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PubMedDate not supplied

[Hyperuricemia and cardiac risK factors: epidemiologic study in the aged].

The aim of our study is to evaluate whether hyperuricemia may be considered a cardiovascular risk factor also in the elderly. 370 subjects over 60-years-old of both sexes were examined of which 148 presented an ischemic heart disease and 222, age and sex homogeneous, were considered as control group. Serum uric acid was determined. A strong difference among the two groups (p < 0.001) was statistically demonstrated. Such modifications were sex independent. A strict correlation of hyperuricemia and hyper trygliceridemia was present; in fact high uric acid levels were mostly found in the group with triglycerides > 200 mg/dl (p < 0.02). In the whole group and in males a stability of uric acid was noted. In females a significant increase among the first (60-69 years) and the second (70-79 years) age class was present. In conclusion, a positive role of hyperuricemia in the ischemic heart disease pathogenesis is possible.

Age Factors↗

PubMedDate not supplied

[Hyperuricemia and plasma renin activity in essential arterial hypertension].

The frequency of hyperuricemia in 253 patients with essential hypertension (EH) was studied. The level of uric acid in serum and frequency of hyperuricemia were determined in patients divided according to sex and renin plasma activity (RPA). High values of uric acid in serum were found in a total of 69 patients (27.3%), of which there were 40 males (30.1%) and 29 females (24.2%). The highest values of uric acid were found in those with high RPA, but the difference was significant only in males (p < 0.05). No correlation was observed between the values of the uric acid in serum and RPA in none of the renin subgroups. On the basis of our study, it was not possible to explain the high values of uric acid in serum in patients with EH, especially in those with high plasma renin activity, as well as the role of renin-angiotensin-aldosterone system in the pathogenesis of hyperuricemia.

Female↗

PubMed1993

[A case of Down syndrome with chronic renal failure caused by long-term asymptomatic hyperuricemia].

The elevation of serum urate levels in patients with Down syndrome has been reported by several investigators, but gout or renal dysfunction due to hyperuricemia has rarely been encountered. We described a case of Down syndrome showing chronic renal failure caused by long-term asymptomatic hyperuricemia. A 30-year-old man, who had persistent subclinical hyperuricemia for nine years, was noted to have pale face, weakness and hypertension. Laboratory findings revealed acute renal dysfunction. He died from uremic lung 7 months later. Autopsy disclosed a finding suggesting chronic urate nephropathy; many gouty microtophi with foreign body reaction in the renal medulla. It is important to estimate serum urate and to control increased serum urate level in order to prevent from renal dysfunction in Down syndrome.

Adult↗

PubMed1996

[Hyperuricemia and the kidney].

The risk for renal insufficiency by uric acid precipitation in medulla of kidney correlates with the degree of uric acid supersaturation in the urine, depending on uric acid concentration and urinary pH. The patients with gout or hyperuricemia have sometimes acidic urine and increased uric acid excretion. Accordingly, these patients frequently accompany by renal insufficiency. Improvement of hyperuricosuria, increasing of urine volume, and alkalinization of urine to pH6 6.5, are effective for the prevention from renal insufficiency. Acute renal failure related to hyperuricemia, can also occured secondary to cell lysis. Tumor lysis syndrome is a critical illness characterized by massive tumor cell death leading to severe hyperuricemia, hyperphosphatemia, hypocalcemia, and acute renal failure after starting chemotherapy to cancers, especially lymphoproliferative malignancies. Administration of allopurinol 500-600 mg and adequate hydration and alkalinization of urine are advocated to prevent acute renal failure. Intensive care with hemodialysis is often required to treat renal failure, because renal failure is reversible in most cases.

Acute Kidney Injury↗

PubMed1996

[Association of hyperuricemia with hyperlipidemia and obesity].

Various epidemiological evidences have shown the increased incidence of hyperuricemia in the subjects with hyperlipidemia and/or obesity. Our clinical study indicated the association was more close in hypertriglyceridemia to hyperuricemia than in hypercholesterolemia. Serum uric acid level increased more in Type IIb with elevated lipoprotein lipase (LPL) than those with low or normal LPL. Elevated LPL may be involved in the retarded uric acid clearance due to increased free fatty acids (FFA) in the serum, resulting in the elevation of uric acid and may be linked to the obesity-insulin resistance syndrome. Increased FFA may play an important role on the association of hyperuricemia with hypertriglyceridemia.

Fatty Acids, Nonesterified↗

PubMed1996

[Alcohol ingestion and hyperuricemia].

Purine nucleotide degradation during ethanol catabolism, inhibition of renal excretion of urate by lactic acid, and high purine content of certain kinds of beverage are responsible for the elevation of serum uric acid level following alcohol drinking. It is well documented that rapid consumption of ATP produces uric acid via purine nucleotide degradation. Since individuals with ALDH2*1 can catalyze ethanol readily, they consume large amount of ATP, and thus produce more hypoxanthine than those with ALDH2*2. Thus, daily drinker and heavy drinker tend to readily induce hyperuricemia after alcohol ingestion. A high purine content in beer may contribute to the increasing frequency of hyperuricemia. Restriction of any kind of alcohol beverages, especially beer, is necessary in the medical control of patients with gout or hyperuricemia.

Adenosine Triphosphate↗

PubMed1977

[De novo purine biosynthesis. In vitro measurement in hyperuricemia (author's transl)].

De novo purine biosynthesis has been investigated in circulating blood lymphocytes in vitro. N-formyl-glycinamide ribonucleotide (FGAR) has been mesured using 14C-formate incorporation in the presence of azaserine, a metabolic inhibitor blocking the metabolical pathway at the level of FGAR synthesis. Such a synthesis was measured in 20 healthy controls, 24 patients with primary gout (11 on allopurinol therapy) and 26 patients with chronic renal failure and secondary hyperuricemia (8 on allopurinol therapy). Among gouty patients without allopurinol therapy, FGAR synthesis was normal in 5 and increased in the others. FGAR synthesis was decreased in patients with renal failure whatever the therapy. However, FGAR synthesis remained increased in patients with a primary gout complicated with renal insufficiency. The test we propose for de novo purine biosynthesis measurement is simple and of value to analyse the patho-physiology of hyperuricemia and its therapy. The test allows an acurate discrimination between primary and secondary hyperuricemia in the presence of renal insufficiency.

Adult↗

PubMed1997

[Hyperuricemia as a risk factor for noninfectious diseases in the inhabitants of Chuvashia].

The relation of hyperuricemia with obesity, arterial hypertension, hyperlipoproteinemia, high intensity of lipid peroxidation, hyperinsulinemia, diabetoid carbohydrate disturbances (abnormal tolerance to carbohydrates and type-II diabetes mellitus) has been investigated in an epidemiological survey of a random population. The study covered 594 citizens of Chuvashia aged 16-65 years (mean age 39.4 +/- 0.5 years). Hyperuricemia is shown to be related with hyperlipidemia, arterial hypertension, obesity, high activity of lipid peroxidation and hyperinsulinemia. It is evident that on the population level hyperuricemia may serve an indicator of hormonal-metabolic athero-, diabetogenic shifts.

Adolescent↗

PubMed1997

[Therapy of hyperuricemia and gout].

Therapy of hyperuricemia and gout has to depend on pathogenesis and stage of the disease. Dietary regimen are in the forefront in treatment of asymptomatic hyperuricemia. Uric acid lowering drugs can only be supported in repeated serum-measures from 9 mg/dl up. The therapy of an acute attack of gout primarily is done with non-steroidal antiinflammatory drugs, in rare cases with colchicine or corticoids. Gouty arthritis in intermission, independent of the extent of hyperuricemia, as well as chronic gout are indications for an uric acid lowering pharmacotherapy, usually for life. A special therapeutic challenge arises out of renal complications and the frequent association with the metabolic syndrome.

Acute Disease↗

PubMed2026

Black Rice Anthocyanin-Hyaluronic Acid Complex Alleviates Hyperuricemia-Associated Renal Injury Through Synergistic Inhibition of the TLR4/NF-κB Pathway and Modulation of Uric Acid Transport.

Hyperuricemia-associated renal injury is closely linked to oxidative stress and inflammation, highlighting the need for safe dietary intervention. This study evaluated the protective effects of a black rice anthocyanin (ATC)-hyaluronic acid complex (HAA) against uric acid (UA)-induced injury. In UA-induced human renal proximal tubular epithelial (HK-2) cells, black rice ATCs, HA, and HAA improved cell viability and antioxidant defenses, as shown by increased glutathione (GSH) levels and catalase (CAT) and superoxide dismutase (SOD) activities. They also reduced malondialdehyde (MDA), reactive oxygen species (ROS), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β). HAA produced a greater reduction in TLR4/NF-κB-related inflammatory gene expression, suggesting that its cytoprotective and anti-inflammatory effects may be associated with modulation of this inflammatory axis. In hyperuricemic mice, HAA lowered serum UA, creatinine, and blood urea nitrogen levels, inhibited hepatic xanthine oxidase and adenosine deaminase activities, and attenuated renal histopathological injury. HAA also reduced the mRNA expression of urate reabsorption-related genes, including GLUT9, OAT4, and OAT10, while increasing that of urate excretion-related genes, including OAT1 and ABCG2, which may contribute to improved urate homeostasis. These findings support the potential of HAA as a functional dietary ingredient for the management of hyperuricemia-associated metabolic disturbances and renal injury.

Hyperuricemia↗

PubMed2006

Effect of losartan versus candesartan on uric acid, renal function, and fibrinogen in patients with hypertension and hyperuricemia associated with diuretics.

BACKGROUND: Hyperuricemia may counter benefits of blood pressure (BP) reduction, although this is controversial. METHODS: We examined the effects of candesartan and losartan on uric acid, creatinine, and fibrinogen. Patients with hypertension and serum uric acid > or = 0.42 mmol/L (7 mg/dL) associated with diuretics were randomized to receive losartan 50 to 100 mg or candesartan 8 to 16 mg for 24 weeks. At randomization and after 24 weeks, systolic and diastolic BP, serum uric acid, creatinine, and fibrinogen were measured. RESULTS: A total of 59 patients were entered into the study (30 in the losartan and 29 in the candesartan group). Mean systolic and diastolic BP were reduced in the candesartan group, from 156 mm Hg at baseline to 132 mm Hg at 24 weeks, and from 90.9 to 80.8 mm Hg respectively, P < .0001), and in the losartan group from 150.3 to 132 mm Hg and from 89.6 to 77.6 respectively, P < 0001). Overall mean values of fibrinogen levels were again reduced from 4.39 g/L at baseline to 4.01 g/L at 24 weeks (P < .02). Mean values of serum uric acid in the losartan and candesartan groups were similar at baseline (0.44 and 0.46 mmol/L, respectively), but they were lower in the losartan group after 24 weeks (0.39 and 0.48 mmol/L, P = .01). Twelve patients (44%) in the candesartan group had a 10% increase in serum creatinine compared with four patients (14.2%) in the losartan group (P < .02). CONCLUSIONS: Candesartan and losartan lowered BP, but only losartan reduced uric acid. The lowering of fibrinogen in both groups may explain the reduction in stroke with angiotensin receptor blockers. The effect of persistent hyperuricemia on renal function requires further study.

Antihypertensive Agents↗

PubMed2005

Hyperuricemia as a risk factor on cardiovascular events in Taiwan: The Chin-Shan Community Cardiovascular Cohort Study.

Little is known about uric acid role for cardiovascular events in the Asian-Pacific countries with relatively low coronary heart disease (CHD) but high stroke events. Also, there is scanty evidence for repeated measures of uric acid levels among population. We examined associations of basic and repeated measures of uric acid level with CHD and stroke events in one Taiwanese adult community prospectively. Cox proportional hazards models, treating uric acid as baseline and time-dependent covariates, were used to assess the 11-year risk of CHD and stroke events. Among 3602 adult subjects older than 35 years, 86 incident CHD and 155 incident stroke cases were identified. The rate ratios of hyperuricemia ranged between 2.00 and 3.96, with higher risk ratios in women than in men. The rate differences and population attributable fractions were also higher in women than in men, implying that women had high risk of uric acid on cardiovascular events. After adjustment for age effect, time-dependent uric acid was associated with significant CHD risk in both genders (hazard risk [HR] 1.43, 95% CI: 1.10-1.87 in men and HR 1.22, 95% CI: 1.03-1.44 in women). But the magnitude of hazard risks decreased after adjusting more atherosclerotic risk factors for CHD. For stroke event, the age-adjusted hazard risk of time-dependent continuous uric acid level was 1.23 (95% CI: 1.00-1.54) in men and 1.36 (95% CI: 1.05-1.75) in women. Multiple adjustment by risk factors demonstrated that uric acid was still a significant predictor for stroke in women (HR 1.32, 95% CI: 1.00-1.73). The similar hazard risk patterns existed for binary categories of hyperuricemia. Subgroup analyses demonstrated uric acid had significant risk only in hypertension and metabolic syndrome subgroups, not in their counterparts. We concluded that uric acid, in the baseline and time-dependent variables, could predict cardiovascular events in the community of relatively low CHD but high stroke risk in Taiwan.

Adult↗

PubMed2005

Hypothesis: fructose-induced hyperuricemia as a causal mechanism for the epidemic of the metabolic syndrome.

The increasing incidence of obesity and the metabolic syndrome over the past two decades has coincided with a marked increase in total fructose intake. Fructose--unlike other sugars--causes serum uric acid levels to rise rapidly. We recently reported that uric acid reduces levels of endothelial nitric oxide (NO), a key mediator of insulin action. NO increases blood flow to skeletal muscle and enhances glucose uptake. Animals deficient in endothelial NO develop insulin resistance and other features of the metabolic syndrome. As such, we propose that the epidemic of the metabolic syndrome is due in part to fructose-induced hyperuricemia that reduces endothelial NO levels and induces insulin resistance. Consistent with this hypothesis is the observation that changes in mean uric acid levels correlate with the increasing prevalence of metabolic syndrome in the US and developing countries. In addition, we observed that a serum uric acid level above 5.5 mg/dl independently predicted the development of hyperinsulinemia at both 6 and 12 months in nondiabetic patients with first-time myocardial infarction. Fructose-induced hyperuricemia results in endothelial dysfunction and insulin resistance, and might be a novel causal mechanism of the metabolic syndrome. Studies in humans should be performed to address whether lowering uric acid levels will help to prevent this condition.

Fructose↗

PubMed2005

Efficacy and safety of rasburicase, a recombinant urate oxidase (Elitek), in the management of malignancy-associated hyperuricemia in pediatric and adult patients: final results of a multicenter compassionate use trial.

The recombinant urate oxidase, rasburicase (Elitek, Sanofi-Synthelabo, Inc.), has recently received regulatory approval for the prevention and treatment of hyperuricemia in children with leukemia, lymphoma, and solid tumors. Prior to approval, 682 children and 387 adults in the US and Canada received rasburicase on compassionate-use basis. Uric acid concentration declined rapidly in both adult and pediatric patients after rasburicase treatment. Similar responses were observed in patients treated with subsequent courses. Possible drug-related adverse events, including allergic reactions, were uncommon. These data confirm that rasburicase is effective and safe for the treatment and prophylaxis of children and adults with malignancy-associated hyperuricemia.

Adolescent↗

PubMed2006

Familial nephropathy associated with hyperuricemia in Spain: our experience with 3 families harbouring a UMOD mutation.

Since 1993 we have studied 5 Spanish families with familial nephropathy associated with hyperuricemia (FJHN). Among these families, 24 patients have been identified. All patients had some combination of hyperuricemia, gout, renal insufficiency, arterial hypertension, and reduced kidney size. The clinical presentation in the different families and in the members of the same family was heterogeneous. Allopurinol treatment did not appear to influence renal disease. From a clinical perspective, this syndrome is a distinctive interstitial nephropathy, inherited as an autosomal dominant trait, that progresses to renal failure and is not halted nor prevented by allopurinol therapy. In 2003, genetic linkage analysis in 3 of the 5 families showed linkage of FJHN to 16p 11.2. One family was not analyzed and one family did not show linkage to this region confirming the genetic heterogeneity of this syndrome. A mutation in UMOD gene was found in these 3 families as the cause of the FJHN. The mutations cluster in exon 4 and exon 5 and were point mutation that results in an amino acid change in the uromodulin or Tamm Horsfall protein. This fact allowed in 2004, the presymptomatic genetic diagnosis of an 8-years-old boy belonging to one of these 3 Spanish families. We conclude that in families with a history of renal failure and/or gout in which FJHN is suspected, UMOD mutation screening may enable a definite diagnosis. When a mutation is found, family members can be tested for a UMOD mutation and pre-symptomatic diagnosis may allow counseling to prevent or halt the progression to renal insufficiency.

Adult↗

PubMed2004

Pharmacokinetics and pharmacodynamics of febuxostat (TMX-67), a non-purine selective inhibitor of xanthine oxidase/xanthine dehydrogenase (NPSIXO) in patients with gout and/or hyperuricemia.

The diurnal change of sUA and the effect of febuxostat on this change were investigated in 10 patients with gout and/or hyperuricemia. The diurnal sUA change after the last dose during the 4-week treatment phase (20 mg, QD) was almost the same as the pre-treatment value. Considering the dose, the AUC(obs) and Cmax of unchanged drug in patients with gout and/or hyperuricemia were estimated to be similar to those of healthy male adults. The results show that a 6-week treatment with febuxostat is safe and well-tolerated in the target patient population for this drug.

Area Under Curve↗

PubMed2003

Efficacy and safety of rasburicase (recombinant urate oxidase) for the prevention and treatment of hyperuricemia during induction chemotherapy of aggressive non-Hodgkin's lymphoma: results of the GRAAL1 (Groupe d'Etude des Lymphomes de l'Adulte Trial on Rasburicase Activity in Adult Lymphoma) study.

PURPOSE: Hyperuricemia and tumor lysis syndrome are well-known complications during induction treatment of aggressive non-Hodgkin's lymphomas (NHLs). Usual prophylaxis and treatment of hyperuricemia consist of hydration, alkalinization, and administration of allopurinol. This study was designed to evaluate the efficacy and the safety of rasburicase (recombinant urate oxidase) in adult patients with aggressive NHL during their first cycle of chemotherapy. PATIENTS AND METHODS: A total of 100 patients from Groupe d'Etude des Lymphomes de l'Adulte centers, with diffuse large B-cell lymphoma (n = 79); anaplastic large-cell lymphoma (n = 6); peripheral T-cell lymphoma (n = 8); transformation of indolent lymphoma (n = 5); Burkitt's lymphoma (n = 1); and lymphoblastic lymphoma (n = 1) were enrolled from May 2001 to June 2002. Before chemotherapy, 66% of patients had elevated lactate dehydrogenase (LDH), including 28% with LDH above 1,000 U/mL. Eleven percent of patients were hyperuricemic (uric acid [UA] > 450 mmol/L or > 7.56 mg/dL). Rasburicase 0.20 mg/kg/d intravenously for 3 to 7 days was started the day before or at day 1 of chemotherapy. UA levels were measured 4 hours after rasburicase injection, then daily during treatment. RESULTS: All patients responded to rasburicase, as defined by normalization of UA levels maintained during chemotherapy. The control of UA was obtained within 4 hours after the first injection of the drug. Creatinine levels and other metabolites were also controlled with the administration of rasburicase. No patient exhibited increased creatinine levels or required dialysis during chemotherapy. CONCLUSION: Rasburicase is the treatment of choice to control UA and prevent tumor lysis syndrome in adult patients with aggressive NHL.

Adult↗

PubMed2003

Hyperuricemia in hypothyroidism: is it associated with post-insulin infusion glycemic response?

This experimental study was designed to examine whether hyperuricemia in hypothyroidism is associated with insulin resistance. For induction of hypothyroidism, rabbits (n = 12) were administered methimazole orally (75 mg/100 g food) for 30 days. T3, T4 and TSH values measured in plasma prior to and at the end of the experimentation period revealed the establishment of hypothyroidism. In the euthyroid and hypothyroid states of rabbits, crystalline porcine insulin was administered (0.1 unit/kg body weight) intraperitoneally and plasma glucose was measured at 0, 15, 30, 45 and 60 minutes. Sum of post insulin infusion glucose values was considered to reflect insulin resistance. Creatinine clearance (GFR) and uric acid clearance (CuA) were determined. Additionally, triglycerides were measured in plasma and Mg2+ both in erythrocytes and in plasma. Due to hypothyroidism: i) The glycemic response to insulin was not altered. ii) GFR and CuA were both decreased but CuA/GFR unchanged. iii) Triglycerides in plasma decreased. iv) Mg2+ concentration increased in plasma whereas decreased in erythrocytes. Several associations were observed between the variables on correlation analysis. On the basis of our data, it could be suggested that insulin resistance does not exist in hypothyroidism. Hyperuricemia observed in hypothyroidism should be considered to be secondary to decreased renal excretion but not as an indicator of insulin resistance.

Animals↗