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PubMed1975

[The effect of glucose substitutes on human uric acid metabolism (author's transl)].

Fructose, sorbitol and xylitol produce a rise in serum uric acid during intravenous injection. This is most pronounced with xylitol. The amount of increase in uric acid depends on the amount given. Irreversible decomposition of preformed adenine nucleotide in the liver is considered most important as a cause. Patients in whom there is already an impairment of the energy output on the part of the liver should not be given fructose or sorbitol and certainly not xylitol intravenously.

Adenine Nucleotides↗
PubMed2005

Relation of serum uric acid with metabolic risk factors in asymptomatic middle-aged Brazilian men.

This study in 352 asymptomatic middle-aged Brazilian men demonstrated that serum uric acid increases linearly with an increasing number (0 to >/=3) of metabolic risk factors (5.78 +/- 1.1, 6.14 +/- 1.0, 6.27 +/- 1.1, and 6.79 +/- 1.3, p <0.001). In patients who had >/=3 metabolic risk factors, there was a higher prevalence of serum uric acid in the highest quartile (7.2 to 10.3 mg/dl) than in the lowest quartile (2.6 to 5.4 mg/dl, 35% vs 12%, p <0.001). Mean serum levels of uric acid were higher in those who had an abnormal ratio of >/=3 for triglyceride to high-density lipoprotein (suggesting insulin resistance) than in those who had a normal ratio (6.6 +/- 1.2 vs 5.87 +/- 1 mg/dl, p <0.001).

Adult↗
PubMed2005

Uric acid, evolution and primitive cultures.

Hypertension is epidemic and currently affects 25% of the world's population and is a major cause of stroke, congestive heart failure, and end-stage renal disease. Interestingly, there is evidence that the increased frequency of hypertension is a recent event in human history and correlates with dietary changes associated with Westernization. In this article, we review the evidence that links uric acid to the cause and epidemiology of hypertension. Specifically, we review the evidence that the mutation of uricase that occurred in the Miocene that resulted in a higher serum uric acid in humans compared with most other mammals may have occurred as a means to increase blood pressure in early hominoids in response to a low-sodium and low-purine diet. We then review the evidence that the epidemic of hypertension that evolved with Westernization was associated with an increase in the intake of red meat with a marked increase in serum uric acid levels. Indeed, gout and hyperuricemia should be considered a part of the obesity, type 2 diabetes, and hypertension epidemic that is occurring worldwide. Although other mechanisms certainly contribute to the pathogenesis of hypertension, the possibility that serum uric acid level may have a major role is suggested by these studies.

Animals↗
PubMed2005

Serum uric acid, dehydroepiandrosterone sulphate, and apolipoprotein E genotype in benign vs. progressive multiple sclerosis.

The majority of patients with multiple sclerosis (MS) experience gradual progression of disability, either as secondary progressive MS (SPMS) or primary progressive MS (PPMS). A subgroup with relapsing-remitting MS shows a benign course with little or no disease progression and minimal disability decades after the first manifestations, so called benign MS (BMS). In our search to identify factors that are associated with progression of MS, we investigated serum levels of uric acid and dehydroepiandrostenedione sulphate (DHEAS), and apolipoprotein (apo)E genotype in 28 patients with BMS, 33 with SPMS, 21 with PPMS, and 29 healthy individuals. We found no significant changes in uric acid levels and apoE genotype between the four groups. Mean DHEAS levels were lower in MS patients compared with healthy controls (P = 0.049), but there were no significant differences between the clinical subgroups of MS. In patients with SPMS and PPMS there was no correlation between progression rate and serum levels of either uric acid or DHEAS. Our results suggest that serum levels of uric acid and DHEAS, and apoE genotype do not differ between patients with a benign and progressive course of MS.

Adult↗
PubMed2004

Increased dietary protein elevates plasma uric acid and is associated with decreased oxidative stress in rapidly-growing broilers.

Uric acid is an important antioxidant and methods to elevate its plasma concentration may be important in animal health. In a first study, the effect of dietary protein on plasma uric acid (PUA) and glucose concentrations were determined in 3-week-old chicks. Twenty-four broiler chicks were randomly assigned to four diets: a commercial control diet (C, 20% crude protein), low protein (LP) containing 10% casein, medium protein (MP) containing 20% casein or high protein (HP) containing 45% casein for a 3-week experiment. PUA concentration increased (P<0.05) in chicks fed HP diet and declined (P<0.05) in chicks fed LP while plasma glucose concentrations were lower (P<0.05) in chicks fed the LP diet at the end of the study. In a second study, PUA and leukocyte oxidative activity (LOA) were determined in broilers fed C, LP, MP or HP diets for 4 weeks. As in the first study, dietary protein directly affected PUA concentrations. In birds consuming HP diets, PUA was negatively correlated (P=0.06) with lowered LOA. These data support the view that increases in dietary protein can increase PUA concentrations, which can ameliorate oxidative stress.

Animals↗
PubMed2006

[Two cases of uric acid stones unsuccessfully dissociated by oral chemolysis].

We report two patients with renal uric acid (UA) stones in whom chemolysis by oral administration of alkaline citrate and allopurinol was unsuccessful. The stone in a 58-year old female did not dissolve because her urinary pH remained low throughout the day after alkaline citrate administration. The stone in a 50-year old man did not dissolve because his urinary pH was 5.5-6.0 after alkaline citrate administration. Alkalization of the urine helps reduce the stone size and the calcification of the stone. Extracorporeal shockwave lithotripsy was performed and the stone composition showed mixed calcium oxalate and calcium phosphate. The indication of oral chemolysis of uric acid stones is discussed.

Administration, Oral↗
PubMed1990

Reaction of MDCK cells to crystals of monosodium urate monohydrate and uric acid.

Madin-Darby canine kidney (MDCK) cells exhibit many of the characteristics of cells of the cortical collecting tubule. Since hypotheses concerning the development of gouty and uric acid nephropathy involve a reaction between such cells and crystals, either of monosodium urate monohydrate (MSUM) or uric acid, the reaction between MDCK cells in culture and the above crystals was studied, both morphologically and functionally. In monolayer cultures, reaction sites developed within four hours of exposure to urate crystals. These increased in number for up to 72 hours and subsided gradually after removal of the crystals. At these reaction sites, crystals were observed to have passed beneath the cell surface and could be demonstrated both within intra-cellular lysosomes as well as within the inter-cellular spaces. When the MDCK cells were maintained as single cells in suspension, phagocytosis of crystals by the majority of the cells could be observed, but the response was much more rapid than in monolayers. During the cell/crystal reaction, significant amounts of lysosomal enzymes and prostaglandin E2 were released and, to a less significant degree, cytosolic enzymes, presumably due to cell lysis. This enzyme release did not occur in MDCK cells grown in protein-free medium, and protein coating of the crystals was necessary for reactivity with cells. In this regard, coating with IgG or lysozyme was more effective than albumin. The reaction with uric acid crystals revealed a reactivity which was lesser in degree but qualitatively similar to that of urate crystals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Portable electrochemical blood uric acid meter.

We describe a new portable uric acid (UA) meter, called the UASure (Apex Biotechnology Corp., Hsinchu, Taiwan). The UASure is an electrochemical blood UA meter designed for fast monitoring of UA concentrations in one drop of capillary blood using an electrochemical test strip. We compared the UASure with the standard method, the Hitachi 7600 modular system (Hitachi, Tokyo, Japan), in 146 volunteers (average age 62.5 +/- 12.8 years). Of these, 65 were known hyperuricemic subjects, 17 of whom received medical therapy. The patients donated their capillary and venous blood samples in random order. Capillary blood and one drop of venous blood were tested immediately by the UASure. The venous blood in the test tube was sent to the central laboratory for serum UA measurement by the Hitachi 7600. The intra-assay coefficients of variation (CVs) of the UASure were 4.79%, 5.77%, and 3.08% at UA levels of 5.8, 7.1, and 13.5 mg/dl, respectively. The UA concentrations tested by the UASure correlated well with those by the Hitachi 7600 (r = 0.87 in venous sampling and r = 0.78 in capillary sampling, P < 0.001). The intraclass correlation was good for venous samples by the UASure (rI = 0.84, 95% CI 0.82-0.90), somewhat below the meaningful criterion for capillary samples by the UASure (rI = 0.77, 95% CI 0.69-0.83). UASure with venous sampling is interchangeable with the standard method for UA measurement.

Aged↗
PubMed1997

Possible role of uric acid as an antioxidant in premature infants.

Uric acid (UA) is a water-soluble antioxidant in human body fluids. In umbilical cord blood of 172 neonates with gestational ages between 22 and 42 weeks, UA concentrations were between 50 and 990 mumol/l. There was no correlation with gestational age. Infants with an umbilical cord pH < 7.0 had markedly lower UA concentrations in cord blood than neonates without severe acidosis. UA levels increased during the first 24 h of life and subsequently declined within 2 weeks to lower levels than in older children. In tracheal aspirates (TA), UA at concentrations of about 10(-4) mol/l was found capable of effectively scavenging free oxygen radicals. Luminol-dependent chemiluminescence activity of isolated TA phagocytes or alveolar macrophages was suppressed by UA dose dependently, with a 100% reduction at UA concentrations of 10(-3) mol/l. On the assumption that oxidative stress contributes to the development of chronic lung disease (CLD), in premature infants the ratio of the antioxidant UA and malondialdehyde (MDA) as a marker of oxidative injury was measured in serially obtained TA of 102 ventilated premature infants with birth weights < 1,500 g. At the age of 3-14 days, infants who later developed severe CLD had significantly lower TA UA/MDA ratios than infants without CLD development. In infants with moderate CLD, UA/MDA ratios were comparable to those in the non-CLD group until day 5. During the next 2 weeks, decreasing ratios of UA/MDA paralleled lung injury with increased oxygen requirement and microvascular permeability. Serum UA concentrations did not differ between groups. It is speculated that UA may be physiologically important as an antioxidant in the epithelial lining fluid of the respiratory tract in neonates during the 1st week of life.

Antioxidants↗
PubMed2004

Emergence of Talanin protein associated with human uric acid nephrolithiasis in the Hominidae lineage.

Recently, we identified a susceptibility locus for human uric acid nephrolithiasis (UAN) on 10q21-q22 and demonstrated that a novel gene (ZNF365) included in this region produces through alternative splicing several transcripts coding for four protein isoforms. Mutation analysis showed that one of them (Talanin) is associated with UAN. We examined the evolutionary conservation of ZNF365 gene through a comparative genomic approach. Searching for mouse homologs of ZNF365 transcripts, we identified a highly conserved mouse ortholog of ZNF365A transcript, expressed specifically in brain. We did not found a mouse homolog for ZNF365D transcript encoding the Talanin protein, even if we were able to identify the corresponding genomic region in mouse and rat not yet organized in canonical gene structure suggesting that ZNF365D was originated after the branching of hominoid from rodent lineage. In mouse and in most mammals, a functional uricase degrades the uric acid to allantoin, but uricase activity was lost during the Miocene epoch in hominoids. Searching for the presence of Talanin in Primates, we found a canonical intron-exon structure with several stop codons preventing protein production in Old World and New World monkeys. In humans, we observe expression and we have evidence that ZNF365D transcript produces a functional protein. It seems therefore that ZNF365D transcript emerged during primate evolution from a noncoding genomic sequence that evolved in a standard gene structure and assumed its role in parallel with the disappearance of uricase, probably against a disadvantageous excessive hyperuricemia.

Alternative Splicing↗
PubMed1986

Sex differences in uric acid metabolism in adults: evidence for a lack of influence of estradiol-17 beta (E2) on the renal handling of urate.

The serum urate concentration of adult women, which is lower than in men of a similar age, is thought to be related to a higher renal clearance of urate in women, possibly due to their higher plasma estrogen levels. Intersexual differences in the renal handling of uric acid was assessed in 9 normal adult women and 9 normal age-matched men. Women showed a significantly lower serum urate concentration as compared to men (3.5 +/- 0.3 v 4.9 +/- 0.7 mg/dL, P less than 0.001), higher fractional excretion of urate (9.8 +/- 1.0 v 7.3 +/- 0.8%, P less than 0.001), and significantly lower tubular urate postsecretory reabsorption (67.2 +/- 1.6 v 76.6 +/- 1.4% of secreted urate, P less than 0.01). To test whether plasma E2 has a uricosuric effect we administered estradiol valerate and estradiol benzoate to either oophorectomized or adult women. Plasma E2 levels and urinary total estrogen excretion increased significantly in both groups but the treatment failed to significantly modify serum urate or the fractional excretion of uric acid. Furthermore, in 4 normal adult women, the tubular phases that modulate the renal excretion of urate were not significantly influenced by increased plasma E2 levels. We conclude that in comparison to men of a similar age, the lower tubular urate postsecretory reabsorption of adult women is in accordance with the intersexual differences in uric acid metabolism. Plasma E2 does not influence renal handling of uric acid or serum urate levels.

Absorption↗
PubMed1978

Determination of uric acid on continuous-flow (AutoAnalyzer II and SMA) systems with a uricase/phenol/4-aminophenazone color test.

This report describes a new specific colorimetric procedure for uric acid assay with AutoAnalyzer II and SMA (Technicon) systems, made specific by the application of uricase. Hydrogen preroxide, formed in this reaction, effects the oxidative coupling of 4-aminophenazone and 2,4-dichlorophenol under the catalytic influence of peroxidase. The red dye formed is measured at 505 or 520 nm. A sample blank measurement is not necessary, and the reagents show very good stability. The test shows linearity up to 714 mumol of uric acid per liter. Results of thie method correlate very well with those by the uricase-ultraviolet and uricase--catalase methods. There is no interference by hemoglobin, bilirubin, lipemia, and various drugs, except a minor interference by alpha-methyldopa. Interference from ascorbate is eliminated by ascorbate oxidase. This method can be regarded as a considerably improved routine test for uric acid on continuous-flow systems in clinical laboratories as compared with the commonly used phosphotungstate method.

Aminopyrine↗
PubMed1982

[The value of a single determination of serum uric acid concentration in the early diagnosis of hypertensive disorders in pregnancy (author's transl)].

In 200 healthy, normotensive nulliparous women, a single determination of serum uric acid concentration was done between weeks 28-32 of gestation in order to identify a possible increased risk of developing hypertensive complications. If serum concentrations higher than 3.6 mg/dl were considered as increased ("positive test"), women who developed toxaemia of late pregnancy (proteinuric hypertension), had a significantly elevated mean serum uric acid concentration already at the beginning of the third trimester (p less than 0.01). The incidence of toxaemia and hypertensive disease without proteinuria was significantly higher in the group of women with an elevated uric acid value (p less than 0.001). Only 9% of pregnant women with a "negative test" ultimately developed a mild form of a hypertensive complication. Conversely, 74% of the patients with a "positive test" remained normotensive. Thus, the predictive value of a "positive test" is low (26%) and that of a "negative test" relatively high (91%).

Adolescent↗
PubMed2006

Effects of allopurinol on beer-induced increases in plasma concentrations and urinary excretion of purine bases (uric acid, hypoxanthine, and xanthine).

To determine the effects of allopurinol on beer-induced increases in plasma and urinary excretion of purine bases (hypoxanthine, xanthine, and uric acid), we performed three experiments on five healthy study participants. In the first experiment (combination study), the participants ingested beer (10 ml/kg body weight) eleven hours after taking allopurinol (300 mg). In the second experiment (beer-only study), the same participants ingested beer (10 ml/kg body weight) alone, while in the third experiment (allopurinol-only study), they took allopurinol (300 mg) alone. There was a two-week interval between each of the studies. Beer-induced increases in plasma concentration and urinary excretion of hypoxanthine in the combination study were markedly higher than those in the beer-only study. On the other hand, the sum of increases in plasma concentrations of purine bases in the beer-only study was greater than in the combination study, whereas the increase in plasma uridine concentration in the combination study did not differ from the beer-only study. In addition, allopurinol administration inhibited the beer-induced increase in plasma concentration of uric acid. These results suggest that abrupt adenine nucleotide degradation may increase plasma concentration and urinary excretion of hypoxanthine under conditions of low xanthine dehydrogenase activity, which is mostly ascribable to allopurinol. Further, the difference in the sum of increases in plasma concentrations of purine bases between the combination study and beer-only study was largely ascribable to a greater increase in urinary excretion of hypoxanthine in the combination study. In addition, allopurinol intake seems to be effective in controlling the rapid increase in plasma uric acid caused by ingestion of alcoholic beverages.

Adult↗
PubMed2002

Comparison of uric acid and ascorbic acid in protection against EAE.

Serum levels of uric acid (UA), an inhibitor of peroxynitrite- (ONOO-) related chemical reactions, became elevated approximately 30 million years ago in hominid evolution. During a similar time frame, higher mammals lost the ability to synthesize another important radical scavenger, ascorbic acid (AA), leading to the suggestion that UA may have replaced AA as an antioxidant. However, in vivo treatment with AA does not protect against the development of experimental allergic encephalomyelitis (EAE), a disease that has been associated with the activity of ONOO- and is inhibited by UA. When compared in vitro, UA and AA were found to have similar capacities to inhibit the nitrating properties of ONOO-. However UA and AA had different capacities to prevent ONOO- -mediated oxidation, especially in the presence of iron ion (Fe3+). While UA at physiological concentrations effectively blocked dihydrorhodamine-123 oxidation in the presence of Fe3+, AA did not, regardless of whether the source of ONOO- was synthetic ONOO-, SIN-1, or RAW 264.7 cells. AA also potentiated lipid peroxidation in vivo and in vitro. In conclusion, the superior protective properties of UA in EAE may be related to its ability to neutralize the oxidative properties of ONOO- in the presence of free iron ions.

Albumins↗
PubMed1985

Uric acid levels in plasma and urine in rats chronically exposed to inorganic As (III) and As(V).

The effect of inorganic arsenic (III) and arsenic (V) on renal excretion and plasma levels of uric acid was examined in rats. Oral administration of 1200 micrograms As/kg/day for 6 weeks diminished uric acid levels in plasma by 67.1% and 26.5% of control after the administration of As(III) and As(V), respectively. Renal excretion of uric acid was significantly reduced during the first 3 weeks following As (III) administration, with a subsequent increase to approach control values at the end of the treatment. When As(V) was administered, the diminution in renal excretion was significant at 6 weeks.

Administration, Oral↗
PubMed1988

Improved rapid assay of uric acid in serum by liquid chromatography.

This improved method for rapid determination of uric acid in serum is based on high-performance liquid-gel-permeation chromatography, with hydrophilic and highly porous vinyl alcohol copolymer as packing material. It has the following advantages: no need for sample deproteinization or use of a precolumn, more than 500 serum samples can be analyzed without having to regenerate or recondition the analytical apparatus, and the analysis for uric acid is a one-step procedure. Correlation coefficients between this method and other methods are very good (r = 0.998, 0.999).

Chromatography, High Pressure Liquid↗
PubMed1995

[An epidemiologic study on pathogenesis of uric acid urolithiasis].

We reviewed 5477 patients with urinary calculi who presented during the years from 1975 to 1993. During this time the percentage of calcium stones has remained at approximately 86%. However over the same period the rate of urinary calculi composed of uric acid has increased and is now about 7.2%. The number of uric acid stones has increased 3.5 times compared to 1975. 355 of 394 (90.1%) with uric acid stones are male. We believe that the increase in the numbers of patients seen with gout, hyperurisemia of a high alcohol intake.

Alcohol Drinking↗