Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “hyperuricemia”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 127 records · Page 7Linked to original sources
PubMed2004

Hyperuricemia and cardiovascular risk factor clustering in a screened cohort in Okinawa, Japan.

The relation between serum uric acid level and cardiovascular risk factors is complex and has been investigated mainly in men. We examined the correlation between serum uric acid level and obesity, hypertension, dyslipidemia, and diabetes mellitus (DM) in both men and women of a screened cohort in Okinawa, Japan. A total of 9,914 individuals (6,163 men and 3,751 women ranging in age from 18 to 89 years) who were screened at Okinawa General Health Maintenance Association were subjects in this study. Hyperuricemia was defined as a serum uric acid level > or = 7.0 mg/dl in men and > or = 6.0 mg/dl in women. The odds ratios (95% confidence intervals) for the presence of hyperuricemia in men were 1.75 (1.56-1.97) for obesity, 1.42 (1.25-1.62) for hypertension, 1.16 (1.02-1.30) for hypercholesterolemia, 1.80 (1.60-2.03) for hypertriglyceridemia, 1.19 (1.02-1.40) for hypo-high density lipoprotein (HDL) cholesterolemia, and 0.61 (0.49-0.75) for DM; in women, they were 2.02 (1.62-2.53) for obesity, 1.64 (1.29-2.10) for hypertension, 1.31 (1.04-1.65) for hypercholesterolemia, 1.95 (1.51-2.51) for hypertriglyceridemia, 1.53 (0.96-2.44) for hypo-HDL cholesterolemia, and 1.20 (0.76-1.90) for DM. Hyperuricemic subjects had higher rates of coexistence of two or more of these cardiovascular risk factors than non-hyperuricemic subjects (63.8% vs. 43.2% in men; 58.9% vs. 27.6% in women). The present study revealed that hyperuricemia is positively associated with obesity, hypertension, and dyslipidemia in both men and women, and that hyperuricemic subjects tend to have a clustering of these cardiovascular risk factors.

Adult↗
PubMed2004

Hyperuricemia as a predictor of hypertension in a screened cohort in Okinawa, Japan.

Several epidemiological studies have shown a positive association between serum uric acid levels and the risk of hypertension. However, subjects in these studies were mostly men, or were incompletely examined for lifestyle-related variables. We prospectively examined the relation between hyperuricemia and the risk of developing hypertension with consideration for alcohol consumption and smoking habits in a large screened cohort of men and women. A total of 4,489 individuals (2,927 men and 1,562 women) who did not have hypertension and were not currently using antihypertensive medication were examined at the Okinawa General Health Maintenance Association in 1977. Subjects were re-examined in 2000. Hyperuricemia was defined as a serum uric acid level >or=7.0 mg/dl in men and >or=6.0 mg/dl in women. Hypertension was defined as systolic blood pressure (SBP) >or=140 mmHg, and/or diastolic blood pressure (DBP) >or=90 mmHg. A total of 289 subjects (201 men and 88 women) were hypertensive (SBP >or=140 mmHg, and/or DBP >or=90 mmHg) in 2000. Multivariate analysis was performed for development of hypertension in hyperuricemic subjects, adjusted for age, family history of hypertension, alcohol consumption, cigarette smoking, obesity, hypercholesterolemia, hypertriglyceridemia, low high-density lipoprotein cholesterol, and diabetes mellitus. The adjusted odds ratio (95% confidence interval) in men was 1.48 (1.08-2.02) and in women was 1.90 (1.03-3.51) (p <0.05, respectively). The results showed hyperuricemia to be a new predictor of hypertension development in both men and women.

Adolescent↗
PubMed2004

[A case of rheumatoid arthritis/Sjogren's syndrome with acute renal failure due to hyperuricemia associated with mizoribine therapy].

A 64-year-old woman was diagnosed as having rheumatoid arthritis in 1999 at a nearby hospital. She had been treated with etodolac, actarit, mizoribine (MZ) and prednisolone. On May 25, 2001, she noticed fever and nausea and was treated with diclofenac sodium and clindamycin. On May 31, a nasal bleeding, tarry stool, hyperuricemia, renal dysfunction and thrombocytopenia developed and she was admitted to our hospital. Administration of drugs except prednisolone was stopped and hemodialysis was carried out on June 1. Fever and nausea improved during several days. Hyperuricemia and renal dysfunction disappeared on June 11. The platelet count became normal after platelet transfusion and she was discharged from our hospital on July 2. She was also diagnosed as having Sjogren's syndrome. In our case, a delay in MZ discharge by transient renal dysfunction might have caused a hyperuricemia, following an aggravation of renal dysfunction. So, care should be taken about latent renal dysfunction during the use of MZ. Moreover, it may be necessary to consider a discontinuation of MZ and administration of hemodialysis in the case of transient renal dysfunction.

Acute Kidney Injury↗
PubMed2002

[Effects of aqueous extract in herba of Lysimachia christinae on hyperuricemia in mice].

OBJECTIVE: To study hypouricemic effect of aqueous extract of Lysimachia christinae on hyperuricemia in mice. METHOD: The uricase inhibitor potassium oxonate was used to induce hyperuricemia in mice, and serum uric acid level was determined with the phosphotungstic acid method. RESULT: The aqueous extract of Lysimachia christinae, when administered orally to the oxonate-induced hyperuricemic mice at the doses of 5.2, 10.4 and 20.8 g.kg-1, was able to elicit dose-dependent hypouricemic effects. At these doses of the extract, the serum urate levels of the oxonate-pretreated mice showed no difference from the normal mice. In normal mice, however, oral administration of the extract at the same doses did not produce any observable hypouricemic effects. CONCLUSION: The aqueous extract of Lysimachia christinae possesses potent hypuricemic effects on models of hyperuricemia in mice pretreated with oxonate.

Animals↗
PubMed2005

Efficacy and safety of recombinant urate oxidase (rasburicase) for treatment and prophylaxis of hyperuricemia in children undergoing chemotherapy.

Rasburicase has been defined as a potent urolytic agent for management of malignancy-associated hyperuricemia. We reviewed the data of 26 children with malignancy at risk for TLS who received rasburicase for treatment or prophylaxis of acute hyperuricemia, producing a significant decrease in uric acid level in all the patients. Tolerance of treatment was excellent. Rasburicase is a safe, highly and rapidly effective agent in the treatment and prevention of malignancies-associated acute hyperuricemia.

Adolescent↗
PubMed2004

Clinical manifestations of patients with hyperuricemia.

OBJECTIVE: To study the clinical manifestations of patients with hyperuricemia in King Chulalongkorn Memorial Hospital. METHOD: A cross sectional study of 188 hyperuricemic patients was done at King Chulalongkorn Memorial Hospital. History, physical examination, and blood samples were drawn to assess complete blood count (CBC), blood urea nitrogen (BUN), creatinine (Cr), liver function test (LFT), and serum uric acid in all patients. RESULTS: Most of the patients (92%) were male, more than 50 years old (69%), the mean age of the patients was 56.7 +/- 12.1 years old. All of the female patients were more than 50 years old. Symptomatic hyperuricemia was found in 93%, the mean duration of symptoms was 63.2 +/- 66.3 months. The mean of the serum uric acid level was 10.0 +/- 2.9 mg/dl. Associated diseases were found in 46% of the patients, and 30% of these patients had more than one disease. Hypertension was the most common followed infrequency by dyslipidemia, diabetes mellitus, ischemic heart disease, and chronic obstructive pulmonary disease consecutively. Renal impairment was detected in about one-third of the patients. CONCLUSION: This study shows that hyperuricemia is common in elderly, male patients. Associated diseases and renal impairment can befoundfrequently, and the patients should be monitored.

Age Distribution↗
PubMed2005

[Hyperuricemia following rotavirus infection].

Elevated serum levels of uric acid are caused by increased production or decreased renal excretion. Another cause of the disorder which is less familiar is hyperuricemia following rotavirus infection. This is a case study of a girl who was admitted for abdominal pain, fever, vomiting and diarrhea. Multiple abdominal lymph nodes up to 2.8 x 3.0 cm size were noted on the ultrasound examination. The patient's laboratory findings were significant for hyperuricemia and elevation of lactic dehydrogenase. The patient had no evidence of dehydration and the combination of her clinical signs and symptoms and laboratory findings were consistent for a malignancy. Proof of the rotaviral antigen in her stool, the fact that uric acid levels returned to normal within five days, and a normal repeat ultrasound examination, ruled out this possibility. This clinical case highlights the association between hyperuricemia and rotavirus infection. An understanding of this association may avoid performing unnecessary diagnostic tests in the patient.

Child, Preschool↗
PubMed1984

Does hyperuricemia protect from rheumatoid inflammation? A clinical study.

The negative association between gout and rheumatoid arthritis is well accepted. The reason for this mutual exclusion is not clear; a protective immunosuppressive effect of hyperuricemia has been included among possible explanations. To test this hypothesis, we reviewed the charts of 160 rheumatoid arthritis patients on whom clinical information and followup for at least a year were available. We selected those patients with persistent hyperuricemia as defined by serum urate levels averaging above 7.5 mg% for at least 6 months. We found 12 patients fulfilling such criteria, and 11 of these were judged to have quiescent, minimally active, or inactive disease during hyperuricemic periods. In 2 patients, flares of the rheumatoid process coincided with normalization of serum urate levels. We propose that persistent hyperuricemia may protect against or decrease the expression of rheumatoid inflammation.

Arthritis, Rheumatoid↗
PubMed1984

IMP dehydrogenase mutants: cell culture model for hyperuricemia.

These studies with wild-type and mutant cells defective in IMP dehydrogenase and the previous data with the adenylosuccinate synthetase-deficient cell line suggest that among the clinical population with dominantly inherited hyperuricemia, patients with partial deficiencies in these enzymes exist. It is hoped that these pharmacogenetic cell culture models for overproduction hyperuricemia will lead to the initiation of a search for hyperuricemia patients with either of these deficiencies. If such patients are found it may be possible to design chemotherapeutic regimens by which effectors (inhibitors) of purine synthesis might ameliorate the overproduction of purines by the de novo pathway.

Animals↗
PubMed1987

Asymptomatic hyperuricemia. Risks and consequences in the Normative Aging Study.

To quantify the consequences of asymptomatic hyperuricemia, this study examined rates for a first episode of gouty arthritis based on 30,147 human-years of prospective observation. A cohort of 2,046 initially healthy men in the Normative Aging Study was followed for 14.9 years with serial examinations and measurement of urate levels. With prior serum urate levels of 9 mg/dl or more, the annual incidence rate of gouty arthritis was 4.9 percent, compared with 0.5 percent for urate levels of 7.0 to 8.9 mg/dl and 0.1 percent for urate levels below 7.0 mg/dl. With urate levels of 9 mg/dl or higher, cumulative incidence of gouty arthritis reached 22 percent after five years. Incidence rates were three times higher for hypertensive patients than for normotensive patients (p less than 0.01). The strongest predictors of gout in a proportional hazards model were age, body mass index, hypertension, and cholesterol level, and alcohol intake. When the serum urate level became a factor in the model, none of these variables retained independent predictive power. At the final examination, only 0.7 percent of participants had a serum creatinine level of 2.0 mg/dl or more, with no evidence of renal deterioration attributable to hyperuricemia. These data support conservative management of asymptomatic hyperuricemia.

Adult↗
PubMed1996

Hyperuricemia and xanthine oxidase in preeclampsia, revisited.

Hyperuricemia is associated with the severity of preeclampsia and with fetal outcome. Traditionally the high uric acid concentration in preeclampsia has been attributed soley to renal dysfunction. Preeclampsia is also characterized by increased free radical formation and elevated oxidative stress. Xanthine dehydrogenase/oxidase produces uric acid. Xanthine dehydrogenase/oxidase is present as two isoforms in vivo. Uric acid production is coupled with formation of reactive oxygen species when the enzyme is in the oxidase form. Several factors can increase the holoenzyme activity and the conversion of xanthine dehydrogenase/oxidase to its oxidase form. These factors include hypoxia-reperfusion, cytokines, and increased substrate availability (xanthine and hypoxanthine). Preeclampsia is characterized by hyperuricemia and signs of increased formation of reactive oxygen species and decreased levels of antioxidants. Preeclampsia is also characterized by shallow implantation, producing a relatively hypoxic maternal-fetal interface, and increased turnover of trophoblast tissue, which can result in higher xanthine and hypoxanthine concentrations and higher levels of circulating cytokines. These mechanisms can lead to increased production of uric acid and free radicals and contribute to the hyperuricemia and increased oxidative stress present in preeclampsia.

Female↗
PubMed2000

Relationship between hyperuricemia and other cardiovascular disease risk factors among adult males in Taiwan.

Hyperuricemia is associated with cardiovascular disease risk factors such as obesity, impaired glucose tolerance, hypertension, and hyperlipidemia. However, this relationship between serum uric acid (SUA) concentrations and cardiovascular disease (CVD) is a controversial one, especially among males. The purpose of this study is to evaluate the association between SUA concentrations and other CVD risk factors among adult males in Taiwan. After multi-stage sampling procedures, we randomly selected 1743 Taiwanese males with a mean age of 35 years (from 22 to 54) in this study. Anthropometric, blood pressure and biochemical variables, including serum uric acid, glucose, total cholesterol and triglyceride concentrations, were measured. Among the study population, the mean SUA concentration was 6.5 +/-1.5 mg/dl. There were 290 (16.6%) subjects with SUA concentrations > or = 8.0 mg/dl (defined as hyperuricemia). Compared to normouricemic subjects, hyperuricemic subjects had significantly greater age-adjusted body weight (75.3 vs. 69.2 kg, p < 0.001), body mass index (BMI, 25.5 vs. 23.6 kg/m2, p < 0.001), higher blood pressure (BP, 120.2 vs. 115.2 mmHg for systolic BP and 78.5 vs. 75.3 mmHg for diastolic BP, both p < 0.001) and blood lipid concentrations (193.8 vs. 182.1 mg/dl for total cholesterol and 123.7 vs. 94.4 mg/dl for triglycerides, both p < 0.001). SUA concentration was positively correlated with body weight, BMI, BP and serum lipid concentrations (all p < 0.001). In multivariate regression analyses, after adjusting for potential confounders, SUA concentration was significantly positively associated with diastolic BP, serum total cholesterol and triglyceride concentrations. An increase of 1 mg/dl of SUA was associated with a 2.1 mg/dl elevation in serum total cholesterol (p < 0.001) and a 5.4 mg/dl increase in triglyceride (p < 0.001). From this study, we found that hyperuricemia in subjects is associated with being overweight, and having high blood pressure and hyperlipidemia. There is a significantly positive association between SUA concentration and other CVD risk factors among adult males in Taiwan.

Adult↗
PubMed2002

Hyperuricemia, hypertension, and proteinuria associated with high-altitude polycythemia.

Chronic exposure to high altitude is associated with the development of erythrocytosis, proteinuria, and, in some cases, hyperuricemia. We examined the relationship between high-altitude polycythemia and proteinuria and hyperuricemia in Cerro de Pasco, Peru (altitude, 4,300 m). We studied 25 adult men with hematocrits less than 65% and 27 subjects with excessive erythrocytosis (EE; hematocrit > 65%) living in Cerro de Pasco, Peru and compared them with 28 control subjects living in Lima, Peru (at sea level) and after 48 hours of exposure to high altitude. Serum urate levels were significantly elevated in patients with EE at altitude, and gout occurred in 4 of 27 of these subjects. Urate level strongly correlated with hematocrit (r = 0.71; P < 0.0001). Urate production (24-hour urine urate excretion and urine urate-creatinine ratio) was increased in this group compared with those at sea level. Fractional urate excretion was not increased, and fractional lithium excretion was reduced, in keeping with increased proximal reabsorption of filtrate. Significantly higher blood pressures and decreased renin levels in the EE group were in keeping with increased proximal sodium reabsorption. Serum urate levels correlated with mean blood pressure (r = 0.50; P < 0.0001). Significant proteinuria was more prevalent in the EE group despite normal renal function. Hyperuricemia is common in subjects living at high altitude and associated with EE, hypertension, and proteinuria. The increase in uric acid levels appears to be caused by increased urate generation secondary to systemic hypoxia, although a relative impairment in renal excretion also may contribute.

Adult↗
PubMed1987

Myogenic hyperuricemia. A common pathophysiologic feature of glycogenosis types III, V, and VII.

To identify the mechanism of hyperuricemia in glycogen storage diseases (glycogenoses) that affect muscle, we studied the effects of exercise and prolonged rest on purine metabolism in two patients with glycogenosis type III (debrancher deficiency), one patient with type V (muscle phosphorylase deficiency), and one patient with type VII (muscle phosphofructokinase deficiency). All had hyperuricemia except for one patient with glycogenosis type III. Plasma concentrations of ammonia, inosine, and hypoxanthine increased markedly in all the patients after mild leg exercise on a bicycle ergometer. The plasma urate concentrations also increased, but with a delayed response. Urinary excretion of inosine, hypoxanthine, and urate increased greatly after exercise, consistently with the increases in plasma levels. Hypoxanthine and urate concentrations were extremely high in the plasma and urine of the patient with glycogenosis type VII. With bed rest, the plasma hypoxanthine level returned to normal within a few hours, and the plasma urate concentration decreased from 18.6 to 10.6 mg per deciliter (1106 to 630 mumol per liter) within 48 hours. Similarly, the urinary excretion of these purine metabolites was reduced by bed rest. These findings indicate that muscular exertion in patients with glycogenosis types III, V, and VII causes excessive increases in blood ammonia, inosine, and hypoxanthine due to accelerated degradation of muscle purine nucleotides. These purine metabolites subsequently serve as substrates for the synthesis of uric acid, leading to hyperuricemia.

Adult↗
PubMed1989

Cyclosporine-induced hyperuricemia and gout.

To evaluate the frequency and the pathogenesis of hyperuricemia and gout during cyclosporine therapy, we studied renal-transplant recipients who were treated with either cyclosporine and prednisone (n = 129) or azathioprine and prednisone (n = 168). Among the patients with stable allograft function and serum creatinine concentrations below 265 mumol per liter, hyperuricemia was more common in the cyclosporine group than in the azathioprine group (84 percent vs. 30 percent; P = 0.0001). Gout developed in nine patients (7 percent) in the cyclosporine group, but no episodes occurred in the azathioprine group. Serum urate levels became elevated in 90 percent of the patients in the cyclosporine group who were treated with diuretics, as compared with 60 percent of those not treated with diuretics (P = 0.001); in the azathioprine group, the corresponding values were 47 percent and 15 percent (P = 0.0001). Serum urate levels did not correlate with trough blood cyclosporine levels in a selected subgroup (n = 40) of patients from the cyclosporine group, who were studied from 4 to 96 weeks after transplantation. Detailed studies of urate metabolism in six cyclosporine-treated patients revealed normal turnover rates for urate and decreases in creatinine and urate clearance, as compared with seven control subjects. We conclude that hyperuricemia is a common complication of cyclosporine therapy and is caused by decreased renal urate clearance. Gouty arthritis is the cause of considerable morbidity among renal-transplant recipients who receive cyclosporine.

Adult↗
PubMed1991

Gout and hyperuricemia.

Although our understanding of hyperuricemia and gout has changed little over the past several years, questions remain in defining the many metabolic abnormalities that can result in these problems. In the past year, several papers have further addressed heritable mechanisms for the development of hyperuricemia, as well as environmental factors that contribute to its onset in adulthood. Consequences of hyperuricemia other than clinical gout have received further attention. Although typical gout is easily recognized and treated, several recent papers have addressed atypical presentations of gout, as well as other causes of podagra that might have been attributed previously to gout. The treatment of patients whose disease is uncomplicated by other conditions remains straightforward. However, the presentation of gout in patients with multiple comorbidities not only increases recognition of the toxicity of nonsteroidal anti-inflammatory drugs and colchicine, but often requires innovative approaches to its treatment.

Adult↗
PubMed2004

Prevalence of comorbid conditions and prescription medication use among patients with gout and hyperuricemia in a managed care setting.

BACKGROUND: : Comorbid disorders and multiple prescription drug use are common among patients with gout and/or hyperuricemia and may influence the clinical course and outcome of gout. OBJECTIVE: : We wanted to document the conditions and associated medications in a large group of patients with gout in a managed care setting. METHODS: : This study was a 2-year, retrospective, administrative claims analysis examining comorbid conditions and medication use among managed care enrollees with gout/hyperuricemia across the United States. RESULTS: : Of the 9482 study subjects (82.1% men, mean age 52 years), 57.9% had hypertension, 45.3% had a lipid disorder, 32.5% had both conditions, and 19.9% had diabetes mellitus. During the 24-month follow-up period, subjects had 5 +/- 3.14 (mean +/- standard deviation) different comorbid conditions and filled prescriptions for of 11.0 +/- 7.90 different medications. The most commonly filled prescriptions included antihypertensive drugs, 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins), and nonsteroidal antiinflammatory drugs (NSAIDs). CONCLUSIONS: : The study indicates a high prevalence of both comorbid conditions and multiple medication use among managed care enrollees with gout and/or hyperuricemia. Heightened awareness of these associated disorders is important because they may warrant treatment of their own accord and often some modification of gout management. Drugs, particularly diuretics and prophylactic aspirin, could potentially contribute to the development of hyperuricemia and gout.

Journal Article↗
PubMed1982

Hyperuricemia as a risk factor for cardiovascular mortality.

The value of hyperuricemia as a risk factor for cardiovascular mortality was investigated in 3195 men and 3160 women aged 40-69 years in Finland. Hyperuricemia was associated with obesity, impaired glucose tolerance, hypertension and history of heart disease. The total mortality of hyperuricemic men and women in 5 years was significantly higher than the mortality of normouricemics. Cardiovascular mortality was not higher in hyperuricemics than in normouricemics. However, in hyperuricemic women without known heart disease cardiovascular mortality was significantly increased in the follow-up period between 5 and 12 years. Total and cardiovascular mortality rates were significantly higher in hyperuricemic men with known heart disease than in corresponding normouricemic men. A rise of serum uric acid may be secondary to more advanced atherosclerosis. Thus, hyperuricemia may be associated with more advanced heart disease and it is not an independent cause of cardiovascular diseases.

Adult↗