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PubMed1976

Hyperuricemia in the hemolytic-uremic syndrome.

Elevated serum uric acid concentrations were found in 18 children with hemolytic-uremic syndrome. The highest recorded level in each patient ranged from 10 to 29 mg/100 ml, and nine patients had concentrations of greater than 20 mg/100 ml. During a 53-hour period of peritoneal dialysis, 5.5 gm of uric acid was removed from one infant. Although acute renal failure was probably the major factor, erythrocyte destruction and hyperlacticacidemia may also have been important in the pathogenesis of the hyperuricemia.

Blood Urea Nitrogen↗
PubMed1999

Mechanism of the uricosuric action of the anti-inflammatory drug E3040 used to treat inflammatory bowel disease I: study using a rat model of hyperuricemia.

E3040, a new class of anti-inflammatory drug, was found to reduce the plasma uric acid level in the first phase of clinical studies. In the present study, the mechanism of the uricosuric action of E3040 was investigated using the hyperuricemia model rat. The fractional excretion of uric acid (FEurate), an indicator of the excretion of uric acid in the renal tubules, at 30, 60 and 90 min after administration of E3040 (50 mg kg(-1)) was significantly elevated as compared with that in the control. This elevation of the FEurate by E3040 was dose-dependent. Although the FEurate was elevated spontaneously 30 min after administration of E3040-sulfate (E-Sul) and glucuronide (E-Glu) (100 mg kg(-1), respectively), the value was not significantly different from the control. Based on these results, it was suggested that E3040 has a uricosuric action, probably in the proximal tubules, and the uricosuric action after administration of E3040 may be mainly due to the parent drug. Concerning the tissue distribution, the kidney concentration of E-Sul after i.v. administration of the E3040 (50 mg kg(-1)) was higher than that of the parent drug (kidney/plasma ratio approximately 2).

Animals↗
PubMed1979

Genetics of hyperuricemia in families with gout.

Complex segregation analysis supports the polygenic hypothesis of Hauge and Harvald and Neel et al, according to which hyperuricemia ascertained through gout is rarely due to a major gene, evidence for which is not significant in two studies that were considered to favor a major locus.

Gene Frequency↗
PubMed2006

Association of the human urate transporter 1 with reduced renal uric acid excretion and hyperuricemia in a German Caucasian population.

OBJECTIVE: Human urate transporter 1 (hURAT1) is a member of the organic anion transporter family (SLC22A12) that mainly regulates tubular urate reabsorption. Loss-of-function mutations result in idiopathic hypouricemia. The present case-control study was designed to analyze whether hURAT1 might also be a candidate gene for hyperuricemia with primary reduced renal urate excretion. METHODS: DNA samples from 389 individuals with reduced fractional excretion of uric acid (FEUA) (< or =6.5%) and from 263 controls (FEUA >6.5%) were sequenced. Genotype frequencies between groups were compared by Cochran-Armitage trend test. RESULTS: Significantly different genotype distributions could be demonstrated for the -788 T >A (promoter; P = 0.014), the C258T (exon 1; P = 0.006), and the C426T (exon 2; P = 0.0002) polymorphisms, but not for the T1309C (exon 8) and the +18 C >T (intron 9) polymorphisms. The strongest association with reduced FEUA was observed for the C426T polymorphism, with odds ratios (ORs) of 1.59 and 2.54 (P = 0.0002) for the CT and TT genotypes, respectively. Adjusted values for FEUA in the C426T genotype, were significantly reduced decreasing to 7.3%, 6.7%, and 6.3% in individuals with the CC, CT, and TT genotypes, respectively (P = 0.004). Haplotypes were constructed from the -788 T >A, C258T, and C426T polymorphisms. Individuals carrying at least 1 ACT haplotype (n = 349) had a significantly higher risk for reduced FEUA than individuals without any ACT haplotype (n = 303) (OR 1.39, P = 0.041). CONCLUSION: These results indicate that polymorphisms in the N-terminus of the hURAT1 gene were significantly associated with reduced renal uric acid excretion. The main regulating factor seems to be located close to the C426T polymorphism or is in strong linkage disequilibrium.

Adult↗
PubMed1998

Lipoproteins in patients with isolated hyperuricemia.

BACKGROUND: There have been described abnormalities in the lipoprotein profile of hyperuricemic patients, it has not been clarified wether these abnormalities are due to the hyperuricemia or to the dyslipema often associated to these patients. Our aim is to study the apolipoprotein profile in hyperuricemic patients without dyslipemia compared to a control population. PATIENTS AND METHODS: 30 hyperuricemic patients and 26 healthy controls. Measurements were of blood uric acid, total cholesterol, total triglycerides, creatinine, HDL-C, and VLDL cholesterol, triglyceride, Apo B, Apo CII and Apo CIII (1 and 2). Uric acid clearance and fractionated excretion were measured in 24 h. urine samples. RESULTS: No significant differences were found between hyperuricemic and control patients in cholesterol, triglycerides and apo B in VLDL, or LDL and HDL cholesterol. The levels of apo B, Apo AI levels and apo CIII/apo CII were similar in the hyperuricaemic and controls. CONCLUSIONS: There are two types of hyperuricaemic patients, one group associated to hyperlipideamia and would be included in the X Syndrome. The other group not associated to other metabolic abnormalities. Is important to distinguish between these two groups to define the prognosis of a given patient because the greater cardiovascular risk linked hyperuricaemic patients could be related to the association to others cardiovascular risks factors.

Adult↗
PubMed1980

Complete destruction of both femoral heads following idiopathic necrosis of the femoral heads in a diabetic patient with hyperuricemia and hyperlipoproteinemia.

A practically complete destruction of both femoral heads including the femoral necks and acetabula was encountered in a 69-year-old patient with diabetes, which varied in intensity. This destruction, documented by radiographs which had been taken 8 years prior, had started as the typical picture of "idiopathic femoral head necrosis". In addition to diabetes, hyperuricemia and hyperlipoproteinemia were present at the time when the femoral head necrosis was first evidenced. One episode of gout was recorded. In recent years, following therapy, the hyperurecemia and hyperlipoproteinemia had normalized. The question is raised, as to whether or not the present radiological findings represent a complication of aseptic femoral head necrosis, combined with a diabetic arthropathy of the hip joints. Details of the angiographic findings and a spondylopathy, which have all the characteristics of a neuropathic spondylopathy, would favor this hypothesis. When associated with a diabetic condition, generalized osteoporosis and hypertrophic spondylosis of such a particular nature require special mention.

Aged↗
PubMed1990

Acute uric acid nephropathy in two gouty patients with moderate hyperuricemia and high urine acidity.

Acute uric acid nephropathy has been described almost uniformly in patients with massive uric acid overload (malignancies with rapid cell destruction, epileptic seizures). Severe hyperuricosuria and intratubular uric acid precipitation result. Here we present two patients with gout, normal uric acid production, and moderate hyperuricemia, both of whom developed acute uric acid nephropathy. Because of pronounced urine acidity (pH values of 4.6 and 5.0 in morning fasting urines), supersaturation with respect to undissociated uric acid exceeded solubility (0.54 mmol/l), despite basal urate secretions of less than 2.2 mmol/24 hours. Additional predisposing factors, such as uricosuric treatment, heavy beer-drinking, over-consumption of purine-rich foods, and hot environment, were superimposed in both cases.

Acute Kidney Injury↗
PubMed1990

Hyperuricemia-hyperlipemia association in the absence of obesity and alcohol abuse.

We carried out a study of 43 male asymptomatic subjects with high levels of uric acid but showing no signs of arterial hypertension, obesity or alcohol abuse. Initially, we investigated cholesterol levels, triglycerides in blood serum and the very low density lipoprotein fraction. The results showed asymptomatic hyperuricemia, frequently associated with mixed hyperlipidemia or hypertriglyceridemia. In our cases, however, the association was not connected to exogenous factors such as obesity or alcohol consumption. We also found the very low density lipoprotein fraction to be anomalous compared to the control group, which suggests that the metabolism of this lipoprotein is altered by the aforesaid association.

Adult↗
PubMed1982

Hyperuricemia in acute illness: a poor prognostic sign.

To clarify the role of the serum urate level and its change as a potential marker for severe tissue hypoxia, we have measured serum urate levels and urine uric acid excretion in 16 patients with acute cardiovascular disease. The six patients who died had a baseline mean serum urate level of 11.1 mg/lg (range, 6.6 to 15.5 mg/dl) and reached a peak mean value of 20.7 mg/dl (range, 13.6 to 33.0 mg/dl). Five of these patients had findings to suggest increased production of uric acid, in addition to decreased excretion of uric acid from impaired renal function. The 10 survivors had a baseline mean serum urate level of 6.8 mg/dl (range, 1.3 to 14.0 mg/dl) and a maximal mean peak value of 7.1 mg/dl (range, 2.9 to 14.0 mg/dl). There was no consistent evidence for increased production or decreased excretion of uric acid. Patients who died had a lower systolic blood pressure, arterial pH and plasma bicarbonate level and a higher heart rate and serum creatinine level compared with the patients ho survived. The observations suggest that marked hyperuricemia at the height of an illness may predict a fatal outcome. Tissue hypoxia may contribute to this sequence of events by leading to the depletion of adenosine triphosphate (ATP) and activation of purine nucleotide degradation to uric acid.

Acute Disease↗
PubMed1982

Variation of rat serum biochemical values following decapitation or anesthesia with ether, halothane or Innovar-VetR: rapid Innovar-VetR-induced hyperuricemia and hyperglycemia.

True reference values (TRV) should ultimately be determined in blood from inactive, unstimulated rats but in practice, acceptable reference values (ARV) may be established using blood from decapitated or anesthetized animals if one is cognizant of variations associated with blood sampling procedures. Data reported here illustrate some variations in serum biochemical values following decapitation or anesthesia. Decapitation does not provide serum in which ARV for sodium, potassium or lactate dehydrogenase can be found but ARV can be determined for glucose, insulin and several other parameters. It is suggested that both TRV and ARV for serum electrolytes be determined using serum from cannulated rats. All three anesthetics raised glucose levels and ether and halothane increased alkaline phosphatase activity. Both halothane and Innovar-VetR decreased insulin:glucose ratios suggesting inhibition of insulin release from the pancreas. Innovar-VetR also produced hypoxia due to severe respiratory depression and bradycardia as well as hyperuricemia, hyperglycemia and hyperphosphatemia. Techniques most likely to provide ARV should be of the shortest possible duration, afford least respiratory and cardiovascular suppression and minimize stimulation of the sympathetic nervous system.

Anesthetics↗
PubMed1988

Hypertriglyceridemia and hyperuricemia: effects of two fibric acid derivatives (bezafibrate and fenofibrate) in a double-blind, placebo-controlled trial.

The effects of bezafibrate and fenofibrate on serum lipoproteins and serum urinary uric acid were compared. In a double-blind, placebo-controlled, cross-over study, each drug was administered in random order for 6 weeks followed by a 3-week drug-free phase to ten men with primary hypertriglyceridemia. Serum triglyceride and cholesterol concentrations decreased significantly with both fenofibrate and bezafibrate, although no significant change in serum apolipoprotein B, serum low density lipoprotein (LDL) cholesterol or serum high density lipoprotein (HDL) cholesterol concentrations was apparent. Serum uric acid levels, which were elevated on placebo and bezafibrate, were significantly reduced by 20% by fenofibrate. This was associated with an increase in renal uric acid clearance of 30% during fenofibrate therapy. Because it seems likely that hypertriglyceridemia and hyperuricemia are linked by a common carbohydrate inducibility, we studied the acute hyperuricemic response to orally administered fructose. Fructose (50 g) caused the anticipated rise in serum urate reaching a peak between 60 and 90 minutes, which was quantitatively greater in the men with hypertriglyceridemia than in healthy controls. The serum uric response to fructose was unaffected by bezafibrate, but was converted to normal by fenofibrate. The hyperuricemic action of fenofibrate is of sufficient magnitude to be of therapeutic value in the management of patients whose hypertriglyceridemia is associated with gout.

Bezafibrate↗
PubMed1994

Influence of daily drinking habits on ethanol-induced hyperuricemia.

We examined the influence of alcohol drinking habits on the serum uric acid level after the ingestion of a small amount of ethanol. Subjects were divided into two groups according to their alcohol drinking habits--regular drinkers, who consume more than 60 g ethanol every day, and nondrinkers/occasional drinkers, who consume less than 20 g ethanol occasionally. Drinking 0.5 g ethanol/kg increased serum uric acid levels in regular drinkers by 52.6 +/- 26.3 mumol/L (0.8 +/- 0.4 mg/dL), whereas it did not in nondrinkers/occasional drinkers. Urinary excretion of uric acid was unaltered in both groups. Hypoxanthine and xanthine in both plasma and urine and serum acetate were increased more in regular drinkers than in nondrinkers/occasional drinkers. Accelerated adenine nucleotide degradation secondary to enhanced ethanol oxidation likely explains the ethanol-induced hyperuricemia in regular drinkers.

Acetates↗
PubMed1976

Neonatal hyperuricemia.

Serum concentrations and urinary excretion of uric acid were measured in ten normal newborn infants and in 13 patients with the idiopathic respiratory distress syndrome. In the normal infants, serum urate increased from a mean value of 6.0 mg/dl in cord blood to 7.0 mg/dl at 24 hours, followed by a decrease to 3.5 mg/dl over the next three days. The infants with IRDS had higher serum urate concentrations during the first three days of life, and the urinary excretion of uric acid over the period of 12 to 36 hours of age was also higher than in the normal infants. In both groups of neonates the correlation of maximal serum urate values with the urinary excretion was positive, which indicates that neonatal hyperuricemia is not due to renal retention but to increased production of uric acid. It is postulated that this overproduction results from increased nucleotide breakdown associated with perinatal hypoxia. Because of high serum and urinary uric acid concentrations, maintenance of adequate hydration and urinary flow as well as alkalinization of urine is recommended.

Birth Weight↗
PubMed1977

Tubular function impairment in patients with asymptomatic hyperuricemia.

Renal function studies were done on asymptomatic hyperuricemic subjects and normouricemic controls matched as to age, sex and blood pressure. Abnormal urinary sediments and proteinuria were found more frequently in asymptomatic hyperuricemic subjects than in the controls. In addition, the maximal osmolar concentrating ability of urine was markedly reduced in the asymptomatic hyperuricemic subjects. There was no difference in renal function measured by phenolsulfonphthalein excretion between the groups. Our results suggest that hyperuricemia alone may contribute to renal tubular impairment.

Adult↗
PubMed1996

Clustering of dyslipidemia, hyperuricemia, diabetes, and hypertension and its association with fasting insulin and central and overall obesity in a general population. Atherosclerosis Risk in Communities Study Investigators.

Clustering of elevated triglycerides, decreased high-density lipoprotein cholesterol (HDL-C), hyperuricemia, diabetes, and hypertension has been related to insulin resistance/high insulin levels and central and/or overall obesity. The extent to which these abnormalities cluster and whether hyperinsulinemia, central adiposity, and overall obesity each independently associate with this clustering were evaluated in 14,481 US whites and African-Americans 45 to 64 years of age. With the exception of hypertension, abnormalities rarely existed in isolated form. Clustering greatly exceeded chance association (P < .001). Although this clustering was greater in relative terms (ratio of observed to expected cluster frequency) in the lean and less centrally obese, it was greater in absolute terms (observed minus expected cluster frequency as a percent of total population) in the more centrally and more generally obese. The greatest excesses were found for clusters that included both hypertriglyceridemia and low HDL-C. Multiple logistic regression models showed strong and independent graded relationships of clusters with quintiles of fasting insulin (fifth quintile odds ratio, 10 to 54, P < .001) and to a lesser degree with quintiles of the waist to hip ratio (2.2 to 5.4, P < .001 for most) and of body mass index (1.6 to 4.5, P < .05 for most). In conclusion, all abnormalities cluster in excess of that predicted by chance, with clusters showing remarkable and graded independent associations with fasting hyperinsulinemia and to a lesser extent with central and overall obesity. Thus, a metabolic syndrome occurs in both lean and obese middle-aged US adults.

Cluster Analysis↗
PubMed2001

European experience in the treatment of hyperuricemia.

The nonrecombinant form of urate oxidase has been routinely used in France since 1975 as standard practice in the initial management of non-Hodgkin's lymphoma (NHL) and acute lymphoblastic leukemia (ALL), and for prevention of tumor lysis syndrome (TLS). A retrospective study was performed to evaluate the frequency of metabolic complications and dialysis in 410 patients with B-cell stage III and IV NHL and L-3 ALL treated in France according to the LMB89 protocol, and to compare these results to those of other series of patients treated without urate oxidase. Of the 57 patients treated at Institut Gustave-Roussy, only five had metabolic complications occurring in the first cycle of chemotherapy. Two patients (3.5%) underwent dialysis: one because of oliguria, the second for preventive reasons. In all the other cases, metabolic problems were successfully resolved or prevented, using nonrecombinant urate oxidase (Uricozyme, Sanofi-Sythélabo, Inc, Paris, France) in combination with hyperhydration. Nonrecombinant urate oxidase is generally well tolerated. However, allergic reactions may occur, with rates varying from 0% to 4.5%. In addition, the extraction technology used to produce the product is limited by a low yield. A recombinant form of urate oxidase (rasburicase) was therefore developed. European clinical development results indicate that this agent produces a sharp and consistent decrease in uric acid levels in patients undergoing cytoreductive therapy. Additionally, there is a very low incidence of anaphylaxis. Studies have demonstrated the efficacy of urate oxidase in lowering uric acid levels, preventing hyperuricemia after the initiation of cytoreductive therapy, and preserving renal function in patients with B-cell advanced stage NHL and ALL.

Adolescent↗
PubMed2001

Urate oxidase in the prophylaxis or treatment of hyperuricemia: the United States experience.

Nonrecombinant urate oxidase (Uricozyme, Sanofi-Synthélabo, Inc, Paris, France) is a highly effective uricolytic agent, but its use is associated with hypersensitivity reaction manifested mainly by bronchospasm in approximately 5% of patients. Recently, several multi-institutional studies have evaluated the efficacy and safety of a recombinant urate oxidase (rasburicase). In a phase I/II study, all 131 patients with newly diagnosed acute lymphoblastic leukemia (ALL) or stage III/IV non-Hodgkin's lymphoma (NHL) experienced rapidly decreased plasma uric acid concentrations after receiving recombinant urate oxidase. Serum creatinine levels also decreased significantly. Toxicity was negligible, and none of the patients required dialysis. In a phase III trial, children with newly diagnosed ALL or stage III/IV NHL were stratified and randomized to receive recombinant urate oxidase or allopurinol. Results showed that the 27 patients who received recombinant urate oxidase had a significantly lower plasma uric acid concentration and a more rapid decline in serum creatinine level than did the 25 who took allopurinol. One patient in the recombinant urate oxidase group had hemolysis of unknown cause, and one in the allopurinol group required hemofiltration for hyperphosphatemia. To further assess the safety profile of recombinant urate oxidase, the data on 245 patients (173 children and 72 adults) who received this agent in a compassionate-use program were reviewed retrospectively. The drug produced dramatic decreases in uric acid concentrations in all patients. Nine patients (four children and five adults) had mild adverse reactions that were drug-related or of unknown etiology. These data suggest that recombinant urate oxidase is safe and effective in the prophylaxis and treatment of hyperuricemia associated with malignancy or chemotherapy.

Allopurinol↗
PubMed2001

Recombinant urate oxidase (rasburicase) in the prevention and treatment of malignancy-associated hyperuricemia in pediatric and adult patients: results of a compassionate-use trial.

To confirm the efficacy of recombinant urate oxidase (rasburicase) and to establish its safety profile, we reviewed the data on 173 children and 72 adults with malignancy who were treated with this new uricolytic agent in a compassionate-use trial. Rasburicase (0.20 mg/kg) was administered intravenously daily for 1 to 7 days and could be given every 12 h for the initial 72 h. Subsequent courses were allowed at a later date. Rasburicase produced a dramatic decrease in uric acid concentrations in all patients whether they received it for prophylaxis (n = 79) or treatment (n = 166) (P < 0.001 in all comparisons between the levels at diagnosis and those after treatment). The median post-treatment levels were 0.5 to 0.7 mg/dl. Repeated administrations were also effective in all 11 evaluable patients. Four children and five adults had mild adverse reactions that were drug related or of unknown etiology. In two of the children, the adverse events occurred during the second course. Rasburicase is highly effective and safe in the prophylaxis or treatment of malignancy- or chemotherapy-associated hyperuricemia in children and adults.

Adolescent↗