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High-dose methylprednisolone therapy in multiple sclerosis increases serum uric acid levels.

Uric acid, which is the final product of purine nucleoside metabolism, is a strong peroxynitrite scavenger. Several studies report on lower serum uric acid levels in multiple sclerosis. In this study, we investigated serum uric acid levels before and after high-dose methylprednisolone treatment (intravenous 1 g/day/5 days) in multiple sclerosis patients. Blood samples from 25 definite multiple sclerosis patients (11 male and 14 female) before and after methylprednisolone treatment (days 0, 6 and 30) and from 20 healthy donors (9 male and 11 female) were analyzed. Serum uric acid levels were measured using a quantitative enzymatic assay (Elitech diagnostics, Sees, France) according to the manufacturer's protocol, and the results were standardized using a commercial uric acid standard solution. We observed significantly increased serum uric acid levels 1 day after the termination of the therapy (day 6). These differences were sustained for 30 days after starting treatment (during remission period). Mean serum uric acid levels were significantly higher in the control group. These results suggest that increasing the uric acid concentration may represent one of the possible mechanisms of action of methylprednisolone in multiple sclerosis.

Adult↗

Effect of social support on stress-related changes in cholesterol level, uric acid level, and immune function in an elderly sample.

Strong social support systems, which in epidemiologic studies are associated with decreased morbidity and mortality, have been hypothesized to mitigate the harmful effects of stressful stimuli on the individual. The authors found that, among 256 healthy elderly adults, individuals with good social support systems tended to have lower serum cholesterol and uric acid levels and higher indices of immune function; these correlations were independent of age, body mass, tobacco use, alcohol intake, and degree of perceived psychological distress. Thus, social support systems may intervene between the stressful stimulus and the physiologic response to that stimulus.

Age Factors↗

Effects of diltiazem on plasma uric acid level and renal uric acid excretion in rats.

The effects of diltiazem on plasma uric acid level (PUA) and renal uric acid excretion were investigated in oxonate-loaded rats. Diltiazem (0.5 mg/kg, i.v.) decreased PUA without producing uricosuria, and it decreased fractional excretion of uric acid and renal blood flow. The present results suggest that diltiazem produces hypouricemia not accompanied by uricosuria, probably by affecting uric acid metabolism, and it may also cause an alteration in the renal handling of uric acid partly due to changes in renal hemodynamics.

Animals↗

Trends in serum uric acid levels 1961--1980.

Uric acid levels of adult male volunteers in a longitudinal study of human aging rose steadily between 1961 and 1978. In the 1,141 men with 3 serial physical examinations, who developed no diseases and who took no drugs known to affect uric acid levels, levels rose from means below 5.5 mg/dl in 1961--1963 to means above 6.5 mg/dl in 1975--1978. The best predictor of a longitudinal increase in uric acid level was a gain in weight, but this, and other significant predictors, explained only a small portion of the increase in this population. Preliminary data available from a fourth examination indicate that the rising trend has leveled off.

Adult↗

Effect of azlocillin on uric acid levels in serum.

Uric acid levels in serum were observed to fall precipitously in a group of 20 hospitalized asthmatic patients receiving azlocillin, bronchodilators, and steroids. None of the 20 hospitalized controls receiving the antiasthma therapy without azlocillin showed any decline in their uric acid levels. The levels for the azlocillin-treated group fell from a mean of 6.4 mg/dl to mean of 2.3 mg/dl, whereas those for the control group initially were 7.0 mg/dl and fell only to a mean of 6.5 mg/dl.

Adolescent↗

The relationship between Achilles tendon rupture and serum uric acid level.

The serum uric acid level of 30 patients with a rupture of the Achilles tendon was compared with that of 30 healthy control subjects matched for age and sex. In patients with a ruptured Achilles tendon the serum uric acid level was significantly higher than in the control subjects. This finding was not dependent on sex or race. It is possible that hyperuricaemia is a contributing factor in rupture of the Achilles tendon and warrants further study. It is suggested that this finding might be related to an adverse effect on the tendon's nutrition.

Achilles Tendon↗

[Diagnostic value of the CSF uric acid level (author's transl)].

Uric acid is the end-product of purine metabolism, and purines are the nitrogenous bases derived from the breakdown of nucleic acids. The CSF uric acid level is thought to be the index of the turnover of the nucleic acid and the degree of the cellular destruction in the brain. CSF uric acid levels were investigated in normal controls (30 cases) and in patients with brain tumor (20 cases), microcephalus (8 cases) and craniostenosis (4 cases). The mean values and standard deviations of CSF uric acid levels in normal controls were as follows; Newborn--9 yrs 0.34 +/- 0.09 mg/dl; 10 yrs--19 yrs 0.50 +/- 0.18 mg/dl; 20 yrs--29 yrs 0.46 +/- 0.05 mg/dl; 30 yrs--39 yrs 0.35 +/- 0.10 mg/dl; 40 yrs--49 yrs 0.35 +/- 0.23 mg/dl. Thereafter 0.72 +/- 0.21 mg/dl. The increased CSF uric acid levels after the age of 50 is thought to be due to the cellular destruction in the brain. CSF uric acid levels increased in patients with highly malignant brain tumor such as grade 3 or 4 astrocytoma and sarcomatous meningioma, but were normal in patients with grade 2 astrocytoma and meningiomas of meingothelial or fibroblastic type. CSF uric acid levels decreased in patients with microcephalus, but were almost normal in patients with craniostenosis. There is a significant correlation between CSF uric acid levels and the degree of brain atrophy in infants.

Adolescent↗

Serum uric acid levels and leukocyte nitric oxide production in multiple sclerosis patients outside relapses.

BACKGROUND: A number of studies found that patients with multiple sclerosis (MS) have low serum levels of uric acid. It is unclear whether this represents a primary deficit or secondary effect. Uric acid is a scavenger of peroxynitrite, which is the product of nitric oxide (NO) and superoxide. Because peripheral blood leukocyte NO production and NO metabolites in serum are raised in MS patients, associations might be expected between serum uric acid levels and peripheral NO production. METHODS: Serum levels of uric acid and NO production by peripheral blood leukocytes were measured in 60 patients with MS without a relapse in the past 3 months, and 30 age- and sex-matched healthy controls. Uric acid was determined with the uricase PAP method, and NO production was assayed by measuring nitrite concentration in supernatants of lysed leukocytes. RESULTS: Serum uric acid levels were not different between MS patients and controls. Compared to controls, patients with MS had significantly higher peripheral blood leukocytes nitrite concentrations (p<0.001). There was no correlation between leukocyte nitrite concentration and serum uric acid levels. CONCLUSIONS: Our findings suggest that in MS patients there is no primary deficit in serum uric acid. NO production by peripheral blood leukocytes is increased, but there is no association with serum uric acid levels.

Adult↗

Association between intronic SNP in urate-anion exchanger gene, SLC22A12, and serum uric acid levels in Japanese.

Serum uric acid levels are maintained by urate synthesis and excretion. URAT1 (coded by SLC22CA12) was recently proposed to be the major absorptive urate transporter protein in the kidney regulating blood urate levels. Because genetic background is known to affect serum urate levels, we hypothesized that genetic variations in SLC22A12 may predispose humans to hyperuricemia and gout. We investigated rs893006 polymorphism (GG, GT and TT) in SLC22A12 in a total of 326 Japanese subjects. Differences in clinical characteristics among the genotype groups were tested by the analysis of variance (ANOVA). In male subjects, mean serum uric acid levels were significantly different among the three genotypes. Levels in the GG genotype subjects were the highest, followed by those with the GT and TT genotypes. However, no differences between the groups were seen in the distributions of creatinine, Fasting plasma glucose (FPG), HbA(1c), total cholesterol, triglyceride, HDL cholesterol levels or BMI. A single nucleotide polymorphism (SNP) in the urate transporter gene SLC22CA12 was found to be associated with elevated serum uric acid levels among Japanese subjects. This SNP may be an independent genetic marker for predicting hyperuricemia.

Asian People↗

Serum uric acid levels in optic neuritis.

Uric acid, an antioxidant, is reduced in multiple sclerosis (MS). Patients with gout have a reduced incidence of MS. Optic neuritis (ON), often the first manifestation of MS, is not known to be associated with reduced uric acid. Patients with recent onset of ON were investigated to determine whether uric acid levels were reduced at presentation. Twenty-one patients with ON were included, 17 females and 4 males. The mean (SD) serum uric acid in the ON female group was 184.4 ( +/-55.1) micromol/L (range, 116-309 micromol/L), whilst in the control group it was 235.2 (+/- 50.2) micromol/L (range, 172-381 micromol/L). The difference was statistically significant (chi2 = 8.93, P = 0.003). In the small male cohort, mean (SD) serum uric acid was 305 (+/- 52.1) micromol/L, whilst in the control group it was 328 (+/- 80.4) micromol/L. These differences were not statistically significant. Reduced antioxidant reserve is possibly an early pathogenic mechanism in inflammatory demyelination, and raises the possibility that low uric acid levels could be an indicator of disease activity. Since optic neuropathies of other causes were not investigated, future research needs to determine whether low uric acid represents a unique feature of optic neuritis or is seen in other optic neuropathies.

Adult↗

Inheritance and alcohol as factors influencing plasma uric acid levels.

Variation in plasma uric acid levels in 206 pairs of male and female twins, aged from 18 to 34 years, was consistent with a simple model including only individual environmental and additive genetic effects and a heritability of h2 = 0.73. Individual environmental variation was estimated to be approximately the same as variation of individuals measured on two occasions. Correlations of DZ pairs were also consistent with sex-linked genetic effects. In men there was a significant genetic correlation with weekly alcohol consumption and as much as 18% of the variation in uric acid levels could be accounted for by genetic variation in alcohol consumption.

Adolescent↗

Plasma 5'-nucleotidase activities and uric acid levels in women with pre-eclampsia.

The present study investigated plasma activity of 5'-nucleotidase, a key enzyme in the production of adenosine, in pre-eclampsia, and evaluated the relationship between changes in 5'-nucleotidase activity, and levels of uric acid, endproduct of the purine metabolism, and the severity of pre-eclampsia. We measured plasma 5'-nucleotidase activities and uric acid levels in women with 18 normal pregnancies, mild and severe pre-eclampsia. In mild and severe pre-eclampsia, plasma 5'-nucleotidase activities and uric acid levels were significantly increased compared with those in normal pregnancy (p < 0.05). Plasma 5'-nucleotidase activity increased according to increases in uric acid levels and the severity of pre-eclampsia. These results suggest that increased plasma 5'-nucleotidase activity may, at least in part, be related to changes in purine metabolism in pre-eclampsia.

5'-Nucleotidase↗

Effects of low birth weight in 8- to 13-year-old children: implications in endothelial function and uric acid levels.

Low birth weight has been associated with an increased incidence of adult cardiovascular disease. Endothelial dysfunction and high levels of serum uric acid are associated with hypertension. In this study, we have determined whether uric acid is related to blood pressure and vascular function in children with low birth weight. We evaluated vascular function using high-resolution ultrasound, blood pressure, and uric acid levels in 78 children (35 girls, 43 boys, aged 8 to 13 years). Increasing levels of uric acid and systolic blood pressure were observed in children with low birth weight. Birth weight was inversely associated with both systolic blood pressure and uric acid; on the other hand, uric acid levels were directly correlated with systolic blood pressure in children of the entire cohort. Low birth weight was associated with reduced flow-mediated dilation (r=0.427, P<0.001). Because the children with low birth weight had elevated uric acid as well as higher systolic blood pressure levels, we evaluated the correlation between these variables. In the low birth weight group, multiple regression analysis revealed that uric acid (beta=-2.886; SE=1.393; P=0.040) had a graded inverse relationship with flow-mediated dilation, which was not affected in a model adjusting for race and gender. We conclude that children with a history of low birth weight show impaired endothelial function and increased blood pressure and uric acid levels. These findings may be early expressions of vascular compromise, contributing to susceptibility to disease in adult life.

Adolescent↗

[Effects of zotepine, a psychotropic agent, on the serum uric acid level of inpatients at a psychiatric hospital].

UNLABELLED: Serum uric acid levels were examined and compared to diagnostic groups of inpatients of a mental hospital. An action lowering serum uric acid level of zotepine was further evaluated in those patients. RESULTS: (1) In patients receiving some kind of psychotropic drugs, except for zotepine, mean serum uric acid level of patients with epilepsy in both sexes was significantly lowered in comparison with that of schizophrenia. Mean serum uric acid levels of male and female patients with alcoholism and organic brain disease were higher than that of schizophrenia without any statistical significance. (2) Mean serum uric acid level of patients treated with various psychotropic drugs, except for zotepine, was higher than that of patients receiving zotepine. (3) Zotepine decreased serum uric acid level parallel with its dosage (r=0.70, p less than 0.001) with a mean reduced rate of 54.1% (p less than 0.001), when serum uric acid levels of 32 patients were examined 3 times over 3 months before and during zotepine administration, respectively. (4) Maximum reduction of serum uric acid level occurred in 3-6 days following zotepine application. Controversely, it takes about 4 weeks to recover baseline level of serum uric acid after stopping zotepine administration. (5) Zotepine had no significant effect not only on the results of creatinine clearance test, but also on BUN level. However, it significantly increased level of uric acid clearance, and rate between uric acid clearance and creatinine clearance. The rate of uric acid clearance vs creatinine clearance correlated with the dosage of zotepine given. Zotepine is thought to decrease serum uric acid level via selective blocking of tubular reabsorption of uric acid in the kidney.

Adult↗