uricase and peroxidase coupled with p-hydroxyphenylacetic acid as a fluorophor. There is a very wide range of proportionality between the concentration of uric acid and the increase of fluorescence intensity. 10 ng of uric acid is still determinable. At most 25 mul of human or 50 mul of rat plasma is sufficient to obtain the accurate valve of endogenous plasma uric acid concentration. The uric acid levels of normal human and rat plasma measured by present method were within the ranges of concentrations previously reported. A comparative study of this method with a standard assay method is also presented.

Animals↗
PubMed1999

Serum uric acid levels in patients with cirrhosis: a reevaluation.

It has been reported that the serum uric acid levels in patients with cirrhosis were decreased compared with healthy subjects. These studies suggested that the lower serum uric acid levels in cirrhotic patients were attributed mainly to an increased effective vascular volume, and consequently to an excessive renal clearance of uric acid. However, the previous observations are challenged by a recent hypothesis for the pathogenesis of hyperdynamic circulation and formation of ascites in cirrhosis. The current study was undertaken to reevaluate serum uric acid levels in patients with cirrhosis. Ninety-eight cirrhotic patients with normal renal functions were included in this study. All biochemical and hemodynamic data were utilized for analysis. The mean serum uric acid level (mean, 6.1+/-1.2 mg/dL; range, 2.7-9.1 mg/dL) was higher than that of the age- and sex-matched healthy control subjects (mean, 5.5+/-1.3 mg/dL; range, 2.9-8.1 mg/dL; p = 0.018). Using multiple regression analysis it was determined that the serum uric acid level was not related to the severity of liver disease, cardiac index, systemic vascular resistance, and hepatic venous pressure gradient but was related closely to age (r = 0.210, p = 0.026) and effective renal plasma flow (r = -0.677, p < 0.0001). Compared with cirrhotic patients without ascites, those with ascites had a significantly higher serum uric acid level (6.7+/-1.6 mg/dL vs. 5.6+/-1.7 mg/dL, p < 0.05) and lower effective renal plasma flow (396+/-125 mL/min vs. 445+/-149 mL/min, p < 0.05). In conclusion, for cirrhotic patients with normal serum creatinine levels, the current study shows that the mean serum uric acid level is higher than that of healthy control subjects. It is not related to the severity of liver failure and systemic and portal hemodynamics, but is related closely to renal functions, especially the renal plasma flow.

Adult↗
PubMed1987

Plasma uric acid levels in ethanol-fed turkey poults treated with allopurinol.

Plasma uric acid levels were determined in ethanol-fed poults following administration of allopurinol. In young poults, allopurinol at a dose of 50 mg/kg significantly depressed plasma uric acid levels 6 hr post-dosing. At 11 hr post-dosing, plasma uric acid levels were significantly elevated in the allopurinol-treated poults when compared with control poults. During a period of ethanol abstinence, allopurinol at a dose of 40 mg/kg significantly depressed plasma uric acid levels up to 8 hr post-dosing. At a dose of 30 mg/kg, plasma uric acid levels were similar to control values at 4 and 6 hr post-dosing. Data suggest that plasma uric acid levels can be depressed in ethanol poults when allopurinol is administered every 8 hr at a dose of 40-50 mg/kg of body weight.

Allopurinol↗
PubMed2003

Lack of prognostic significance of early elevated serum uric acid levels in low birthweight infants.

This study examined the utility of serum uric acid concentrations in the first day of life to identify infants with severe brain injury (grade III or IV intraventricular hemorrhage and/or periventricular leukomalacia). The serum uric acid concentrations in infants with severe brain injury were compared to those without. Severe brain injury was assessed in 151 infants with birthweight < or = 1,251 g admitted before 24 h of life. The risk of severe brain injury was related to 5-min Apgar scores (odds ratio 0.79, CI 0.63-0.98, p < 0.05) and seizures in the first day of life (odds ratio 4.44, CI 1.004-19.66, p < 0.05), but the mean uric acid levels did not differ between those with and without severe brain injury [5.11 +/- 1.88 mg/dl (303.9 +/- 111.8 micromol/l) vs. 5.77 +/- 2.13 mg/dl (343.2 +/- 126.7 micromol/l), p = 0.200]. Uric acid levels were related to serum creatinine (p < 0.001), time of uric acid sample (p < 0.001), maternal hypertension (p < 0.001), and base deficit (p = 0.032). Of the 80 infants seen in neurodevelopmental follow-up at a median 11 months postconceptional age, uric acid concentrations did not differ between the abnormal (n = 20) and normal subjects [5.38 +/- 1.72 mg/dl (320.0 +/- 102.3 micromol/l) vs. 6.02 +/- 2.55 mg/dl (358.1 +/- 151.8 micromol/l), p = 0.197]. Uric acid may not be a useful early marker for premature infants with severe brain injury.

Apgar Score↗
PubMed1991

Uric acid stimulates vascular smooth muscle cell proliferation by increasing platelet-derived growth factor A-chain expression.

Recent data suggest that uric acid is generated locally in the vessel wall by the action of xanthine oxidase. This enzyme, activated during ischemia/reperfusion by proteolytic conversion of xanthine dehydrogenase, catalyzes the oxidation of xanthine, thereby generating free radicals and uric acid. Because of the potential role of ischemia/reperfusion in vascular disease, we studied the effects of uric acid on rat aortic vascular smooth muscle cell (VSMC) growth. Uric acid stimulated VSMC DNA synthesis, as measured by [3H]thymidine incorporation, in a concentration-dependent manner with half-maximal activity at 150 microM. Maximal induction of DNA synthesis by uric acid (250 microM) was approximately 70% of 10% calf serum and equal to 10 ng/ml platelet-derived growth factor (PDGF) AB or 20 ng/ml fibroblast growth factor. Neither uric acid precursors (xanthine and hypoxanthine) nor antioxidants (ascorbic acid, glutathione, and alpha-tocopherol) were mitogenic for VSMC. Uric acid was mitogenic for VSMC but not for fibroblasts or renal epithelial cells. The time course for uric acid stimulation of VSMC growth was slower than serum, suggesting induction of an autocrine growth mechanism. Exposure of quiescent VSMC to uric acid stimulated accumulation of PDGF A-chain mRNA (greater than 5-fold at 8 h) and secretion of PDGF-like material in conditioned medium (greater than 10-fold at 24 h). Uric acid-induced [3H]thymidine incorporation was markedly inhibited by incubation with anti-PDGF A-chain polyclonal antibodies. Thus uric acid stimulates VSMC growth via an autocrine mechanism involving PDGF A-chain. These findings suggest that generation of uric acid during ischemia/reperfusion contributes to atherogenesis and intimal proliferation following arterial injury.

Animals↗
PubMed1981

Uric acid in the etiology of psoriasis.

The potential etiologic relationship between uric acid in its microcrystalline monosodium urate form and psoriasis was examined by 1) substantiating the reported correlation between hyperuricemia and psoriasis using the phosphotungstate method; 2) examining psoriatic tissue samples for the presence of urates under a microscope using polarized light and a compensator; 3) attempting to induce psoriasis-like symptoms in laboratory animals with purine-to-uric acid metabolism by increasing serum uric acid level; and 4) observing psoriasis-hyperuricemic patients following treatment for their hyperuricemia with Allopurinol. As expected, both men and women psoriatics had higher uric acid levels than did their counterparts in a control group. Monosodium urate crystals were found in samples from psoriatic plaques by both methods used. They were clustered particularly around sweat pores and Munro abscesses, but were found only occasionally in epidermal tissue taken from nonpsoriatics. Psoriasis-like symptoms were induced in laboratory animals (the South American boa, Constrictor constrictor) when they were fed doses of uric acid. Patients with psoriasis and hyperuricemia showed marked improvement in psoriasis when treated for their hyperuricemia. Psoriasis, like gout, may be, at least partly, a result of disorder of purine metabolism and monosodium urate crystals may be responsible for the cell proliferation that is characteristic of psoriatic plaques. Monosodium urate crystals were found by the author to be strikingly segmented. This structure may result in ease of fragmentation, thus increasing the difficulty in identifying urates in any tissue.

Allopurinol↗
PubMed1977

Familial hypouricemia due to isolated renal tubular defect. Attenuated response of uric acid clearance to probenecid and pyrazinamide.

A 37-year-old female was found to have hypouricemia (1.1-1.9 mg%) with markedly increased uric acid clearance (24.7039.5 ml/min). Uric acid excretion was only slightly affected by pyrazinamide, a drug which suppresses renal tubular uric acid secretion, and by probenecid, a drug which inhibits tubular uric acid reabsorption. The attenuated response in this subject to both drugs suggest a renal tubular defect in the proximal high capacity-high affinity uric acid reabsorption mechanism. No other renal tubular or metabolic abnormalities were detected. A survey of the family-three sisters and two brothers, revealed two similarly affected sisters. The abnormality described in this family is defined as familial renal hypouricemia due to an isolated renal tubular defect with attenuated response of uric acid clearance to probenecid and pyrazinamide.

Adult↗
PubMed1992

A study of uric acid pretreatment for the protection of rat gastric mucosa against toxic damage.

Uric acid was evaluated for its potential to protect the gastric mucosa against the injuries caused by 80% ethanol, 0.6 m-HCl and 0.2 M-NaOH in rats. Uric acid at doses of 50, 100 or 300 mg/kg body weight provided dose-dependent protection against the ulcerogenic effects of all three agents. Other effects caused by ethanol only were studied. Serum uric acid concentrations were statistically significantly increased by both uric acid and ethanol treatments. Treatments of rats by gavage with 1 ml 80% ethanol was found to cause depletion of stomach-wall mucus, to lower the concentrations of protein, nucleic acids and non-protein sulphydryl groups in the stomach wall, and to cause histopathological lesions, including necrosis, erosions, congestion and haemorrhage, of the stomach wall. Treatment with uric acid, at doses of 50, 100 or 300 mg/kg body weight, by gavage, provided some measure of protection against all of these effects, and the protection was generally dose dependent. The protective effects of uric acid against damage to the gastric-wall mucosa may be mediated through its effects on mucus production and non-protein sulphydryl concentrations, and/or its free-radical scavenging properties.

Animals↗
PubMed2002

The analysis of uric acid in urine using microchip capillary electrophoresis with electrochemical detection.

Clinical studies have linked irregular concentrations of uric acid in urine to several diseases. Conventional methods for the measurement of uric acid are however temperature-dependent, expensive, and require labile reagents. The miniaturization of analytical techniques, specifically capillary electrophoresis, offers an ideal alternative for clinical analyses such as uric acid determination. The added benefits include reduced reagent and analyte consumption, decreased maintenance costs, and increased throughput and portability. A microchip capillary electrophoresis-electrochemical system for the analysis of uric acid in urine is described. The poly(dimethylsiloxane) (PDMS)/glass microchip utilizes amperometric detection via an off-chip platinum working electrode. Linear responses from 1 to 165 microM and 15 to 110 microM were found for dopamine and uric acid, respectively. The limit of detection for both compounds was 1 microM. Once characterized, the system was used to measure the concentration of uric acid in a dilute urine sample in less than 30 s. The measured uric acid concentration was verified with the uricase reaction and found to be acceptable. Six additional urine samples were evaluated with the microchip device and the uric acid concentration for each sample was found to be in the expected clinical concentration range.

Dopamine↗
PubMed1995

The influence of dairy products on plasma uric acid in women.

Elevated levels of plasma uric acid have been linked to increased risk of cardiovascular diseases and their complications. As dairy proteins have been found to decrease plasma uric acid without increasing glomerular filtration rate, a sample of postmenopausal women living in Montreal was studied to investigate the nature of this relationship. Participants (158 Roman Catholic nuns) were randomly assigned to one of two test diets for a period of four weeks: the dairy foods group (n = 81) consumed approximately 30 grams of dairy protein daily and the dairy-free diet group (n = 77) ate no dairy foods at all. Subjects completed two one-day food records, a core questionnaire and a dairy foods diet history; blood specimens were obtained, and blood pressure, height and weight were measured. Average nutrient intakes differed as a consequence of the test diets, with significantly greater intakes of protein, fat, saturated fat, monounsaturated fat, potassium and calcium (p < 0.01) in the dairy group after the study period, and lower dietary levels of protein, cholesterol, calcium and retinol (p < 0.01) in the dairy-free group. Plasma uric acid was unchanged after the dietary intervention in the dairy group, but increased by 7.8 mumol/l (p = 0.03) in subjects on the dairy-free diet; however, diastolic blood pressure decreased in response to calcium (beta = -22.9, SE = 10.0, p = 0.02) among those whose diet included dairy foods.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Distribution↗
PubMed1998

Serum uric acid levels in cardiovascular diseases.

OBJECTIVE: Comparison of the serum uric acid levels of healthy people (n=71) and patients with cardiovascular diseases (CVD) (n=62). SUBJECTS AND METHODS: The patients included had either experienced acute myocardial infarction (AMI) (n=31), atherosclerosis (AT) (n=23) or ischaemia (n=8). The mean values (x+/-SD) of serum uric acid levels of the control group, the patients with CVD as a whole, and patients with AMI, AT and ischaemia were 4.15+/-0.45 mg%, 5.6+/-2.06 mg%, 5.96+/-2.60 mg%, 5.38+/-1.22 mg% and 4.94+/-1.40 mg%, respectively. A statistically higher level of serum uric acid was found in the controls compared to the CVD patients (P < 0.05). CONCLUSION: The higher serum uric acid levels found in CVD patients suggests that any protective antioxidant effect which uric acid has is overwhelmed by other negative effects on pathogenesis.

Adult↗
PubMed1976

[Automatic ultramicrotechnic for the determination of plasma uric acid].

An automatic micromethod is described for the estimation of plasma uric acid. The hydrogen peroxide formed when uric acid is oxidised by uricase, condenses by oxidation two molecules of p-hydroxyphenil-acetic acid in the presence of peroxidase. The product formed (dicarboxymethyl-5,5' dihydroxy-2,2' biphenyl) is fluorescent. This method permits one to estimate quantitites of uric acid of the order of 1 microng and permits measurement of uric acid in 50 microll of plasma. The values obtained for human plasma are compared to those supplied by a reductrimetric technique (SMA 12-60).

Autoanalysis↗
PubMed1990

[Evidence of abnormal kidney processing of uric acid in patients with insulin-dependent diabetes mellitus].

Renal uric acid handling in 62 insulin dependent diabetic (IDD) patients of both sexes, without clinical or biochemical signs of nephropathy or hypertension was studied and compared to healthy age matched control groups. IDD adults (n = 38, age 45-64) presented uremia similar to controls (n = 9 age 45-64). Neither, the tubular charge or filtration charge (CFU) or the uric acid excretion fraction showed statistically significant differences. Young IDD (n = 24, age 13-37) presented levels uric acid than significantly (p less than 0.001) lowers to young controls (n = 10, age 13-38) and adults IDD (p less than 0.001). The CFU is lower in both, young and adult IDD when compared to young controls (p less than 0.02). Nevertheless, the CFU is higher in young IDD than in controls of the same age (p less than 0.001) or in adult IDD (p less than 0.001). In summary, we conclude the existence of an abnormal (uric acid) renal management caused by a tubular defect probably lying on the proximal tubular segment where the uric acid secretion is carried out.

Adolescent↗
PubMed2002

Serum uric acid levels in multiple sclerosis patients correlate with activity of disease and blood-brain barrier dysfunction.

Several findings suggest lower levels of serum uric acid in multiple sclerosis (MS) patients. The aim of this study is to investigate relationships of uric acid serum levels in relapse-remitting (RR) MS patients with clinical activity of disease and blood-brain barrier (BBB) condition. Sixty-three definite RRMS patients and 40 controls divided into two groups: 20 healthy donors and 20 patients with other inflammatory neurological diseases (OINDs) were analysed. By using a quantitative enzymatic assay according to the manufacture's protocol and a commercial uric acid standard solution, serum uric acid levels were measured and the results were standardized. To investigate BBB function, magnetic resonance imaging after administration of gadolinium was used. MS patients were found to have significantly lower serum uric acid levels (193.89 +/- 49.05 micromol/l; mean value +/-SD) in comparison with healthy donors (292.7 +/- 58.65 micromol/l; P=0.000) and OIND patients (242.7 +/- 46.66 micromol/l; P=0.001). We found that MS patients with relapse had significantly lower serum uric acid levels (161.49 +/- 23.61 micromol/l) than MS patients with remission (234.39 +/- 41.96 micromol/l; P=0.000) and more over, MS patients with BBB disruption had significantly lower serum uric acid levels (163.95 +/- 26.07 micromol/l) than those with normal BBB (252.48 +/- 25.94 micromol/l; P=0.000). Further, we also found that serum uric acid level independently correlated with disease activity, BBB disruption, and gender. These results indicate that lower uric acid levels in MS patients are associated with relapse and suggest that uric acid might be beneficial in the treatment of MS.

Adolescent↗
PubMed1987

[Circadian rhythm of uric acid levels of the serum in gout].

Uric acid concentration in the serum was investigated 3 times a day using the uricase method in 15 gout inpatients on a hypopurine diet with age- and sex-adjusted caloric content. The highest uric acid concentration was noted at 7 a. m., the lowest concentration value at 11 p. m. The highest renal clearance values were noted from 7 a. m. till 3 p. m., the lowest ones from 11 p. m. till 7 a. m. Similar regularities were noted in 15 rheumatoid arthritic patients, however uric acid concentration in the serum was lower and its renal excretion was 1.7 times more effective.

Adult↗
PubMed1984

Serum uric acid concentrations in offspring of conjugal diabetic parents.

Serum uric acid concentrations were measured in offspring of conjugal diabetic parents, in diabetic patients, and in matched nondiabetic controls. The mean uric acid level in offspring of conjugal diabetic parents was significantly higher than in the controls and diabetic patients (P less than 0.001 in the nonobese and P less than 0.05 in the obese). Diabetic patients did not show significant differences in the serum uric acid concentration compared to the controls. The elevated level of serum uric acid in offspring of conjugal diabetic parents could possibly be an early biochemical marker of diabetes.

Adult↗
PubMed2003

Effects of combination treatment using anti-hyperuricaemic agents with fenofibrate and/or losartan on uric acid metabolism.

OBJECTIVE: To assess the effect of a combination treatment using anti-hyperuricaemic agents with fenofibrate and/or losartan on uric acid metabolism in hypertriglyceridaemic and/or hypertensive patients with gout. METHODS: Twenty seven patients with gout were included in a fenofibrate plus anti-hyperuricaemic agents combination study, and 25 in a losartan plus anti-hyperuricaemic agents combination study. Serum uric acid concentration, uric acid clearance, and 24 hour urinary uric acid excretion were measured before and two months after the addition of fenofibrate (300 mg once daily) or losartan (50 mg once daily) to anti-hyperuricaemic agents. RESULTS: Combination therapy of fenofibrate or losartan with anti-hyperuricaemic agents, which included benzbromarone (50 mg once daily) or allopurinol (200 mg twice a day), significantly reduced serum uric acid concentrations in accordance with increased uric acid excretion. CONCLUSION: A combination of fenofibrate or losartan with anti-hyperuricaemic agents is a good option for the treatment of gout patients with hypertriglyceridaemia and/or hypertension, though the additional hypouricaemic effect may be modest.

Adult↗