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PubMed1991

The relationship between glucose and uric acid metabolism: influence of short term allopurinol on glucose metabolism.

Many investigators suggest that insulin resistance of the peripheral tissues is the primary defect that results in non-insulin dependent diabetes mellitus (NIDDM). It is also generally accepted that multifactorial controls, playing in concert for gene expression trigger this disease. Previous research reports indicated that uric acid metabolism plays a role in the pathogenesis of NIDDM. To investigate this hypothesis, we studied 53 NIDDM patients by using a double blind cross over control study, of allopurinol and placebo administration. We found a statistically significant elevation in the level of hemoglobin A1c (HbA1c) after the allopurinol intervention period of 12 weeks compared with the placebo period of the same duration (p less than 0.003). The elevation was also found in a subgroup with Body Mass Index (BMI) less than 25 kg/m2 (p less than 0.001) and BMI more than or equal to 25 kg/m2 (p less than 0.05). No statistically significant differences between fasting plasma glucose, glucose tolerance test, serum insulin, total cholesterol, triglycerides, high density lipoprotein cholesterol, creatinine, prior to and after use of allopurinol were noted except for serum uric acid (p less than 0.001). No relationship between changes in HbA1c and changes in uric acid, analysed by linear regression analysis and correlation was demonstrated (r = 0.15, p = 0.29). We conclude that the changing of hemoglobin A1c may be a direct effect of allopurinol or support the role of uric acid in the pathogenesis of NIDDM.

Adult↗
PubMed1989

Incorporation of intraportally infused [15N]ammonia into urinary uric acid in cockerels pretreated with methionine sulfoximine.

1. Measurements were made in situ to determine the incorporation of intraportally infused ammonia-15N into urinary uric acid in cockerels pre-treated with methionine sulfoximine (MSM), a glutamine synthetase inhibitor. 2. The incorporation of 15N into urinary uric acid was 34% of the infused amount in MSM-treated birds. This was not significantly different from the value of 46% for control birds. 3. Pre-treatment with MSM inhibited the activity of liver glutamine synthetase to 7% of the control value and decreased the incorporation of the infused ammonia-15N into plasma glutamine amide-N to 3% of the control. 4. Increases in glutamine concentrations in the blood, liver and kidney caused by the infusion of ammonia were also completely inhibited by the MSM treatment (P less than 0.05). 5. It is concluded that in the cockerel ammonia-N can be incorporated into uric acid other than by glutamine formation.

Ammonia↗
PubMed2006

Comparison of plasma uric acid levels in five varieties of the domestic turkey, Meleagris gallopavo.

Plasma uric acid (PUA) is a consensus physiological biomarker for many phenotypes in vertebrates because it is a reliable indicator for processes such as oxidative stress and tubular function. In birds, it is considered a major antioxidant and is also the primary endproduct of nitrogen metabolism. Despite this importance, knowledge of baseline levels of PUA in physiologically normal birds, including the turkey, Meleagris gallopavo, is limited. Here, we compared PUA levels in a total of 106 apparently normal male and female birds at 8 and 32 wk of age from 5 strains of the domestic turkey, including Bourbon Red, Narragansett, Blue Slate, Royal Palm, and Spanish Black. Though differences in PUA were not significant at 8 and 32 wk of age, BW, variety, and sex effects were highly significant. When adjusted for BW, female birds had, on average, a higher PUA per kilogram of BW than male birds. When adjusted for both sex and BW, Royal Palm birds had the lowest average PUA, and Blue Slate had the highest PUA. Results of these investigations represent the first comparative analysis of PUA in physiologically normal turkey varieties. They suggest that differences in basal plasma levels of uric acid in physiologically normal turkeys are influenced by sex, weight, and genetic background but may be independent of age.

Aging↗
PubMed1984

[A problem on the uric acid value of rats for clinical evaluation].

Routine monitoring on levels of serum uric acid in the rats has been widely employed as an important factor in the nucleic acid metabolism, despite of the presence of the uricase in them. In this paper, it is confirmed that the levels of allantoin in serum and urine of the normal rats were higher than those of uric acid. Therefore, the concentration of allantoin in serum and urine of the rats with abnormal nucleic acid metabolism caused by adenine administration were measured. The results indicated that the value of serum allantoin was more sensitive to abnormal nucleic acid metabolism.

Adenine↗
PubMed1989

The insulin response to oral glucose, concentrations of total cholesterol, triglycerides and uric acid in women with idiopathic hirsutism.

The glucose and insulin responses to an oral glucose tolerance test, concentrations of total cholesterol, triglycerides and uric acid were evaluated in women with idiopathic hirsutism (IH). Clinical data and laparoscopy of the ovaries were used in diagnosis. According to body weight the patients were divided into two groups: obese (OB-IH) and non-obese (NO-IH). In the IH and NO-IH groups the glucose response was significantly greater than in the control group (p less than 0.05). The insulin response to oral glucose was significantly higher in the IH and OB-IH groups compared with the control group (p less than 0.01). The concentrations of total cholesterol and triglycerides were significantly increased in the IH and OB-IH groups compared to those of normal women (p less than 0.01). All groups had significantly higher levels of uric acid compared with the control group (p less than 0.01). The results of our study suggest that alterations of carbohydrate, lipid and uric acid metabolism are present in patients with IH and further studies are needed to establish their mechanisms.

Adolescent↗
PubMed1978

[Juvenile gout with decreased activity of hypoxanthine-guanine-phosphoribosyl transferase and pheochromocytoma: partial persistence of tophi despite uric-acid reducing treatment for 12 years (author's transl)].

A now 45-year-old man with marked chronic tophous gout and recurrent nephrolithiasis has been followed for 12 years. First gouty symptoms appeared at age 18. Uric-acid reducing treatment freed the patient of symptoms, and bony and soft-tissue tophi in part regressed. The early onset and high urinary uric-acid excretion indicated increased uric-acid production. Decreased activity of the enzyme hypo-xanthine-guanine-phosphoribosyl transferase was demonstrated to be the cause of the hyperuricaemia, which led to an excessive purine synthesis. An almost complete loss of activity of this enzyme is the basis of the Lesch-Nyhan syndrome. In the described patient all of the neurological and behavioural disorders of the Lesch-Nyhan syndrome were absent. A pheochromocytoma was found to be the cause of malignant hypertension, which had been present for many years.

Adrenal Gland Neoplasms↗
PubMed2004

Uric acid stones following hepatic transplantation.

We report the case of a 52 year old man with a history of insulin-requiring diabetes and hepatitis B with cirrhosis who received an orthotopic liver transplant. One year later he developed renal colic and was found to have a 3 mm stone at the left ureterovesical junction. Numerous other stones formed and infrared spectroscopy analysis demonstrated all to be composed of 100% uric acid. Urine collections demonstrated a low urine pH of 5.1 without hyperuricosuria. His stones were effectively prevented with potassium citrate therapy. Few incidence data are available for uric acid stone occurrence in solid organ recipients. Calcineurin inhibitors are thought to often cause hyperuricemia on the basis of decreased urate excretion. However, this effect would not be expected to cause hyperuricosuria nor uric acid stones. This class of drugs may also be associated with low urine pH, perhaps on the basis of hypoaldosteronism, but the contribution of such a syndrome to uric acid stone formation is not established.

Calcineurin Inhibitors↗
PubMed1983

Uric acid utilization by Mycobacterium intracellulare and Mycobacterium scrofulaceum isolates.

Forty-nine human and environmental isolates of Mycobacterium intracellulare and Mycobacterium scrofulaceum were tested for their ability to grow on uric acid and a number of its degradation products. Nearly all (88 to 90%) strains used uric acid or allantoin as a sole nitrogen source; fewer (47 to 69%) used allantoate, urea, or possibly ureidoglycollate. Enzymatic activities of one representative isolate demonstrated the existence of a uric acid degradation pathway resembling that in other aerobic microorganisms.

Humans↗
PubMed1975

Gout as a complication of Bartter's syndrome. A possible role for alkalosis in the decreased clearance of uric acid.

A prevalence of hyperuricemia of 50% and of acute gouty arthritis of 20% has been observed in a group of patients with Bartter's syndrome. All patients except one presented initially with complaints unrelated to uric acid metabolism. The cause of their hyperuricemia and subnormal clearance of uric acid is unexplained. Systemic alkalosis, a prominent feature of Bartter's syndrome, can decrease the clearance of uric acid and may contribute to the hyperuricemia and gout that have been observed. Physicians should be aware of the possibility of gout as a clinical complication of Bartter's syndrome and of the inhibitory effects of alkalosis on urate clearance.

Acute Disease↗
PubMed1997

Intestinal formation of hypoxanthine and uric acid during endotoxemia.

The objective of this study was to examine the intestinal metabolism of high-energy purine compounds as sensitive indicators of tissue ischemia during endotoxemia. Arterial (art) and portal venous (PV) concentrations as well as the intestinal net concentration changes of adenosine (ADO), hypoxanthine (Hypo), and uric acid (UA) were measured at baseline and after 60 and 120 min in rats that were subjected to a 1-hr continuous infusion of endotoxin (1.5 mg/kg; group E), and in control animals (group C). Furthermore, the arterial (SaO2) and portal venous oxygen saturation (S(PV)O2) was determined at the same time points. Animals in both groups remained normotensive throughout the study period and no differences in mean arterial blood pressure were observed. In both groups, adenosine concentrations remained constant throughout the study and no changes in the net concentration difference (NCD) of adenosine between arterial and portal venous blood were observed [ADO(NCD); baseline: group E, -23 +/- 46 nmole/L; group C, 17 +/- 84 nmole/L; 120 min: group E, 14 +/- 38 nmole/L; group C, 5 +/- 40 nmole/L]. In contrast to control animals, hypoxanthine and uric acid concentrations increased in arterial and portal venous blood in endotoxemic rats after 120 min. This was accompanied with an increase in the intestinal net concentration differences of both hypoxanthine and uric acid, indicating the gut as the predominant source of these two compounds during endotoxemia [Hypo(NCD); baseline: group E, -36 +/- 53 nmole/L; group C, -53 +/- 185 nmole/L; 120 min: group E, 538 +/- 211 nmole/L; group C, 99 +/- 100 nmole/L] [UA(NCD); baseline: group E, 2.04 +/- 1.62 micromole/L; group C, -0.04 +/- 1.11 micromole/L; 120 min: group E, 9.58 +/- 3.04 micromole/L; group C, 0.35 +/- 1.34 micromole/L]. Furthermore, in endotoxemic rats the portal venous oxygen saturation decreased despite unaltered arterial oxygen saturation [SaO2; baseline: group E, 95.2 +/- 0.9%; group C, 94.2 +/- 0.9%; 120 min: group E, 95.4 +/- 0.7%; group C, 96.4 +/- 0.9%] [S(PV)O2; baseline: group E, 86.2 +/- 3.1%; group C, 85.7 +/- 1.4%; 120 min: group E, 69.1 +/- 4.5%; group C, 82.3 +/- 1.9%]. These results indicate the presence of tissue ischemia in the intestinal tract during early, normotensive endotoxemia. Furthermore, because of the direct toxic damage mediated by oxygen radicals that are generated during the production of uric acid, intestinal mucosal injury observed during endotoxemia may be related to an enhancement of the ATP-degradation pathway.

Adenosine↗
PubMed2005

Serum uric acid independently predicts mortality in patients with significant, angiographically defined coronary disease.

BACKGROUND: Uric acid is a nontraditional risk factor implicated in the development of coronary artery disease (CAD). This study prospectively evaluated the predictive value of serum uric acid (SUA) levels for mortality after angiographic diagnosis of CAD. METHODS: Blood samples were collected from 1,595 consecutive, consenting patients with significant, angiographically defined CAD (stenosis 70%). Baseline and procedural variables were recorded and levels of SUA were measured. Patients were followed to death or to the time of contact (mean 2.6 years, range 1.8-5.0 years). RESULTS: Patients averaged 65 +/- 11 years of age, 78% were male and 170 subjects died during the follow-up period. In univariate analysis of prospectively defined quintiles, SUA predicted all-cause mortality (fifth quintile vs. first four quintiles: hazard ratio 1.9, p < 0.001). In multivariable Cox regression controlling for 20 covariables, independent predictive value for mortality was retained by SUA (hazard ratio 1.5, confidence interval 1.02-2.1, p = 0.04). In subgroup analysis based on diuretic use status, SUA independently predicted mortality among patients not using diuretics, while SUA was not a significant predictor of mortality among those who used diuretics. CONCLUSIONS: In patients with significant, angiographically defined CAD, SUA predicted mortality independent of traditional risk factors. This suggests that elevated SUA may be a risk factor for mortality in patients with significant cardiovascular disease and may be a stronger secondary than primary risk factor in CAD.

Aged↗
PubMed2002

Adaptation to multiday ozone exposure is associated with a sustained increase of bronchoalveolar uric acid.

The phenomenon of ozone tolerance is described, but the underlying mechanisms remain unknown. We tested whether adaptation to multiday ozone exposure was related to an upregulated pulmonary antioxidant defence. Six calves were exposed to 0.75 ppm ozone, 12 h day(-1) for seven consecutive days. Pulmonary function tests and bronchoalveolar lavage (BAL) were performed before, after the first (D1), third (D3) and seventh (D7) exposure. Differential cell count, total proteins, 8-epi-PGF2alpha, glutathione and uric acid were determined in BAL. Dynamic lung compliance and arterial oxygen tension were significantly decreased and lung oedema impaired pulmonary function on D1. By repeating ozone exposures, progressive functional adaptation occurred. Ozone induced a significant increase of BAL neutrophil percentage on D1. On D3 and D7, neutrophil percentage was progressively decreased, but remained significantly elevated. BAL total proteins were significantly increased on D1 and decreased progressively until D7. 8-Epi-PGF2alpha was significantly increased on D1 and was returned to baseline on D3 and D7, whilst glutathione significantly increased on D3 and returned to baseline on D7. Uric acid was increased ten-fold on D1. On D3, uric acid was increased six-fold and was persistently elevated at D7. This study suggests that ozone adaptation of functional and inflammatory variables is accompanied with sustained BAL uric acid elevation.

Animals↗
PubMed1983

Prevention of recurrent uric acid and calcium oxalate stones by administration of the xanthine oxidase inhibitors Milurit 100 and Milurit 300.

Disturbances in purine metabolism with hyperuricaemia and/or hyperuricosuria are a risk factor in uric acid and Ca oxalate stone formation. By way of a competitive xanthine oxidase inhibition, the formation of uric acid is reduced by allopurinol. In investigations on two groups of patients, Milurit could be demonstrated to decrease the uric acid levels in serum and urine. No differences could be seen in the dosages of 3 x 100 mg or 1 x 300 mg Milurit. Therefore, in stone recurrence prevention, the administration of Milurit 300 is recommended.

Adolescent↗
PubMed1990

[The effect of oral calcium loading on the serum concentrations and urinary excretion of uric acid in patients with recurrent calcium nephrolithiasis and hypercalciuria].

The authors have established that to higher calciuria in patients with calcium nephrolithiasis correspond higher vales of uric acid serum concentrations and urine excretion than in the controls. In the oral calcium tolerance test a significant correlation was found between the changes in the uric acid urine excretion and those in the diuresis. The following conclusions are put forward. I. In the patients with recurrent calcium nephrolithiasis and hypercalcinosis one should look for active impairment of uric acid metabolism which should be kept in mind when an antirecurrence treatment is planned. 2. The established parallel increase of uricosuria and calciuria in the oral calcium tolerance test means that to patients with recurrent calcium nephrolithiasis and gout a rich calcium diet should not be prescribed since it increases the risk of formation of calcium oxalate stones.

Administration, Oral↗
PubMed2006

Unearthing uric acid: an ancient factor with recently found significance in renal and cardiovascular disease.

Uric acid is strongly associated with cardiovascular and renal disease, but is usually not considered to have a causal role. However, recent experimental, epidemiological, and clinical studies provocatively suggest that uric acid may contribute to the development of hypertension, metabolic syndrome, and kidney disease in some patients. Clinical studies are urgently needed to examine this important possibility.

Animals↗