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PubMed1988

Differential effects of exercise intensity on serum uric acid concentration.

To investigate the effects of exercise intensity and short-term training on alterations in plasma uric acid, two series of experiments were performed using untrained male subjects. In series 1, 6 subjects (age 19 to 23 yr) cycled at 120% VO2max for 1 min followed by 4 min recovery until fatigue or until 24 repetitions had been completed. In series 2, 7 subjects (age 19 to 25 yr) cycled continuously at 65% VO2max for 2 h. In both experiments, short-term training was performed by repeating the exercise protocol for three consecutive days. In series 1, a progressive increase of 40% (P less than 0.05) was observed on day 1 in plasma uric acid concentration over the duration of the exercise. On day 2, pre-exercise values remained elevated over day 1 (mean +/- SD, 476 +/- 77 vs 352 +/- 30 mumol.l-1) and showed a further 23% increase (P less than 0.05) with exercise. Although resting uric acid concentrations on day 3 were elevated (P less than 0.05) over day 1, the exercise levels between day 1 and day 3 were not different (P greater than 0.05). In contrast, in series 2, prolonged sub-maximal exercise failed to stimulate increases in uric acid concentration either between days or within days. It is concluded that exercise intensity rather than total work output is a critical factor mediating increases in blood uric acid concentration. These results are consistent with the interpretation that uric acid formation may arise from purine nucleotide degradation and fast-twitch fiber utilization during conditions of high energy utilization.

Adult↗
PubMed1998

Effect of uric acid and chemical analogues on oxidation of human low density lipoprotein in vitro.

Oxidative modification of low density lipoprotein (LDL) is implicated in the early development of atherosclerosis. In the present study, attention has been focused toward the potential protective effects of uric acid and purine-based chemical analogues in copper-promoted oxidative changes to human LDL in vitro. Between 5-100 mumol/l uric acid protected LDL from oxidative degradation in a concentration dependent manner. However, 5 mumol/l were not capable of inhibiting the consumption of LDLs natural antioxidative components, alpha-tocopherol and beta-carotene, but led to a more than two-fold prolongation, up to 3 h, of the lag phase before onset of polyunsaturated acid (PUFA) oxidation. 100 mumol/l uric acid, which is still below the human serum level of 300 mumol/l, reduced consumption of alpha-tocopherol and beta-carotene by about 50% and largely suppressed PUFA oxidation for up to 4 h. A more lipophilic series of methyl analogues of uric acid exhibited less activity. Neither 1,3-dimethyl uric acid, nor the 1,3,7- or 1,7- or 3,7-methylated compounds, all at 100 mumol/l, exceeded the antioxidative potential of 10 mumol/l uric acid. At concentrations up to 100 mumol/l xanthine and its analogues lacked virtually any protective effects toward the LDL constituents. In conclusion, the present study indicates that uric acid at concentrations similar to its physiological levels, and also related analogues are able to suppress oxidative degradation of LDL components. In view of the various mechanisms underlying atherogenesis in vivo, the protective effect in terms of modulating redox reactions and oxidative events in the blood or at the arterial wall appears of potential importance.

Antioxidants↗
PubMed2005

Sex-related differences in relations of uric acid to left ventricular hypertrophy and remodeling in Japanese hypertensive patients.

Both hyperuricemia and echocardiographically determined left ventricular (LV) mass have a well-determined association with cardiovascular morbidity and mortality. However, whether or not there is a sex difference in the association of serum uric acid level with LV mass has never been systematically explored. We examined the sex-specific relation of serum uric acid level and echocardiographic indexes of LV structure in never-treated patients with essential hypertension. We enrolled 160 never-treated hypertensive patients (89 men and 71 women) to assess the possible relationship between LV mass and serum uric acid levels. LV measurements were performed according to the recommendations of the American Society of Echocardiography and the Penn Convention. LV mass was indexed by height, body surface area and height raised to the 2.7th power. A positive significant correlation between LV geometry (LV mass, indexed LV mass and relative wall thickness) and serum uric acid level was found in male hypertensive patients but not in female hypertensive patients. Independent determinants of serum uric acid levels in male hypertensive patients were LV mass and serum creatinine levels. In addition, male hypertensive patients with concentric hypertrophy showed the highest serum uric acid levels. In comparison, independent determinants of serum uric acid levels in female hypertensive patients were age and serum creatinine levels. In conclusion, these findings indicate a sex difference in the association of uric acid with LV geometry in Japanese hypertensive patients. In addition, the finding that the highest levels of serum uric acid were observed in our male hypertensive patients with concentric hypertrophy confirmed the previous reports that these patients have the highest risk for cardiovascular morbidity and mortality.

Aged↗
PubMed2005

A causal role for uric acid in fructose-induced metabolic syndrome.

The worldwide epidemic of metabolic syndrome correlates with an elevation in serum uric acid as well as a marked increase in total fructose intake (in the form of table sugar and high-fructose corn syrup). Fructose raises uric acid, and the latter inhibits nitric oxide bioavailability. Because insulin requires nitric oxide to stimulate glucose uptake, we hypothesized that fructose-induced hyperuricemia may have a pathogenic role in metabolic syndrome. Four sets of experiments were performed. First, pair-feeding studies showed that fructose, and not dextrose, induced features (hyperinsulinemia, hypertriglyceridemia, and hyperuricemia) of metabolic syndrome. Second, in rats receiving a high-fructose diet, the lowering of uric acid with either allopurinol (a xanthine oxidase inhibitor) or benzbromarone (a uricosuric agent) was able to prevent or reverse features of metabolic syndrome. In particular, the administration of allopurinol prophylactically prevented fructose-induced hyperinsulinemia (272.3 vs.160.8 pmol/l, P < 0.05), systolic hypertension (142 vs. 133 mmHg, P < 0.05), hypertriglyceridemia (233.7 vs. 65.4 mg/dl, P < 0.01), and weight gain (455 vs. 425 g, P < 0.05) at 8 wk. Neither allopurinol nor benzbromarone affected dietary intake of control diet in rats. Finally, uric acid dose dependently inhibited endothelial function as manifested by a reduced vasodilatory response of aortic artery rings to acetylcholine. These data provide the first evidence that uric acid may be a cause of metabolic syndrome, possibly due to its ability to inhibit endothelial function. Fructose may have a major role in the epidemic of metabolic syndrome and obesity due to its ability to raise uric acid.

Animals↗
PubMed1979

Uric acid: a risk factor for coronary heart disease?

The association between serum uric acid and the prevalence of ECG abnormalities was analyzed for 24.997 employed men and women, white and black, age 18--64 years, from the Chicago Heart Association (CHA) Detection Project in Industry. In addition, the relationships between uric acid and 5-year mortality from all causes, from cardiovascular diseases (CVD), and from coronary heart disease (CHD) were analyzed for 7804 white men and women age 45--64 years from this study and 967 white men age 44--63 years from the Chicago People's Gas Company Study. For men, the association between uric acid and the prevalence of ECG abnormalities and with mortality appear to be secondary to associations between uric acid and other risk factors. For women, however, the associations could not be explained by other risk factors.

Arrhythmias, Cardiac↗
PubMedDate not supplied

Estimation of plasma uric acid in pregnancy induced hypertension (PIH). Is the test still relevant?

Plasma uric acid and creatinine were estimated at each visit of 59 consenting women attending ante-natal clinic. Results in the third trimester of pregnancy confirmed that the plasma uric acid was able to differentiate between normal pregnancy and those with PIH at P < 0.002. The results of those with ordinary hypertension and the women who developed pre-eclampsia were similar. Plasma creatinine was found to be able to differentiate between women with ordinary hypertension (97.45 +/- 25.03 umol/L) and those with pre-eclampsia (288.75 +/- 191.97 umol/L) at P < 0.01. For patients with pre-eclampsia who developed convulsions, there invariably was a further rise in the plasma uric acid levels. Monitoring of plasma creatinine level among patients with PH will help to predict those at risk of developing pre-eclampsia. In the same way, monitoring of plasma uric acid level in those with pre-eclampsia will help to predict those that will develop eclampsia. The tests are inexpensive but sensitive, which is in contrast to many more expensive electronic alternatives.

Adult↗
PubMed1985

[Blood uric acid and arterial hypertension in pregnancy. Interpretation and prognostic value].

The serum uric acid level varies during pregnancy. Based on the graph of this assay over time, the authors have distinguished three different ranges with very different foeto-maternal prognoses in hypertensive pregnant women. They conducted a retrospective study of 77 cases of hypertensive pregnant women with a total of 173 assays of the serum uric acid and a prospective study of 49 cases of normal pregnancies with 65 assays of the serum uric acid. The authors define a dangerous zone in which foeto-maternal complications were observed in 94 per cent of cases; a zone with a good prognosis in which complications were observed in only 2 per cent of cases; and an intermediate "warning" zone (covering one third of the assays), in which essentially foetal complications were observed in 32 per cent of cases. An interpretation of the serum uric acid in relation to the term of the pregnancy is therefore useful to determine the foeto-maternal prognosis in the majority of cases and constitutes a valuable parameter for monitoring the pregnancy and for the adaptation of the treatment to the severity of the disease.

Female↗
PubMed1999

Inverse association between coffee drinking and serum uric acid concentrations in middle-aged Japanese males.

Consumption of caffeine-rich beverages, which have diuretic properties, may decrease serum uric acid concentrations. We examined cross-sectionally the relationship of coffee and green tea consumption to serum uric acid concentrations in 2240 male self-defence officials who received a pre-retirement health examination at four hospitals of the Self-Defence Forces between 1993 and 1994. The mean levels of coffee and green tea consumption were 2.3 and 3.1 cups/d respectively. There was a clear inverse relationship between coffee consumption and serum uric acid concentration. When adjusted for hospital only, those consuming less than one cup of coffee daily had a mean serum uric acid concentration of 60 mg/l, while that of those drinking five or more cups of coffee daily was 56 mg/l (P < 0.0001). No such relationship was observed for green tea, another major dietary source of caffeine in Japan. The relationship between coffee consumption and serum uric acid concentration was independent of age, rank in the Self-Defence Forces, BMI, systolic blood pressure, serum creatinine, serum total cholesterol and serum HDL-cholesterol concentrations, smoking status, alcohol use, beer consumption and intake of dairy products. These findings suggest that coffee drinking may be associated with lower concentrations of serum uric acid, and further studies are needed to confirm the association.

Alcohol Drinking↗
PubMed2003

Peroxynitrite flux-mediated LDL oxidation is inhibited by manganese porphyrins in the presence of uric acid.

We have studied the role of three Mn(III)porphyrins differing in charge, alkyl substituent length and reactivity, on LDL exposed to low fluxes of peroxynitrite (PN) in the presence of uric acid. Mn(III)porphyrins (5 microM, MnTE-2-PyP(5+), MnTnOct-2-PyP(5+), and MnTCPP(3-)) plus uric acid (300 microM) inhibited cholesteryl ester hydroperoxide formation, changes in REM as well as spared alpha- and gamma-tocopherol. MnTnOct-2-PyP(5+), the more lipophilic compound, was the most effective in protecting LDL lipids, while MnTCPP(3-) exerted the lesser protection. Mn(III)porphyrins react fast with PN ( approximately 10(5)-10(7) M(-1) s(-1)) to yield a O=Mn(IV) complex. The stoichiometry of uric acid consumption was approximately 1.7 moles per mol of PN, in agreement with reactions with both the O=Mn(IV) complex and nitrogen dioxide. A shift from an anti- to a pro-oxidant action of the Mn(III)porphyrin was observed after uric acid was significantly consumed, supporting competition reactions between LDL targets and uric acid for the O=Mn(IV) complex. Overall, the data is consistent with the catalytic reduction of PN in a cycle that involves a one electron oxidation of Mn(III) to Mn(IV) by PN followed by the reduction back to Mn(III) by uric acid. These antioxidant effects should predominate under in vivo conditions having plasma uric acid concentration range between 150 and 500 microM.

Humans↗
PubMed2002

The effects of the addition of micronised fenofibrate on uric acid metabolism in patients receiving indapamide.

OBJECTIVE: Hyperuricaemia is associated with indapamide administration. In contrast, micronised fenofibrate can significantly decrease serum uric acid levels. However, there are no data on the effect of combination therapy of indapamide with micronised fenofibrate on uric acid metabolism. METHODS: We studied 20 non-diabetic hypertensive patients with mixed dyslipidaemia in whom serum metabolic parameters, including uric acid levels in serum and urine, were measured before and after eight weeks of indapamide administration (2.5 mg once daily). This study was continued for a further eight weeks, when the indapamide was combined with micronised fenofibrate (200 mg once daily). RESULTS: Indapamide significantly decreased mean systolic and diastolic blood pressure (BP) from 153 +/- 9/97 +/- 8 mmHg to 138 +/- 8/93 +/- 4 mmHg (p< 0.05 for both comparisons). A significant increase in serum uric acid levels occurred after indapamide administration (from a mean value of 5.6 +/- 1.3 mg/dl (0.33 +/- 0.07 mmol/l) to 6.4 +/- 1.1 mg/dl (0.38 +/- 0.06 mmol/l), p < 0.01]. This effect was associated with a decrease in the fractional excretion of uric acid (from a mean value of 9.5 +/- 5% to 7 +/- 5.5%, p < 0.05). The addition of micronised fenofibrate significantly decreased plasma fibrinogen levels as well as total cholesterol, low-density lipoprotein cholesterol, apolipoprotein B (ApoB) and triglycerides, and increased high-density lipoprotein cholesterol and ApoA, levels. Fenofibrate administration was followed by a significant decrease in serum uric acid levels to 4.7 +/- 1.2 mg/dl (0.28 +/- 0.07 mmol/l), p < 0.01, owing to a substantial increase in fractional urate excretion to 11 +/- 3%, p < 0.01. CONCLUSION: The addition of micronised fenofibrate can correct the hyperuricaemic effect of indapamide administration.

Adult↗
PubMed1998

Reduced level of plasma antioxidant uric acid in schizophrenia.

There is evidence of dysregulation of the antioxidant defense system in schizophrenia. The purpose of the present study was to examine whether uric acid, a potent antioxidant, is reduced in the plasma of patients with schizophrenia. To this end, a within-subject, repeated measures, on-off-on haloperidol treatment design was utilized. Male schizophrenic patients with either a haloperidol treatment (n=47) or a drug-free condition (n=35) had significantly lower levels of plasma uric acid than the age- and sex-matched normal control subjects (n=34). Following haloperidol withdrawal, plasma uric acid levels were further reduced in schizophrenic patients (P=0.018; paired t-test, n=35). However, no relationship was found between uric acid levels and the length of the drug-free period (< 5 or > 5 weeks) or days drug free. In addition, the plasma levels of uric acid in patient groups were significantly and inversely correlated with psychosis. There was a trend for lower uric acid levels in relapsed patients relative to clinically stable patients. Smoking, which can modify plasma antioxidant capacity, was not found to have prominent effects on uric acid levels. The present finding of a significant decrease of a selective antioxidant provides additional support to the hypothesis that oxidative stress in schizophrenia may be due to a defect in the antioxidant defense system.

Adult↗
PubMed1988

Serum uric acid unrelated to cancer incidence in humans.

We examined the hypothesis that low levels of serum uric acid are associated with elevated cancer risk. A subpopulation (163,830 members) of a large health maintenance organization was followed for a mean of 9.8 years after a multiphasic health checkup at which serum uric acid level was measured. Total cancer incidence as well as site-specific incidence (for lung, colon, and prostate cancer in men and lung, colon, breast, uterine, and cervical cancer in women) was ascertained from hospital discharge records and the Surveillance, Epidemiology and End Results program in the San Francisco-Oakland Bay area. Age-adjusted cancer incidence was not elevated in the lower deciles of serum uric acid level. After adjusting for age, race, education, smoking, alcohol consumption, and body mass, using proportional hazards models, the risk of cancer was not elevated at lower levels of uric acid. Our results suggest that if increased risk of cancer is associated with low serum uric acid, this risk is associated with serum uric levels below those commonly seen in human populations.

Adult↗
PubMed1960

The relation of serum uric acid to haemoglobin level in patients with cardiac and respiratory disease.

An investigation was made of the serum uric acid in 130 male patients with long-standing cardiac or pulmonary disease. The mean serum uric acid was 4.66 mg. per 100 ml. with a standard deviation of +/-0.99. The serum uric acid increased parallel with a rise in the haemoglobin level. The coefficient of correlation was +0.5, which was nearly six times the standard error. The frequency of hyperuricaemia (over 6 mg. per 100 ml.) was 11 times in 47 patients with a haemoglobin level above 110% as compared with twice in 83 patients when the haemoglobin level was below this figure. The highest levels of serum uric acid were seen in patients with cyanotic congenital heart disease. Two of the patients with hyperuricaemia gave a suggestive history of gout, and this was believed to have been caused by the secondary polycythaemia. Serum uric acid levels were significantly higher, as were the haemoglobin concentrations, in the obese compared with the patients who were not obese.

Heart Diseases↗
PubMed1989

Serum uric acid and 11.5-year mortality of middle-aged women: findings of the Chicago Heart Association Detection Project in Industry.

The relationships of serum uric acid to mortality from all causes, the cardiovascular diseases, and cancer were evaluated in 6797 white women age 35-64 years followed for an average of 11.5 years in the Chicago Heart Association Detection Project in Industry (CHA). Serum uric acid levels at baseline were strongly and significantly associated with all causes mortality in this cohort, with control for multiple risk factors and with exclusion of hypertensives on treatment. When the analysis was performed on age-specific groups 35-44, 45-54, and 55-64 years of age, the association was observed primarily in women in the oldest age group. All cardiovascular deaths, deaths due to coronary heart disease, and all cancer deaths were also associated with serum uric acid levels in the 55-64 year old group. The relationships persisted with control for multiple risk factors and with exclusion of treated hypertensives. A site-specific analysis of cancer deaths demonstrated elevations in mean serum uric acid levels for nearly all sites. Differences in mean serum uric acid levels between decedents and survivors tended to be largest in the first 5 years of follow-up for the cardiovascular deaths, but for cancer decedents they tended to be larger for subsequent years of follow-up. As an initial report on the association of serum uric acid and cancer in women in this age group, the results of this study require confirmation. Although hormonal influences may play a role, pathophysiologic mechanisms relating serum uric acid to mortality in white women aged 55-64 are currently unknown.

Adult↗
PubMed1996

High uric acid: a metabolic marker of coronary heart disease among alcohol abstainers.

The association between serum uric acid level and risk of coronary heart disease (CHD) over 21 years was investigated among 6411 middle-aged Japanese-American men who were participants in the Honolulu Heart Program. In an age-stratified Cox regression model, high serum uric acid (quartile 4 [>6.7 mg/dl], relative to quartile 1 [<5.0 mg/dl]) was a significant predictor of definite CHD (RR = 1.33; 95% confidence interval = 1.08-1.63; p = 0.006). However, when adjustment for confounders (body mass index, heavy alcohol consumption, triglycerides, diastolic blood pressure, blood glucose, and the ratio of animal to vegetable protein) was made, the association of high uric acid with coronary events was substantially reduced and became nonsignificant (RR = 1.14; 95% confidence interval = 0.92-1.42; p = 0.21). There was a significant interaction between serum uric acid and drinking status (P = 0.03). Thus, the risk of definite CHD associated with high urate levels (quartile 4), relative to low levels (quartile 1), was elevated in the abstainers (RR = 1.40; 95% confidence interval = 1.01-1.93; p = 0.02), but not in light and moderate drinkers (RR = 1.1 1; 95% confidence interval = 0.79-1.55; p = 0.58) or among the heavy drinkers (>40 ml of ethanol/day; RR = 0.57; 95% confidence interval = 0.27-1.21; p = 0.08). It is concluded that elevated uric acid may be associated with higher CHD among alcohol abstainers. Whether raised urate is an etiological factor for CHD or a manifestation of existing arterial disease in nondrinkers deserves further investigation.

Adult↗
PubMed1981

Uric acid in a single urine sample from neonates with perinatal hypoxia.

In a referral neonatal intensive care unit, PaO2 values of 40 newborn infants were compared with the serum and urinary uric acid levels. The latter was estimated from the first urine obtained after admission. A significant inverse correlation was found between PaO2 and serum uric acid concentration and between PaO2 and urinary uric acid per creatinine ratio, but no correlation was seen between PaO2 and urinary uric acid concentration. The urinary uric acid per creatinine ratio was determined on the 1st, 2nd and 5th days of life in 27 normal prematures, 28 hypoxic prematures, 23 normal full-term infants and 25 hypoxic full-term neonates. Significantly higher values were obtained in both hypoxic groups on the 1st day, and in hypoxic prematures even on the 2nd day. Although creatinine as a reference substance is regarded as unreliable in the neonatal period, if a single urine sample is only available, determination fo the uric acid per creatinine ratio seems to be warranted, since higher values may retrospectively point to hypoxia.

Humans↗
PubMed1979

Amniotic fluid creatinine and uric acid levels in high risk pregnancy.

Comparison of two methods of creatinine and uric acid assay in amniotic fluid showed that the two-point-reaction rate measurement of creatinine and the enzymatic assay of uric acid give more reliable results than the methods used previously. At the end of pregnancy, increased creatinine and uric acid levels were found. In cases of blood group incompatibility the values were mostly in the normal range, while in diabetic or toxaemic mothers higher, normal and lower values were equally found. It has been concluded that a single investigation does not suffice for the estimation of fetal maturity. Only repeated tests showing an increase in the creatinine and uric acid levels offer reliable information.

Amniotic Fluid↗
PubMed1998

[The effects of fluid ingestion and its composition on uric acid metabolism during high intensity long term exercise].

The purpose of this study was to analyze the effects of fluid ingestion and its composition on uric acid metabolism after exercise. Six healthy males volunteered for the study which was comprised of three different experiments; Exp. 1, Exp. 2, and Exp. 3. In all the experiments, subjects performed treadmill exercise (70%VO2max) for 70 minutes respectively. For seven hours after exercise, subjects ingested mineral water at 10 degrees C ad-lib in Exp. 1, 1.5 times the volume of mineral water consumed in the first experiment in Exp. 2, and the same volume of sports drink as in the first experiment in Exp. 3. No significant differences were observed in oxygen uptake and heart rate during exercise among the three experiments, so it was considered that the produced serum uric acid (SUA) levels in the three experiments were about the same level. However, the decrease in SUA, urinary uric acid excretion (UUA), clearance of uric acid (CUA) and fractional excretion of uric acid (FEUA) in Exp. 3, in which the sports drink was consumed instead of mineral water were higher than in Exp. 1 and Exp. 2. On the other hand, no significant differences were found in Exp. 2 and Exp. 3. A significant relationship between UUA and FEUA was found among the three experiments, while there was no corrleation between UUA and urine volume. These results show that; 1) the sports drink ingestion can increase the efficiency of recovery from high serum uric acid after exercise, 2) the increase in uric volume due to high mineral water intake does not elevate UUA, and 3) the increase in UUA due to sports drink ingestion was associated with the increase of FEUA.

Adult↗