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PubMed2000

Does hyperuricemia affect mortality? A prospective cohort study of Japanese male workers.

A positive association between hyperuricemia and cardiovascular disease has been reported, but no study has evidenced yet the precise role of serum uric acid in the development of cardiovascular disease. In addition, no epidemiological studies have so far documented a decreased risk of cancer among people with hyperuricemia, even though the antioxidant action of uric acid has recently been stressed to inhibit DNA damage. The present prospective cohort study investigates the relationship between hyperuricemia and health hazards in a Japanese working population. The subjects were 49,413 Japanese male railroad workers, aged 25-60 years at enrollment. Serum uric acid and other baseline data were provided by annual health-survey records from 1975 to 1982. The vital status of the subjects was traced until the end of 1985 for those who remained alive. During an average 5.4-year study period, 984 deaths were recorded. Those with serum uric acid over 8.5 mg/dl showed elevated relative risks (RRs) of death in all causes (RR 1.62, p<0.01), coronary heart disease ( RR 1.52), stroke (RR 2.33, p<0.01), hepatic disease (RR 3.58, p<0.01), and renal failure ( RR 8.52, p<0.01), as compared with those with serum uric acid levels of 5.0-6.4mg/dl. The RR of death in all causes still remains statistically significant when adjusted by age and serum total cholesterol (2.00, p<0.01), age and alcohol intake (1.85, p<0.001), age and smoking (1.69, p<0.001), age and gout treatment (1.61, p<0.05), and also age and BMI (1.50, p< 0.05). On the other hand, the RR of all causes decreased but was still above 1.0 when adjusted by age and blood glucose (1.62), age and systolic blood pressure (1.32), age and GOT (1.23), and also age and history of cardiovascular disease (1.17). These results showed that hyperuricemia has a strong association with the RRs of death in all causes, coronary heart disease, stroke, hepatic disease and renal failure, and indicated that serum uric acid seems to be a considerable risk factor for reduced life expectancy.

Adult↗
PubMed1998

The epidemiology study of hyperuricemia and gout in a community population of Huangpu District in Shanghai.

OBJECTIVE: To investigate the prevalence of hyperuricemia and gout in a community population of Huangpu District in Shanghai. METHODS: In the target community, 2037 dwellers were interviewed with relevan questionnares from house to house. According to even house number 1017 blood samples were taken for serum uric acid (SUA) levels measured with the uricase-peroxidase enzymatic method. RESULTS: The prevalence of hyperuricemia was 14.2% in men (SUA > 70 mg/L, 62 cases), 7.1% in women (SUA > 60 mg/L, 41 cases), 10.1% in both sexes. Seven gout patients were all men. The prevalence of gout in 2037 dwellers in Huangpu District was 0.77% in men and 0.34% in both sexes. CONCLUSIONS: The mean SUA level in each age group in this survey was much higher than that of a previous study 1 carried out in Shanghai, Beijing and Guangzhou in 1980 (P < 0.05). And the prevalence of hyperuricemia was increased rapidly (in men: from 1.4% in the survey of 1980 to 14.2% in our survey; in women: from 1.3% in the survey of 1980 to 7.1% in our survey). Compared with Idonesia data in 1992, the prevalence of hyperuricemia and gout in our survey was lower than that in Indonesia (P < 0.05), which suggests that racial and genetic predispositions are key causative factors.

Adolescent↗
PubMed1992

The epidemiology of gout and hyperuricemia in a rural population of Java.

The prevalence of gout and hyperuricemia was investigated by a survey of a total population of 4683 rural adults. The successful response rate was 95.2%. Of the respondents 85.3% of the individuals were examined. The prevalence of gout and hyperuricemia in men was 1.7 and 24.3%, respectively. The male to female ratio was 34:1 for gout and 2:1 for hyperuricemia. The observed higher prevalence of gout and hyperuricemia in this male Malayo-Polynesian population compared with Caucasian data, in spite of a lower life expectancy and subsistence economy, suggests that genetic and racial predisposition are key causative factors.

Adolescent↗
PubMed1988

[Neonatal oliguria associated with hyperuricemia].

Acute renal failure syndrome in the newborn has many etiologic factors. Hyperuricemia as unique etiology of this syndrome has been seldom cited in literature, although is a well know factor operating together with others. From nine newborns with oliguria, hyperuricemia vas a contributing factor in appearance of the syndrome in seven. In the other two cases hyperuricemia was the sole possible etiologic factor in development of oliguria which was classified as functional. Hyperuricemia alone may be the unique etiologic factor in functional oliguria of the newborn being further investigations needed to understand its precise mechanism.

Acute Kidney Injury↗
PubMed1993

Community-based epidemiological study on hyperuricemia in Pu-Li, Taiwan.

A community-based survey to study the prevalence and factors associated with hyperuricemia was carried out by the Yang-Ming Crusade from 1987 to 1988 in Pu-Li Township, Taiwan. A total of 1,738, out of 2,573 registered residents over 30 years of age, were contacted for at least one of the two home-visit interviews or for a fasting blood test. The prevalence of hyperuricemia (> or = 458.2 mumol/L for men; > or = 392.7 mumol/L for women) was 17.3%. The prevalence increased with age. Men had a higher prevalence than women (20.3% vs 14.6%). To study the significant correlates of hyperuricemia, univariate analyses and logistic regression were used. The logistic regression analysis showed that after simultaneously controlling the covariates, four variables were significantly correlated with hyperuricemia: blood pressure, creatinine, triglyceride and organ meat consumption.

Adult↗
PubMed1996

[Non-drug therapeutics of idiopathic hyperuricemia].

Non-drug therapeutics of idiopathic hyperuricemia especially on dietetics and kinesitherapy, and character and therapy of syndrome-X-plus are reviewed. Recently, regulation of total calorie intake is emphasized rather than prohibition of highpurinemic food. Kinesitherapy is not always recommended: Exercises beyond anaerobic threshold aggravate hyperuricemia. Syndrome-X-Plus is a newly suggested condition causes myocardial ischemia in which hyperuricemia is found to be a critical factor, and therefore, improvement of hyperuricemia may prevent the disease.

Alcohol Drinking↗
PubMed1997

[Evaluation of the relation of job stress and food intake to hyperuricemia].

To evaluate the relation of job stress and food intake to hyperuricemia, a case-control study was performed in male subjects who had undergone complete physical examinations. Cases (n = 113) were those with hyperuricemia of over 7.5 mg/dl and controls (n = 113) were those with serum uric acid of less than 7.5 mg/dl. Stepwise regression analysis was performed using sixteen items which were significantly related to hyperuricemia by McNemar's method. Consequently, four items; "negative attitude toward work (Odds ratio 5.22, p < 0.01)", "tendency to become competitive in the job and other areas (Odds ratio 5.54, p < 0.01)" in type A behavior, "high meat consumption (Odds ratio 6.94, p < 0.01)", and "high fat intake (Odds ratio 4.05, p < 0.01)", were significantly related to hyperuricemia.

Adult↗
PubMed2003

Rasburicase (recombinant urate oxidase) for the management of hyperuricemia in patients with cancer: report of an international compassionate use study.

BACKGROUND: Hyperuricemia and tumor lysis syndrome (TLS) are serious complications that can occur during chemotherapy for hematologic malignancies, even if standard management procedures, including administration of allopurinol, are undertaken. Rasburicase, a recombinant urate oxidase that converts uric acid (UA) into the soluble compound allantoin, has been shown to control hyperuricemia faster and more reliably than allopurinol.(1) METHODS: A compassionate use trial, running from January 1999 to December 2001, provided access to rasburicase for patients in nine countries who were at risk for TLS during the initiation of chemotherapy. Of the 280 patients enrolled in the study, 278 received rasburicase and were included in the analysis. A total of 166 pediatric patients who had leukemia (approximately 74%), lymphoma (approximately 24%), or solid tumors (approximately 3%) were treated with rasburicase. One hundred twelve adults with either leukemia (68%) or lymphoma (30%) also were treated. Rasburicase (0.20 mg/kg) was administered intravenously once a day for 1 to 7 days, at the investigator's discretion. Two doses daily could be administered during the first 3 days. A response was defined as a reduction in UA level or maintenance of a UA level less than 7.5 mg/dL (or less than 6.5 mg/dL, for children age < 13 years). RESULTS: UA levels at 24-48 hours after administration of the last dose of rasburicase were available for 122 pediatric patients and 97 adult patients. The mean UA level in 29 hyperuricemic children decreased from 15.1 mg/dL to 0.4 mg/dL, whereas in 27 hyperuricemic adults, the mean level decreased from 14.2 mg/dL to 0.5 mg/dL. Prophylactic administration of rasburicase to prevent TLS during chemotherapy reduced UA levels from a mean of 4.4 mg/dL to 0.8 mg/dL in 93 nonhyperuricemic children and from 4.8 mg/dL to 0.4 mg/dL in 70 nonhyperuricemic adults (for all reductions in UA levels, P < 0.001). The response rate was 100%. Rasburicase was very well tolerated. Serious adverse events related to rasburicase were observed in one patient. CONCLUSIONS: The results of the current study confirm that rasburicase is safe and highly effective in the prevention and treatment of chemotherapy-induced hyperuricemia in both children and adults.

Adolescent↗
PubMed2006

Recombinant urate oxidase (Rasburicase) for the treatment of hyperuricemia in pediatric patients with hematologic malignancies: Results of a compassionate prospective multicenter study in Korea.

BACKGROUND: Hyperuricemia accompanying tumor lysis syndrome is a serious complication in neoplasia with rapid proliferation and destruction. To confirm the efficacy of recombinant urate oxidase (rasburicase) and its safety profile, a phase IV compassionate use prospective study was performed in Korean pediatric patients with hematologic malignancies. PROCEDURE: Rasburicase was administered at 0.2 mg/kg/day once daily for 3-5 days (twice daily allowed during the first 72 hr) by intravenous route for hyperuricemia (uric acid > 7.5 mg/dl). The study period was 5 weeks and consisted of a baseline assessment within 48 hr before the administration of rasburicase, 3-5 days of assessment during treatment and a follow-up assessment at 4 weeks after its final administration. RESULTS: The uric acid endpoint (< or =7.0 mg/dl) was reached in 97.3% (36/37) of the patients and uric acid levels were significantly reduced in all patients (P < 0.001). Drug related toxicities were mild and reversible without any grade 4 or serious adverse event associated with rasburicase. CONCLUSION: This study confirms that rasburicase is a safe and effective agent for the treatment of hyperuricemia associated with hematologic malignancies in pediatric patients.

Adolescent↗
PubMed2006

Hyperuricemia and gout following pediatric renal transplantation.

Hyperuricemia and gout are common complications in adult renal transplant recipients. In pediatric recipients, however, hyperuricemia seems to be rare, but data are scarce. Thirty-two children (21 males, 11 females) were investigated for a median time of 4.8 years (range: 0.4-11.2 years) following renal transplantation. The median age of this pediatric study group was 13.9 years (range: 5.7-20.3 years), and the calculated glomerular filtration rate (GFR) was 61 ml/min per 1.73 m(2) (range:12-88 ml/min per 1.73 m(2)). All patients were given calcineurin inhibitors, with 22 and ten children receiving cyclosporine A (CSA) and tacrolimus (TAC), respectively. The median plasma uric acid was 385 micromol/l (range: 62-929 micromol/l); 15 children (47%) were above the age-related normal range. Only one patient experienced gouty arthritis. There was a significant correlation between plasma uric acid concentration and both time span after transplantation and plasma creatinine, and an inverse correlation to GFR (p<0.05). No significant correlation was found between plasma uric acid and body mass index (BMI). Plasma uric acid concentrations were neither different among CSA- and TAC-treated children, nor did they correlate with drug exposure or blood trough levels of CSA or TAC. Plasma uric acid concentration was not different when compared to children with chronic renal failure (CRF) of a similar degree in native kidneys. We conclude that hyperuricemia is common among pediatric renal transplant recipients and rather a consequence of chronic renal transplant dysfunction than the use of calcineurin inhibitors. Gout, however, is rare.

Adolescent↗
PubMed2006

Association of methylenetetrahydrofolate reductase (C677T) polymorphism with hyperuricemia.

BACKGROUND AND AIMS: Homozygosity for the thermolabile variant of 5,10-methylene tetrahydrofolate reductase (C677T) has been suggested to be positively associated with the risk of vascular disease and neural tube defects. In addition, recent studies have suggested that elevated serum uric acid predicts ischemic heart disease, and epidemiological data on ethnic groups have suggested that genetic factors are determinants of serum uric acid levels. In this study, we tested the hypothesis that 5,10-methylenetetrahydrofolate reductase (C677T) polymorphism may be associated with hyperuricemia. METHODS AND RESULTS: Samples from 518 healthy individuals (268 men and 250 women) were analyzed for MTHFR genotyping and serum uric acid. The participants were categorized to homozygous wild type (CC), heterozygous for wild type and thermolabile (CT), or homozygous for the thermolabile (TT) variant. Serum uric acid was significantly higher in males and females with TT genotype than those with either CC or CT genotype (p=0.0001, ANOVA). Univariate and multivariate analysis showed that 5,10-methylenetetrahydrofolate reductase (C677T) polymorphism was a strong correlate and predictor of uric acid in males (r=0.28, p=0.0001, beta=0.673, p=<0.001) and in females (r=0.27, p=0.0001, beta=0.599, p=<0.001). Odds ratio analysis has also shown that the risk of hyperuricemia was greater in males (OR 3.1, CI 1.8-5.2, p=0.001) and females (OR 3.3, CI 1.9-5.7, p=<0.001) with CT genotypes and in males (OR 3.7, CI 1.3-10.7, p=0.014) and females (OR 3.2, CI 1.1-9.7, p=0.032) with TT genotypes than in those with CC genotypes. CONCLUSION: Results from this study suggest that mutation of 5-MTHFR C677T contributes to the higher uric acid levels in both males and females and may be a risk factor for hyperuricemia.

Adult↗
PubMed2005

Hereditary hyperuricemia and renal disease.

Hyperuricemia and gout have long been known to run in families. As well as an apparently multifactorial genetic component to classic gout itself, 2 rather unusual sex-linked single-gene disorders of purine biosynthesis or recycling have been defined: deficiency of the enzyme hypoxanthine-guaninephosphoribosyl transferase (HPRT), and overactivity of PPriboseP synthase. Both result in overproduction of urate, hyperuricemia, and secondary overexcretion that may lead to acute or chronic renal damage. Familial juvenile hyperuricemic nephropathy (FJHN) and autosomal-dominant medullary cystic kidney disease (ADMCKD) are more common but less well-defined hyperuricemic conditions resulting from a decrease in the fractional excretion of filtered urate, with normal urate production. Although having features in common, ADMCKD is distinguished in particular by the presence of medullary cysts. One major group of both disorders is associated with mutations in the gene for uromodulin, but this accounts for only about one third of cases, and genetic heterogeneity is present. Whether the genes involved in these latter disorders contribute to the polygenic hyperuricemia and urate underexcretion of classic gout remains unexplored.

Genetic Predisposition to Disease↗
PubMed2006

Genetic factors associated with gout and hyperuricemia.

Hyperuricemia and gout are common conditions that have long been known to have a heritable component. Obesity, diabetes, and chronic kidney failure are conditions with multifactorial inheritance that are associated with gout. In addition, social factors such as protein and alcohol intake affect serum uric acid levels. The current review discusses basic uric acid metabolism and the multigenetic inheritance of hyperuricemia. Several monogenic disorders affecting uric acid metabolism are reviewed. The genetics, pathophysiology, diagnosis, and treatment of familial juvenile hyperuricemic nephropathy/medullary cystic kidney disease, autosomal dominant disorders associated with hyperuricemia and progressive kidney failure, are described.

Blood Group Antigens↗
PubMed2006

Effect and mechanism of total saponin of Dioscorea on animal experimental hyperuricemia.

In this study, we investigated the effects and mechanisms of Total Saponin of Dioscorea (TSD) on animal experimental hyperuricemia. Mouse and rat hyperuricemic models were made by orally administering yeast extract paste once a day (30 and 20 g/kg, respectively), for 7 days. Yeast would disturb normal purine metabolism by increasing xanthine oxidase (XOD) activity and generating large quantities of uric acid. This model is similar to human hyperuricemia, which is induced by high-protein diets, due to a purine and nucleic acid metabolic disturbance. Another mouse hyperuricemia model was generated by intraperitoneal injection once with uric acid 250 mg/kg or potassium oxonate 300 mg/kg. Potassium oxonate, a urate oxidase inhibitor, can raise the serum uric acid level by inhibiting the decomposition of uric acid. Likewise, injecting uric acid can also increase serum uric acid concentration. The concentration of uric acid in serum or urine was detected by the phosphotungstic acid method, and the activity of XOD was assayed by a test kit. The results showed that TSD (240, 120 and 60 mg/kg, ig) could significantly lower the level of serum uric acid in hyperuricemic mice. TSD (120 and 60 mg/kg, ig) could also lower the level of serum uric acid in hyperuricemic rats, reduce the activity of XOD in the serum and liver of hyperuricemic rats, and increase the level of urine uric acid concentration as well as 24-hour total uric acid excretion. In conclusion, TSD possesses a potent anti-hyperuricemic effect on hyperuricemic animals, and the mechanism may be relevant in accelerating the excretion and decreasing the production of uric acid.

Animals↗
PubMed2005

Rasburicase therapy in acute hyperuricemia and renal dysfunction.

Neoplastic disorders may be complicated by acute renal failure (ARF). Different tumors may cause ARF: solid tumors involving the kidney, solid tumors not of hematological origin and not primarily involving the kidney or, more frequently, rapidly developing hematological tumors. The pathogenesis of ARF is different depending on the type of cancer, but the most frequent clinical feature is the acute tumor lysis syndrome, characterized by hyperuricemia, hyperphosphatemia, hyperkalemia, hypocalcemia and acute, frequently oliguric, ARF. The presence of a neoplastic disorder and associated acute illness may sometimes lead to the presence of immunodysfunction, septic complications and multiple organ dysfunction. In these settings patients develop systemic inflammation and diffuse endothelial damage, related to different mediators. Among these substances, in cancer patients, high circulating levels of uric acid are a common finding. Hyperuricemia is caused by the increase of purine metabolism, which is result of the increased cellular turnover or the aggressive cancer chemotherapy regimens that worsen cell lysis and release of purine metabolites. Even if hyperuricemia is not the first insult to the kidney, its development might represent a concomitant factor aggravating other previous or simultaneous insults. The most efficient therapy for lowering uric acid is rasburicase, a recombinant form of urate oxidase, a nonhuman proteolytic enzyme that oxidizes uric acid to allantoin. It is efficacious in reducing serum uric acid levels with associated diuresis more effectively and much faster than allopurinol, and to correct renal dysfunction more rapidly than allopurinol.

Acute Disease↗
PubMed2005

Hyperuricemia in kidney transplantation.

Hyperuricemia is a common problem among renal transplant recipients. Its prevalence is clearly attributable to cyclosporine (CsA) use, although individual patients may have other risk factors as well. CsA lowers the urinary clearance of uric acid. The specific mechanism for this is unknown, but may involve alteration in tubular transport. Hyperuricemia may add on to several other factors in contributing to progressive deterioration of graft function and ultimately graft loss. The therapy of hyperuricemia may be particularly challenging in transplant patients.

Chronic Disease↗
PubMed2006

Hyperuricemia and incidence of hypertension among men without metabolic syndrome.

The aim of this project was to study the risk of developing hypertension over a 6-year follow-up in normotensive men with baseline hyperuricemia (serum uric acid >7.0 mg/dL) but without diabetes/glucose intolerance or metabolic syndrome. We analyzed the data on men without metabolic syndrome or hypertension at baseline from the Multiple Risk Factor Intervention Trial. These men (n=3073; age: 35 to 57 years) were followed for an average of 6 years by annual examinations. Follow-up blood pressure among those with baseline was consistently higher than among those with normal serum uric acid concentration. We used Cox regression models for adjustment for the effects of serum creatinine, body mass index, age, blood pressure, proteinuria, serum cholesterol and triglycerides, alcohol and tobacco use, risk factor interventions, and use of diuretics. In these models, normotensive men with baseline hyperuricemia had an 80% excess risk for incident hypertension (hazard ratio: 1.81; 95% CI: 1.59 to 2.07) compared with those who did not. Each unit increase in serum uric acid was associated with a 9% increase in the risk for incident hypertension (hazard ratio: 1.09; 95% CI: 1.02 to 1.17). We conclude that the hyperuricemia-hypertension risk relationship is present among normotensive middle-aged men without diabetes/glucose intolerance or metabolic syndrome.

Adult↗
PubMed2006

Recent developments in our understanding of the renal basis of hyperuricemia and the development of novel antihyperuricemic therapeutics.

Although dietary, genetic, or disease-related excesses in urate production may contribute to hyperuricemia, impaired renal excretion of uric acid is the dominant cause of hyperuricemia in the majority of patients with gout. The aims of this review are to highlight exciting and clinically pertinent advances in our understanding of how uric acid is reabsorbed by the kidney under the regulation of urate transporter (URAT)1 and other recently identified urate transporters; to discuss urate-lowering agents in clinical development; and to summarize the limitations of currently available antihyperuricemic drugs. The use of uricosuric drugs to treat hyperuricemia in patients with gout is limited by prior urolothiasis or renal dysfunction. For this reason, our discussion focuses on the development of the novel xanthine oxidase inhibitor febuxostat and modified recombinant uricase preparations.

Carrier Proteins↗