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PubMed1986

Correlations between deviations from expected cirrhosis mortality and serum uric acid and dietary protein intake.

Mortality from cirrhosis in many countries deviates markedly from that expected for a given per capita alcohol intake. Since lipid peroxidation is thought to be one of the mechanisms involved in the pathogenesis of liver disease and since uric acid is a natural antioxidant, we investigated the possibility that deviation in mortality rates from cirrhosis in different countries might be related to serum uric acid levels in the populations studied. Deviations from expected cirrhosis mortality were calculated as a percentage and correlated with the serum uric acid levels in nine countries. Since animal protein is a major source of dietary purines, the percentage deviation was also correlated with animal protein intake (g/capita/day) for 15 countries. Significant Pearson r correlations were obtained between the percentage deviation in cirrhosis mortality and serum uric acid (-.70, p less than .05) and animal protein ingestion (-.67, p less than .02). This suggests that higher levels of serum uric acid or higher intake of protein may protect against the development of cirrhosis.

Adult↗
PubMed1990

The influence of benzbromarone and its combination with hydrochlorothiazide on renal excretion of uric acid and electrolytes.

The results of a study investigating the effect of single oral administration of B (benzbromarone), and a combination of B + H (hydrochlorothiazide), in 10 healthy volunteers suggest the following conclusions: 1) In agreement with literary data, B at a dose of 100 mg has a significant hypouricemic effect with a 39% decrease after 6 h, and a 53% decrease after 24 h. 2) B and B + H significantly enhance renal clearance and fractional excretion of uric acid but there was no demonstrable significant inverse relation between these parameters and the plasma level of uric acid. 3) B affects PUA (plasma concentration of uric acid) also by some extrarenal action which is not related to the pre-existing alteration of uric acid metabolism. 4) Simultaneous single administration of B + H does not reduce the effect of B on renal excretion and on the plasma level of uric acid. 5) A single dose of B causes a slight but significant decrease in fractional potassium excretion without any demonstrable effect on fractional excretion of sodium and that of all osmotically active substances.

Administration, Oral↗
PubMed1992

Increased urinary loss of uric acid in adults with acute respiratory failure requiring mechanical ventilation.

INTRODUCTION: The purpose of this study was to test a hypothesis of increased urinary excretion of uric acid as an indicator of adenosine triphosphate (ATP) degradation in adult patients with acute respiratory failure, and to look for a correlation to the clinical outcome. STUDY DESIGN: Prospectively 31 patients with acute respiratory failure were studied. The patients were divided into two groups according to the clinical outcome: the need for solely supplemental oxygen (group 1), death or mechanical ventilation (group 2). METHODS: Uric acid was determined by spectrophotometry. RESULTS: Mean uric acid excretion was 39 mumol/kg (range, 7 to 92 mumol/kg) body weight/per 24 h in group 1 (16 patients) compared with 65 mumol/kg/24 h (range, 8 to 253 mumol/kg/24 h) in group 2 (13 patients were mechanically ventilated, and two patients died). The difference was highly significant (p less than 0.0001). CONCLUSION: Increased amount of urinary uric acid was related to the severity of acute respiratory failure in adults.

Acute Disease↗
PubMed2002

Efficacy of benzbromarone compared to allopurinol in lowering serum uric acid level in hyperuricemic patients.

This study was aimed to evaluate the efficacy of benzbromarone compared to allopurinol in lowering serum uric acid level in hyperuricemic patients with normal renal function (serum creatinine < or = 1.5). The authors conducted a crossover study consisting of two four-week treatment periods of allopurinol 300 mg/day and benzbromarone 100 mg/day separated by a four-week washout period. Fourteen patients with mean age and duration of hyperuricemia of 60.78 +/- 8.62 and 6.93 +/- 3.69 years, respectively, were recruited and all completed our study protocol. This study was a crossover design consisting of two four-week treatments of allopurinol and benzbromarone separated by a four-week washout period. The serum uric acid level was reduced from 9.89 +/- 1.43 mg/dl to 5.52 +/- 0.83 mg/dl and from 9.53 +/- 1.48 to 4.05 +/- 0.87 mg/dl by allopurinol and benzbromarone, respectively. The efficacy of benzbromarone in lowering serum uric acid level was significantly superior to allopurinol (p=0.005). No patient reported clinical side effects during treatment with either drug. In conclusion, the authors have shown that benzbromarone is more effective than allopurinol in the reduction of serum uric acid levels in hyperuricemic patients with normal renal function.

Adult↗
PubMed1989

The metabolic relation between hypoxanthine and uric acid in man following maximal short-distance running.

This study was performed to assess the metabolic relation between hypoxanthine and uric acid following short-distance maximal running. Eleven trained males, mean age 22 years (16-31), were instructed to run 800 m in the shortest time possible. Blood samples were collected before warm-up, before the run, immediately after the run and periodically up to 24 h following the run. Blood lactate was determined after warm-up, and at 5, 10, and 30 min following the run. Mean VO2 max for the subjects was 65.8 (4.7) (SD) ml kg-1 min-1 and mean oxygen demand for the running was 118 (8)% of VO2 max. Plasma hypoxanthine levels rose from 3.3 (1.4) to a peak of 48.2 (19.0) mumol l-1 at 20 min following the run and at 180 min had almost returned to pre-run levels. Plasma uric acid levels rose from a pre-run value of 267 (34) to a peak value of 431 (87) mumol l-1 at 45 min following the run. Uric acid concentrations had not returned to normal at 10 h following the run. The blood lactate level peaked at 5 min with 13.7 (2.0) mmol l-1. The results obtained in this study indicate a metabolic relationship between the formation of hypoxanthine and the formation of uric acid. The data also indicate that xanthine oxidase is active following short-distance intensive running.

Adult↗
PubMedDate not supplied

Raised serum TNF-alpha, blood sugar and uric acid in preeclampsia in third trimester of pregnancy.

In preeclampsia, insulin resistance occurs but the exact cause is unknown. It is uncertain whether women destined to develop preeclampsia have preexisting insulin resistance or it is acquired with the development of the disease. Fasting blood samples were collected from 10 normal control pregnant women and from 30 cases of preeclampsia in the third trimester of pregnancy to measure circulating level of glucose, uric acid and tumor necrosis factor-alpha (TNF) concentrations. Preeclampsia was diagnosed as per standard guideline adapted from national high blood pressure education program working group. In control group (n=10) mean age was 25+/-3.71 years, mean sugar level was 86.73+/-13.06 mg/dl, uric acid level was 3.25+/-+/-.59 mg/dl and TNF-alpha level was 9.93+/-9.56 pg/dl. In preeclampsia group mean age was 25.56+/-3.96 years, mean sugar level was 93.46+/-18.6 mg/dl, uric acid was 6.00+/-1.64 mg/dl and TNF-alpha level was 67.66+/-61.83 pg/dl. Statistical analysis done using Kruskal Wallis's test showed significantly raised levels of TNF-alpha (p<0.001), uric acid (p<0.001) and blood sugar (p=0.201) in preeclampsia cases. In preeclampsia there was positive significant correlations of raised TNF-alpha with uric acid (p<0.005). Spearman's test for correlation showed positive correlation of TNF-alpha with blood sugar (p<0.043) in cases of preeclampsia. The findings suggest the involvement of cytokines (TNF-alpha) in preeclampsia and may have a role in gestational diabetes mellitus and insulin resistance. In the present study, there was positive association of raised level of TNF-alpha with blood sugar / and uric acid levels.

Adult↗
PubMed1995

Biotransformation and uric acid lowering effect of benzbromarone in patients with liver cirrhosis - evidence for active benzbromarone metabolites?

The disposition of benzbromarone and its uric acid lowering effect were investigated in 8 patients with compensated liver cirrhosis in order to obtain evidence whether dose requirements differ from subjects with normal liver function. Following a single oral dose of 100 mg benzbromarone, the plasma concentrations of the parent drug and the two hydroxylated main metabolites M1 and M2 as well as uric acid were determined up to at least 72 h. All patients were found to be rapid benzbromarone eliminators. In patients 2-8 the extent of systemic availability of benzbromarone, as estimated by the average AUC(0-infinite), was similar to previous observations in healthy individuals, whereas the values of both metabolites M1 and M2 tended to be lower in patients with liver cirrhosis. Cmax of benzbromarone and M1 also were lower in patients, M2 was equivalent to the data in subjects with normal liver function. tmax and the plasma elimination half-life t(1/2) varied within the same range as previously observed in healthy individuals. One patient exhibited much higher values in AUC(0-infinite); and Cmax of benzbromarone and both metabolites, and in addition of the elimination half-life of M1 and M2, whereas the plasma elimination of benzbromarone itself was not delayed. An effect of altered liver function cannot be excluded in this patient. Ten hours after benzbromarone administration the mean plasma uric acid in patients 2-8 was reduced by 31.5% and in patient 1 by 44.2% as compared to pretreatment values. Baseline levels were not regained until 72 h. These data are compatible with a prolonged uric acid lowering effect of an active benzbromarone metabolite. Altogether, the present observations do not suggest dose adjustment to be necessary in patients with compensated liver cirrhosis Child A and B.

Adult↗
PubMed1991

[Serum uric acid and factor VII hyperactivity in the elderly].

To study the relationship between serum uric acid, lipid fractions, and coagulation factor VII (FVII) in the elderly, we measured FVII coagulation activity (FVIIc). FVII antigen (FVIIag), in 138 normal subjects without alcohol intake ranging in age from 60 to 98 years. We also measured blood lipid fractions including apolipoprotein A-I, A-II, B, E, and serum cholinesterase activity (ChE). Serum uric acid levels significantly correlated with FVIIc (p less than 0.01) and FVIIag levels (p less than 0.05) as well as with tryglycerides, VLDL, LDL, total cholesterol, and ChE in elderly men, but not in women. However, multiple regression analysis showed these correlations in elderly men were not significant, after excluding the effect of triglycerides and VLDL. These results also suggest that elevation of uric acid may be a coronary risk factor in elderly men through high FVII levels.

Aged↗
PubMed2004

Uric acid: A new look at an old risk marker for cardiovascular disease, metabolic syndrome, and type 2 diabetes mellitus: The urate redox shuttle.

BACKGROUND: The topical role of uric acid and its relation to cardiovascular disease, renal disease, and hypertension is rapidly evolving. Its important role both historically and currently in the clinical clustering phenomenon of the metabolic syndrome (MS), type 2 diabetes mellitus (T2DM), atheroscleropathy, and non-diabetic atherosclerosis is of great importance. RESULTS: Uric acid is a marker of risk and it remains controversial as to its importance as a risk factor (causative role). In this review we will attempt to justify its important role as one of the many risk factors in the development of accelerated atherosclerosis and discuss its importance of being one of the multiple injurious stimuli to the endothelium, the arterial vessel wall, and capillaries. The role of uric acid, oxidative - redox stress, reactive oxygen species, and decreased endothelial nitric oxide and endothelial dysfunction cannot be over emphasized.In the atherosclerotic prooxidative environmental milieu the original antioxidant properties of uric acid paradoxically becomes prooxidant, thus contributing to the oxidation of lipoproteins within atherosclerotic plaques, regardless of their origins in the MS, T2DM, accelerated atherosclerosis (atheroscleropathy), or non-diabetic vulnerable atherosclerotic plaques. In this milieu there exists an antioxidant - prooxidant urate redox shuttle. CONCLUSION: Elevations of uric acid > 4 mg/dl should be considered a "red flag" in those patients at risk for cardiovascular disease and should alert the clinician to strive to utilize a global risk reduction program in a team effort to reduce the complications of the atherogenic process resulting in the morbid - mortal outcomes of cardiovascular disease.

Journal Article↗
PubMed1990

Serum uric acid correlates in elderly men and women with special reference to body composition and dietary intake (Dutch Nutrition Surveillance System).

In 460 apparently healthy Dutch elderly, aged 65-79 years, serum uric acid correlates were studied by linear regression analyses, for men and women separately. Diuretic therapy, total serum cholesterol (women only) and creatinine clearance (in bivariate analysis only) were significantly associated with serum uric acid level. Positive associations of serum uric acid with body weight, body mass index, body fatness (men) and lean body mass (men) were observed, with and without adjustment for diuretic therapy, creatinine clearance and age. Serum uric acid levels, whether adjusted or not for these variables and for body mass index, were positively associated with alcohol intake (men) and consumption of meat and fish (women), and inversely with consumption of bread, margarine and milk products (women). These results indicate that limited medication with diuretics, weight control and restriction of alcohol use may help to prevent hyperuricemia in the elderly.

Aged↗
PubMed1977

Plasma uric acid and plasma albumin in healthy subjects.

In healthy male subjects there was a positive correlation between plasma uric acid and plasma albumin (r = 0 - 43, P less than 0 - 005, n = 49) when repeated measurements of both variables were used for each subject. Changes in plasma albumin induced by in vivo ultrafiltration were not accompanied by changes in plasma uric acid. The correlation of plasma uric acid with plasma albumin cannot be attributed to protein binding of urate. The two variables are probably related indirectly through a common association with an unknown factor or factors.

Adolescent↗
PubMed1991

Uric acid as an inhibitor of cyclophosphamide-induced micronuclei in mice.

Swiss albino male mice, 6-8 weeks old, were treated orally with different doses of uric acid dissolved in water for 7 days. Some of the mice in each group were injected i.p. with cyclophosphamide (25 mg/kg) and killed after 30 h. The blood of all animals was analyzed for uric acid levels. The femoral cells of the mice in different groups were collected and studied. Uric acid was found to be devoid of mitodepressant or clastogenic activity at 10-100 mg/kg/day. Pretreatment with uric acid was found to provide significant protection against cyclophosphamide-induced bone marrow depression and micronucleated polychromatic erythrocytes.

Animals↗
PubMed1988

[Clinical studies of the recurrence of urolithiasis (3). Influence of sodium intake on urinary excretion of calcium, uric acid, oxalate, phosphate and magnesium].

Relationship between urinary sodium excretion and urinary excretion of calcium, uric acid, oxalate, phosphate and magnesium was analyzed in 93 ambulatory patients with urolithiasis. There was a significant correlationship between urinary sodium excretion and urinary excretion of calcium, uric acid, oxalate (only in male stone formers), phosphate and magnesium, respectively. Under a salt restricted diet (NaCl 3-5 gm/day) for 3 days, urinary sodium excretion of 16 inpatients with urolithiasis was reduced remarkably together with significant reduction of urinary excretion of calcium, uric acid and oxalate. Urinary excretion of phosphate and magnesium showed no change. From these findings we conclude that restriction of sodium intake is an effective treatment for prevention of stone recurrence.

Calcium↗
PubMed2003

Identification of a novel gene and a common variant associated with uric acid nephrolithiasis in a Sardinian genetic isolate.

Uric acid nephrolithiasis (UAN) is a common disease with an established genetic component that presents a complex mode of inheritance. While studying an ancient founder population in Talana, a village in Sardinia, we recently identified a susceptibility locus of approximately 2.5 cM for UAN on 10q21-q22 in a relatively small sample that was carefully selected through genealogical information. To refine the critical region and to identify the susceptibility gene, we extended our analysis to severely affected subjects from the same village. We confirm the involvement of this region in UAN through identical-by-descent sharing and autozygosity mapping, and we refine the critical region to an interval of approximately 67 kb associated with UAN by linkage-disequilibrium mapping. After inspecting the genomic sequences available in public databases, we determined that a novel gene overlaps this interval. This gene is divided into 15 exons, spanning a region of approximately 300 kb and generating at least four different proteins (407, 333, 462, and 216 amino acids). Interestingly, the last isoform was completely included in the 67-kb associated interval. Computer-assisted analysis of this isoform revealed at least one membrane-spanning domain and several N- and O-glycosylation consensus sites at N-termini, suggesting that it could be an integral membrane protein. Mutational analysis shows that a coding nucleotide variant (Ala62Thr), causing a missense in exon 12, is in strong association with UAN (P=.0051). Moreover, Ala62Thr modifies predicted protein secondary structure, suggesting that it may have a role in UAN etiology. The present study underscores the value of our small, genealogically well-characterized, isolated population as a model for the identification of susceptibility genes underlying complex diseases. Indeed, using a relatively small sample of affected and unaffected subjects, we identified a candidate gene for multifactorial UAN.

Amino Acid Sequence↗
PubMed1998

Uric acid inhibits L-DOPA-CU(II) mediated DNA cleavage.

It has been proposed that considerable DNA damage may be caused by endogenous metabolites produced during the body's normal metabolic processes. We have previously shown that L-DOPA, in the presence of Cu(II) leads to oxidative DNA breakage in vitro. Uric acid is considered to be a naturally occuring antioxidant and is present in plasma at a relatively high concentration. In this paper we report that uric acid inhibits L-DOPA-Cu(II) mediated DNA cleavage at concentrations similar to or lower than those found in plasma. Xanthine, which is the structural analogue of uric acid is a more potent inhibitor of the reaction. Uric acid was also shown to directly quench the generation of hydroxyl radicals by L-DOPA-Cu(II). The results have been discussed in relation to the putative protective role of uric acid against endogenous DNA damage by oxygen radicals.

Animals↗
PubMed2006

Shock wave lithotripsy for uric acid stones.

OBJECTIVE: To report our experience of extracorporeal shock wave lithotripsy (SWL) for patients with uric acid stones. METHODS: From December 1987 to December 2003, a total of 443 patients with uric acid stones in the kidney or ureter accepted SWL using ultrasound-guided lithotripters together with alkali therapy. Among them, 168 patients with an average stone burden of 9.1 mm were treated using an EDAP LT-01 piezoelectric lithotripter. The other patients, with an average stone burden of 9.6 mm, were treated using a Dornier Compact S electromagnetic lithotripter. RESULTS: The average duration of treatment using the EDAP LT-01 device was 52.1 minutes with a pulse frequency of 1.25-2.5 shocks per second at 100% power. The average treatment parameters on the Dornier Compact S device were 3,196 shocks at 14.8 kV. For the EDAP LT-01, the 3-month stone-free rate was 86.4%, with a retreatment rate of 24.2%. For the Dornier Compact S, the 3-month stone-free rate was 90.3%, with a retreatment rate of 29.0%. Auxiliary therapy with the push-back technique was needed in 0.45% of patients with upper ureteral stones that could not be localized using ultrasound. The treatment results were best for stones smaller than 20 mm. No anaesthesia was required for any patient. CONCLUSION: SWL with ultrasound localization for uric acid stones is safe and effective. The combination of SWL with urine alkalization may further improve the stone-free rate.

Adult↗
PubMed2001

Purine nucleotide catabolism in rat liver: labelling of uric acid and allantoin after treatment with oxonic acid and allopurinol.

In our previous experiments on rat liver we found that 15' after intraperitoneal administration of 14C-formate the specific radioactivity of allantoin was always higher than that of uric acid. The present experiments have been carried out to interpret this unexpected result, which was only observed in liver and we studied: a) the incorporation of 14C-glycine into uric acid and allantoin; b) the effects of two competitive inhibitors of xanthine oxidase and uricase, oxonic acid and allopurinol respectively, on levels of uric acid and allantoin in liver and on their specific radioactivity after administration of labelled precursor. The results suggested: a) that under normal conditions, the formation of allantoin is so fast that it exceedes export from liver to serum, and thus the radioactivity of labelled precursors accumulates in allantoin; b) that when allopurinol or oxonic acid are administered, the rate of export exceeds that of allantoin formation and the incorporation of radioactivity into allantoin is lower; c) that not all the data, however, could be interpreted on this basis, but seems to require the existence of different pools of uric acid, which are transformed separately into allantoin.

Allantoin↗