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 1,225 records · Page 68Linked to original sources
PubMed1980

Plasma cholesterol, triglyceride and uric acid in urban and rural communities in Papua New Guinea.

Fasting plasma cholesterol, triglycerides and uric acid were measured in 109 Melanesian residents of Port Moresby and 71 residents of a Papuan coastal village. Cholesterol and triglyceride levels were low, mean cholesterol 3 . 74 and 3 . 70 mM/l and triglycerides 0 . 64 and 0 . 59 mM/l respectively in urban and rural residents, with no relation to age or sex. Uric acid was higher in urban men (0 . 37 mM/l) than either urban women (0 . 26 mM/l) or rural men and women (0 . 25 and 0 . 24 mM/l). The levels of plasma cholesterol found in this study are similar to previous reports on rural populations in Papua New Guinea. The apparent failure of plasma lipids to increase significantly in urbanised residents of port Moresby who had a significantly higher prevalence of both diabetes mellitus and obesity is unexplained.

Adult↗
PubMed1976

The use of aldehyde dehydrogenase to determine H2O2 -producing reactions. I. The determination of the uric acid concentration.

The sequence of reactions catalyzed by uricase, catalase and aldehyde dehydrogenase for determination of the uric acid concentration was evaluated for human serum and urine samples. More than 60 substances were tested for possible interferences. Alcohol dehydrogenase, formaldehyde and homogentistic acid can disturb the proposed assay, but at concentrations which are not usually encountered in human serum or urine. In the presence of protein at least 99% of the uric acid was recovered.

Alcohol Oxidoreductases↗
PubMed1990

Determination of uric acid in canine serum and urine by high performance liquid chromatography.

A reproducible high performance liquid chromatography (HPLC) method was developed for analysis of uric acid in canine serum and urine. The method consists of precipitating serum proteins with phosphotungstic acid prior to HPLC analysis. Urine is analyzed after dilution with buffer. Chromatography is performed on a reversed-phase C-18 column with UV detection at 292 nm. Sensitivity of the method will allow reproducible measurement of uric acid at concentrations of 0.05 mg/dl in serum and 0.1 mg/dl in urine. The HPLC method has been used to quantify hundreds of canine serum and urine samples. The method is superior to UV absorption or colorimetric methods because its lower limit of detection allows measurement of uric acid at concentrations found in canine serum and urine.

Journal Article↗
PubMed1979

Re-examination of effect of paracetamol on serum uric acid measured by phosphotungstic acid reduction.

The drug paracetamol (N-acetyl-p-aminophenol; acetaminophen) caused a spurious increase in serum uric acid measured by phosphotungstic acid reduction methods. However, the increase was less than 0.12 mmol/1 at plasma levels of paracetamol found in overdosage (40 mg/100 ml) and was small at therapeutic concentrations (less than 4 mg/100 ml). It is concluded that few patients with joint pain who have taken paracetamol paracetamol as an analgesic will have clinically misleading values for serum uric acid.

Acetaminophen↗
PubMed1976

[Which uric acid value is in need of treatment?].

Asymptomatic hyperuricemia should be treated only if the plasma uric acid levels are around 10 mg/100 ml or more on several determinations. In addition, patients on a purine-free diet who excrete more than 600 mg uric acid per 24 h should be treated. In both cases, treatment is intended to be prophylactic against gouty nephropathy. At present there is no evidence that primary hyperuricemia alone is a risk factor for early atherosclerosis and especially coronary artery disease. However, more attention should be paid to the accompanying risk factors such as obesity, hyperlipoproteinemia, diabetes mellitus and hypertension.

Allopurinol↗
PubMed1990

[Percutaneous dissolution of uric acid and cystine stones causing acute ureteral obstruction].

Four cases with ureteral obstruction due to uric acid or cystine stones were treated successfully by percutaneous irrigation with sodium bicarbonate or tromethamine-E. These cases underwent percutaneous nephrostomy for the reason of prolonged complete obstruction (case 1), sustained pyelonephritis (case 2) or decreased renal function (case 3 and 4). Two catheters were placed through the nephrostomy tract before irrigation, 6 Fr. ureteral catheter just above the ureteral stone and 10 Fr. pigtail or 12 Fr. Malecot catheter in the renal pelvis. The ureteral stones were markedly reduced in size and passed spontaneously after 6-11 days' duration of irrigation in three cases. In case 2, the remaining stone was removed transurethrally after 14 days' duration of irrigation, and was found to be composed of organic matrix. Percutaneous dissolution is considered to be a safe and reliable method and may be an alternative way of treating uric acid or cystine stone causing acute ureteral obstruction.

Acute Disease↗
PubMed1964

URIC ACID TRANSPORT SYSTEM: APPARENT ABSENCE IN ERYTHROCYTES OF THE DALMATIAN COACH HOUND.

The Dalmatian coach hound appears to lack a mediated transport system for uric acid, which can be demonstrated in the erythrocytes of other dogs by hypoxanthine inhibition of uric acid uptake. This transport deficiency may be a manifestation of a genetic defect which has different metabolic consequences in the liver, in the kidney, and in other tissues, depending on the direction of their differentiation

Animals↗
PubMed1986

Immobilization of uricase on protamine bound to glass beads and its application to determination of uric acid.

Uricase was found to be stabilized by protamine from salmon testis. Protamine was then bound to controlled-pore glass beads aminohexyl CPG 500 using glutaraldehyde. Microbial uricase was readily immobilized on the protamine bound to glass beads. The immobilized uricase proved to be stable even at 70 degrees C, whereas free uricase was inactivated at 45 degrees C and showed activity over a broader pH range than free uricase. Automated analysis of uric acid was facilitated using the immobilized uricase. The standard curve for uric acid was linear in the range of 2 to 10 micrograms/sample and passed through the origin. This automated procedure was also applicable to the determination of uric acid in human serum. Protamine bound to glass beads is expected to be useful for the simple immobilization and stabilization of enzymes.

Animals↗
PubMed1984

Renal handling of uric acid in patients with recurrent calcium nephrolithiasis and hyperuricosuria.

Hyperuricosuria is a frequent finding in patients with recurrent calcium nephrolithiasis (RCN) that has been related to purine overingestion . The influence of diet and the renal handling of uric acid were investigated in patients with RCN to assess the pathogenic mechanism of excessive urate excretion. Among 50 patients with recurrent nephrolithiasis 42 formed renal stones containing calcium and 9 of these 42 patients demonstrated concomitant asymptomatic hyperuricosuria while on a self-selected diet. Ingestion of a purine-free diet normalized the uric acid excretion in 4 of these 9 patients. The other 5 patients showed persistent hyperuricosuria while on a purine-free diet. In order to assess a possible dysfunction in the renal handling of uric acid, pharmacological tests were undertaken in these 9 patients. Pyrazinamide administration almost completely suppressed urate excretion, excluding a presecretory reabsorption defect. Urate excretion in response to probenecid administration was decreased in 4 patients and increased in 1. This finding is in accordance with a postsecretory reabsorption defect in the former and an augmented tubular secretion of urate in the latter. This study proves that both dietary factors and tubular transport defects are involved in patients with recurrent calcium nephrolithiasis and hyperuricosuria.

Adult↗
PubMed1977

Interference of sodium azide with measurement of serum uric acid by the direct acid ferric reduction procedure.

We examined the effect of sodium azide on the quantitation of serum uric acid by the direct acid ferric reduction procedure. Ferric phenanthroline was used as redox indicator. Sodium azide, in a concentration commonly used as preservative (2 g/liter, 27.2 mmol/liter), increased the absorption at 505 nm and increased apparent uric acid values in specimens, as shown by calculations based on an azide-free standard. Spectral studies indicated that this interference was a result of the color produced by sodium azide in the reaction mixture. The mechanism for azide interference was the interaction of sodium azide and ferric ions to form ferric azide, which also absorbs extensively at 505 nm.

Azides↗
PubMed1978

Serum uric acid levels in untreated and PUVA-treated patients with psoriasis.

Hyperuricemia occurs frequently in patients with psoriasis. An increased purin breakdown due to the enhanced epidermal turnover was stressed as a reasonable explanation. To prove this theory serum uric acid, cholesterol, triglyceride levels and the average body overweight were determined in 318 untreated psoriatic patients and the parameters were correlated with the extent of psoriatic skin involvement. In more than 100 psoriatic patients treated by oral photochemotherapy (PUVA), uric acid serum levels were examined additionally after the PUVA clearing phase and during PUVA maintenance treatment. The present study demonstrates: (1) There is no relationship between the frequency of hyperuricemia and the extent of psoriatic skin involvement, indicating that the increased epidermal turn over may not play a role in psoriatic hyperuricemia. (2) The most reasonable explanation for elevated uric acid in psoriasis seems to be a combination of genetic predisposition and hyperalimentation. (3) No significant change was found in the incidence of hyperuricemia under the influence of photochemotherapy.

Cholesterol↗
PubMed2006

Uric acid and the vasculature.

Hyperuricemia is a frequent finding in diseases in which the clinical manifestations are thought to be secondary to a state of generalized vascular endothelial dysfunction and related to the cardiovascular disease present in conditions associated with the metabolic syndrome, such as hypertension or diabetes. Traditionally, uric acid has not been given an active role in the pathologic process underlying these conditions. However, there is now a growing body of experimental and clinical evidence that points to a mechanistic role for uric acid in cardiovascular disease. The mechanisms that are most often thought to link uric acid and endothelial dysfunction involve inflammation and generation of oxidative stress in the vasculature. These observations allowed new clinical applications and formulations of therapies, such as the introduction of xanthine oxidase inhibitors in the management of congestive heart failure.

Blood Vessels↗
PubMed1982

Study of the microstructure of renal stones: uric acid and calcium oxalate.

This paper represents the results of experimental study on the microstructure of uric acid and calcium oxalate crystallites in renal stones. The size distribution parameters and morphological characteristics of the microcrystals forming the stone were determined using SEM and image analysing system. Information on the fabric of the renal stones examined indicates that the mean volume diameter is 15.5 microns for uric acid and 32 microns for calcium oxalate stones. The polydispersity index gamma, the shape factor phi, and the distribution of particle shape show close similarity. Quantitative studies on stone microstructure could furnish valuable information on stone genesis.

Calcium Oxalate↗
PubMed2003

Is there a pathogenetic role for uric acid in hypertension and cardiovascular and renal disease?

Hyperuricemia is associated with hypertension, vascular disease, renal disease, and cardiovascular events. In this report, we review the epidemiologic evidence and potential mechanisms for this association. We also summarize experimental studies that demonstrate that uric acid is not inert but may have both beneficial functions (acting as an antioxidant) as well as detrimental actions (to stimulate vascular smooth muscle cell proliferation and induce endothelial dysfunction). A recently developed experimental model of mild hyperuricemia also provides the first provocative evidence that uric acid may have a pathogenic role in the development of hypertension, vascular disease, and renal disease. Thus, it is time to reevaluate the role of uric acid as a risk factor for cardiovascular disease and hypertension and to design human studies to address this controversy.

Animals↗
PubMed1997

Comparative analysis of biochemical parameters for differentiation of pleural exudates from transudates Light's criteria, cholesterol, bilirubin, albumin gradient, alkaline phosphatase, creatine kinase, and uric acid.

The differentiation of pleural effusions as being either transudate or exudate is the first step in the diagnosis of pleural effusions. The aim of this study was to compare the efficiency of the various biochemical parameters to the traditional criteria of Light et al., for differentiating exudates from transudates. Ninety-three pleural fluid and sera specimens were obtained and classified as transudates or exudates on the basis of their diagnosis. Of the 93 pleural fluids, 21 were transudates, 72 were exudates. The efficiencies of different parameters for detection of exudates were as follows: The criteria of Light 96%; effusion cholesterol concentration 77%; serum-fluid albumin gradient 67%, pleural/serum alkaline phosphatase ratio 83%; effusion creatine kinase levels 91%; pleural/serum creatine kinase ratio 83%, and effusion uric acid 71%. Pleural/serum uric acid ratio was insignificant for the purpose of this study.

Adolescent↗
PubMed1983

The effect of spironolactone on lipid, glucose and uric acid levels in blood during long-term administration to hypertensives.

Spironolactone, an aldosterone antagonist, was given in a daily dose of 100 mg to 15 patients with primary hypertension for one year. Fasting levels of lipids, uric acid, glucose, insulin, potassium and growth hormone were measured before and after 6 and 12 months of treatment. Total cholesterol, LDL cholesterol, glucose, potassium and growth hormone were unchanged, HDL cholesterol fell from (mean +/- SD) 1.5 +/- 0.6 to 1.1 +/- 0.3 mmol/l (p less than 0.05) after 6 months of treatment and remained lowered (1.0 +/- 0.3 mmol/l) (p less than 0.01) after 12 months of treatment. There was a transient fall after 6 months of treatment in triglycerides from 2.4 +/- 1.5 to 2.0 +/- 1.1 mmol/l (p less than 0.05), uric acid from 380 +/- 73 to 342 +/- 58 mumol/l (p less than 0.05) and an increase in insulin from 16 +/- 9.5 to 28.6 +/- 26.8 mU/l (p less than 0.05). The blood glucose curves above fasting levels after glucose loading were unchanged during spironolactone treatment, whereas the area under the net insulin curve was higher after 6 months of treatment (163 +/- 103 mU X h/l) than before treatment (105 +/- 71 mU X h/l), indicating a small and transient insulin resistance. Thus, spironolactone impaired the glucose tolerance transiently and gave small and almost transient changes in fasting serum lipid and uric acid levels.

Adult↗