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PubMed2004

[A community-based case-control study on risk factors of hyperuricemia among residents in the community].

OBJECTIVE: To investigate the risk factors of hyperuricemia among residents aged >/= 20 years. METHODS: A community based case-control study was conducted in 286 patients with 858 controls without hyperuricemia. Available data were analyzed by mono-factorial and multi-factorial logistic regression methods using SPSS 10.0 software. RESULTS: 17 factors related to exposure were identified for hyperuricemia the mono-factorial analysis when; five factors were selected through multiple factoral logistic regression model at P = 0.05 level. The risk factors on hyperuricemia were: hypertriglyceridemia (OR = 3.069), alcohol consumption (OR = 2.032), obesity (OR = 1.802), taste of spicy food (OR = 1.877) and hyperglycemia (OR = 1.622). CONCLUSION: Hyperuricemia is a disease associated with environment and style-life. Changing lifestyle, such as decreasing alcohol consumption and adopting proper structure of diet may prevent or decrease the chance of getting hyperuricemia and gout.

Adolescent↗
PubMedDate not supplied

Hyperuricemia in an infant with Taussig-Bing anomaly and interruption of the aortic arch.

Hyperuricemia is commonly recognized in adolescents and adults with cyanotic congenital heart disease. We report a case of a male infant with hyperuricemia, Taussig-Bing anomaly, and interruption of the aortic arch. The patient underwent correction of interrupted aortic arch and pulmonary arterial banding at the age of 7 days. Hyperuricemia appeared when he was 2 months old (max 17.7 mg/dl) and persisted until he underwent a Jatene operation at the age of 10 months. The hyperuricemia improved gradually after the disappearance of hypoxia and polycythemia. The laboratory findings suggest that hyperuricemia can result from uric acid overproduction due to secondary polycythemia, impairment of uric acid excretion by the kidney, or the acceleration of anaerobic metabolism. Allopurinol and benzbromarone together were partially effective treatments for hyperuricemia in this patient with cyanotic congenital heart disease.

Abnormalities, Multiple↗
PubMed1983

Gout and hyperuricemia associated with sickle-cell anemia.

Since the initial description, in 1958, of gouty arthritis occurring in association with SCA, more than 12 cases have been reported. The high proportion of women and the relatively young ages are noteworthy. Since 1968, studies of patients with SCA have shown a high prevalence of hyperuricemia, beginning during childhood. The initial event in the development of hyperuricemia presumably is increased synthesis of nucleic acids occurring as part of the erythropoietic response to hemolysis. Catabolism of the nucleic acids generates urate. Increased production of UA normally is compensated for by increased urinary excretion of UA. This response occurs in patients with SCA, but during the third decade of life hyperuricosuria can be reduced, probably by damage to the renal tubules caused by infarction and hypoxia resulting from sickling. Impairment of the compensatory renal response leads to more severe and sustained hyperuricemia, and gouty arthritis may then develop. A number of questions about hyperuricemia and gout in SCA remain unanswered. The prevalence of gout among patients with SCA, both in general and in relation to age and sex, has not been determined. The relationships between specific aspects of SCA and of hyperuricemia and gout need to be determined. These include any effect of sickle cell crises on SUA and attacks of gout, and correlation of abnormalities in renal handling of urate with other indices of tubular function and with the pathologic anatomy of the kidney. Finally, it is important to learn whether hyperuricemia and hyperuricosuria contribute to the renal manifestations of SCA; if so, allopurinol might be useful in the prevention and treatment of the renal disease.

Adolescent↗
PubMed1998

Lone hyperuricemia during pregnancy: maternal and fetal outcomes.

OBJECTIVE: Study of maternal and fetal consequences of lone hyperuricemia during pregnancy and demonstration that lone hyperuricemia is not a risk factor regarding the onset of preeclampsia. STUDY DESIGN: Retrospective study of two groups of women, one found to have lone hyperuricemia during pregnancy (n=102) and the others with normal serum uric acid levels (n=100). RESULTS: The only consequence identified of the lone hyperuricemia was a lower birth weight of children born to mothers found to have lone hyperuricemia for more than 2 weeks (P<0.05). CONCLUSIONS: Lone hyperuricemia is not a risk factor regarding the onset of preeclampsia. It is therefore unnecessary to measure serum uric acid level during a normal pregnancy.

Adult↗
PubMed2001

Hyperuricemia, gout, and renal function after liver transplantation.

BACKGROUND: Hyperuricemia is a recognized complication of renal and cardiac transplantation, but the development of hyperuricemia and gout following liver transplantation have received less attention. We have retrospectively assessed the prevalence of hyperuricemia in 134 consecutive liver transplant recipients. RESULTS: Forty-seven percent of the liver transplant recipients studied had hyperuricemia. Serum creatinine was higher in hyperuricemic than in nonhyperuricemic patients. Peak uric acid correlated significantly with corresponding serum creatinine (rs=0.694). Only 6% developed gout. All the patients with gout and 10 hyperuricemic patients with renal impairment but without gout were treated with allopurinol. Over a median period of 3 months, mean serum creatinine fell from 177 micromol/l to 160 micromol/l (P=0.01), without change in type or dose of immuno-suppression. CONCLUSIONS: There is an important association between liver transplantation and hyperuricemia. Treatment with allopurinol results in a significant reduction in serum creatinine in patients with gout and in those with hyperuricemia and renal impairment.

Adult↗
PubMed1999

Placental pathologies are not associated with hyperuricemia in preeclamptic pregnancies.

The mechanism of hyperuricemia in preeclampsia remains unknown. As the breakdown of the nuclear rich syncytiotrophoblast might result in the increased formation of uric acid from purine catabolism, the purpose of this study was to investigate whether placental pathologies were associated with hyperuricemia in preeclamptic pregnancies. We retrospectively reviewed medical reports with the availability of maternal serum uric acid levels and placental pathology reports of 83 singleton, preeclamptic pregnant women at Yale-New Haven Hospital. Preeclampsia was defined by the American College of Obstetricians and Gynecologists criteria. Hyperuricemia was defined as, at least greater than or equal to, two standard deviations of normal mean values for gestational age. The placental pathological findings include infarction, syncytial knots, abruption, intravillous thrombosis, and villous pathology (i.e., edema, villitis). The relevance of hyperuricemia to the individual placental pathologic finding and the numbers of placental pathologic findings were investigated. Statistical analyses were performed using contingency table methods. We found that there was no significant correlation between hyperuricemia and individual or multiple placental pathologic findings. We concluded that placental pathologies secondary to ischemic changes may not fully explain hyperuricemia in preeclamptic pregnancies. A prospective study using morphometric measurements is needed to understand the exact role of ischemic placental damage on the maternal serum uric acid level.

Data Interpretation, Statistical↗
PubMedDate not supplied

[The prevalence of gout and hyperuricemia among the workers of a meat-packing plant complex].

An attempt was made to study the incidence of gout and hyperuricemia among the workers of the Moscow meat-packing plant exposed to high food purine loads. Using extensive clinical material (535 men and 1121 women) the authors established that gout was diagnosed 33 times more often in men of this plant than in the muscular population of other towns of the country. Moderate hyperuricemia was revealed in every second of the examinees. Marked hyperuricemia was noted 1.8 times more often, it being 3.4 times more often in men working at this plant as compared to the whole muscular population of the country. There was a direct dependence of the level of hyperuricemia in men working in this industry on their service record. The levels of moderate hyperuricemia in all groups of men and in some groups of women directly depended on the amount of daily purine loads. Marked hyperuricemia among the examined men is a factor of risk in the development of load and among the examined women an indicator of risk (i. e. warning) of possible metabolic changes which require an adequate dietetic and therapeutic correction.

Age Factors↗
PubMed1988

[Hyperlipoproteinemia in primary gout and asymptomatic hyperuricemia].

More than 800 patients suffering from primary gout or asymptomatic hyperuricemia were examined for the values of total cholesterol and triglycerides and the pattern of lipoproteins. The values for HDL (high-density-lipoprotein = alpha-lipoprotein), LDL (low-density-lipoprotein = beta-lipoprotein) and VLDL (very-low-density-lipoprotein = pre-beta-lipoprotein), found in lipid electrophoresis, were significant abnormal as well in the group of patients with gout (n = 147) as in the group of patients with asymptomatic hyperuricemia (n = 700) versus the healthy controls. It was remarkable, that the values of lipoproteins in asymptomatic hyperuricemia almost were abnormal just as often as in primary gout. Approximately 80% of both groups showed an increased LDL, around 35% a decreased HDL, and an increased VLDL was found in 72% of patients with gout and in 54% of asymptomatic hyperuricemia. Pathological changes of all lipoproteins (HDL, LDL and VLDL) appeared in 23% of patients with gout and in 20% of patients with asymptomatic hyperuricemia. Only 2.7% of patients with gout and 4.8% with hyperuricemia showed a normal lipometabolism.

Adolescent↗
PubMed2006

Hyperuricemia as a risk factor for contrast-induced nephropathy in patients with chronic kidney disease.

OBJECTIVES: Hyperuricemia as a risk factor for contrast-induced nephropathy (CIN) has not been studied. BACKGROUND: The aim of the present study was to assess the influence of hyperuricemia on the development of CIN in patients undergoing coronary angiography. METHODS: This was a prospective cohort study. A total of 266 patients with a mean age of 58.33 +/- 7.85 years and serum creatinine > or = 1.2 mg/dl were divided into two groups (hyperuricemic, n = 126, and normouricemic, n = 140). CIN was defined as an increase of > or = 25% in creatinine over baseline within 48 hr of angiography, and hyperuricemia as serum uric acid > or = 7 mg/dl in males and > or = 6.5 mg/dl in females. RESULTS: CIN occurred in 15.1% of the hyperuricemic group and 2.9% of the normouricemic group (P < 0.001). Serum creatinine increased from 1.45 +/- 0.20 to 1.67 +/- 0.45 mg/dl in the hyperuricemic group and from 1.42 +/- 0.16 to 1.56 +/- 0.23 mg/dl in the normouricemic group (P < 0.001). Hyperuricemia [odds ratio (OR) 4.71; 95% confidence interval (95% CI) 1.29-17.21; P = 0.019] and a high incidence of multi-vessel coronary involvement (OR 3.59; 95% CI 1.12-11.48; P = 0.032) in the hyperuricemic group were predictors of CIN. Hypoalbuminemia (P = 0.001) and age > or = 70 years (P = 0.023) were other risk indicators of CIN. Length of hospital stay (P < 0.001) and CIN requiring renal replacement therapy (P = 0.017) were significantly higher in hyperuricemic group. Serum uric acid level > or = 7 mg/dl in males and > or = 5.9 mg/dl in females were found to be the best cut-off value for prediction of CIN. CONCLUSION: Our data support the hypothesis that patients with hyperuricemia are at risk of developing CIN.

Chi-Square Distribution↗
PubMed2006

[Hyperuricemia and gout: diagnosis and therapy].

In our modern society hyperuricemia is one of the most frequent metabolism disturbances. So far, every fourth man and every tenth woman suffer from an asymptomatic or a symptomatic hyperuricemia named gout. Mostly, over nutrition and malnutrition as well as other secondary factors with a genetically determined renal secretion disturbance of uric acid lead to an increase of serum uric acid. By deposition of uric acid crystals in tissues with intermittent immunologic activation of inflammation cells a manifestation of gout can be seen. The clinical image of gout varies widely. It may manifest as acute or chronic arthritis, tophi on the skin, subcutaneous tissue and the skeletal system as well as urate nephropathy. To eliminate the consequences of hyperuricemia in the long term, apart from a thorough anamnesis of nutritional habits a general examination of metabolic parameters is necessary to exclude a metabolic syndrome and other causes for a secondarily caused hyperuricemia. As gout is very often primarily caused by a renal secretion disturbance of uric acid special diagnostics should be done. Basing on literature research and inclusion of experts opinions this article represents the therapeutically options in treatment of hyperuricemia and gout with their resulting side effects and contraindications.

Allopurinol↗
PubMed2004

Serum uric acid-lowering therapies: where are we heading in management of hyperuricemia and the potential role of uricase.

Although allopurinol has been available for approximately 50 years, hyperuricemia and its sequelae are not only prevalent, but the incidence and costs associated with this disorder continue to increase. However, several new therapies have been developed. Recombinant urate oxidase has been useful in the treatment of tumor lysis hyperuricemia, and pegylated urate oxidase shows promise in patients with hyperuricemia and gout. Febuxostat and Y-700 are new oral xanthine oxidase inhibitors that are in human clinical trials. Tailoring of antilipid therapy in selected hyperuricemic and hyperlipidemic patients with fenofibrate may be of benefit in lowering blood cholesterol and uric acid levels. Similarly, treatment of selected hyperuricemic patients who also are hypertensive with losartan or amlodipine may be beneficial in lowering blood pressure and hyperuricemia. Despite these advances, new treatments for hyperuricemia are needed.

Allopurinol↗
PubMed2006

New developments in clinically relevant mechanisms and treatment of hyperuricemia.

The prevalence of gout has increased markedly in the United States in the past two decades, and new treatments for hyperuricemia are being developed. Recent molecular identification of urate transporter-1 (URAT1) as the central mediator of renal urate reabsorption has provided novel understanding of the pathogenesis of hyperuricemia, and the target site for current and possibly future primary uricosuric agents. Recent studies have also highlighted uricosuric effects of several drugs (losartan, atorvastatin, fenofibrate) that are prescribed for primary indications other than hyperuricemia. The niche of these agents in current management of hyperuricemia is discussed. We also review the ongoing development of recombinant uricase preparations and of novel xanthine oxidase inhibitors exemplified by febuxostat. These agents should provide novel options for patients with chronic, refractory gout and hyperuricemia, particularly in association with allopurinol hypersensitivity and renal insufficiency.

Febuxostat↗
PubMed2005

Status of endothelial dependent vasodilation in patients with hyperuricemia.

Hyperuricemia has been associated with an increased risk for cardiovascular disease and increased mortality. However, the biologic mechanisms that link elevated serum uric acid to cardiovascular disease are uncertain. This study tested the hypothesis that elevated serum uric acid is associated with impaired endothelial function in hyperuricemic patients without any overt cardiovascular disease. Seventeen male patients with hyperuricemia (mean age 42+/-4 years) and 9 control subjects (mean age 45+/-5 years) were studied. All subjects were nonsmokers. All patients had never been treated for hyperuricemia, were on no medications, and were free of any other known diseases. Endothelial function was evaluated by flow-mediated dilation measured by ultrasound. Flow-mediated dilation was significantly impaired in patients with hyperuricemia (4.0+/-0.7%) compared with control subjects (6.4+/-0.8%) (p=0.044). Flow-mediated dilation correlated inversely with uric acid levels (r=-0.4, p=0.05). Nitrate-induced dilation was 12.3+/-1.0% in patients with hyperuricemia and 11.8+/-2.3% in control subjects (p=0.82). Impaired endothelial-dependent vasodilation is present in hyperuricemic patients even in the absence of any overt cardiovascular disease. The elevated serum uric acid, per se, may constitute a novel risk factor for endothelial dysfunction.

Adult↗
PubMed2005

Restored expression and activity of organic ion transporters rOAT1, rOAT3 and rOCT2 after hyperuricemia in the rat kidney.

We previously reported that in hyperuricemic rats, renal impairment occurred and organic ion transport activity decreased, accompanied with a specific decrease in the expression of rat organic anion transporters, rOAT1 and rOAT3, and organic cation transporter, rOCT2. In the present study, we investigated the reversibility of the organic ion transport activity and expression of organic ion transporters (slc22a) during recovery from hyperuricemia. Hyperuricemia was induced by the administration of a chow containing uric acid and oxonic acid, an inhibitor of uric acid metabolism. Four days after discontinuance of the chow, the plasma uric acid concentration returned to the normal level, and renal functions such as creatinine clearance and BUN levels were restored, although the recovery of tubulointerstitial injury was varied in sites of the kidney. Basolateral uptake of p-aminohippurate (PAH) and tetraethylammonium (TEA), and both protein and mRNA levels of rOAT1, rOAT3 and rOCT2 in the kidney gradually improved during 14 days of recovery from hyperuricemia. Basolateral PAH transport showed a higher correlation with the protein level of rOAT1 (r(2)=0.80) than rOAT3 (r(2)=0.34), whereas basolateral TEA transport showed a strong correlation with rOCT2 protein (r(2)=0.91). The plasma testosterone concentration, which is a dominant factor in the regulation of rOCT2, was gradually restored during the recovery from hyperuricemia, but the correlation between the plasma testosterone level and rOCT2 protein expression in the kidney was not significant. These results suggest that the regulation of organic ion transporters, rOAT1, rOAT3 and rOCT2, by hyperuricemia is reversible, and the organic ion transport activity restores according to the expression levels of these transporters.

Animals↗
PubMed2005

Uric acid and chronic renal disease: possible implication of hyperuricemia on progression of renal disease.

Although hyperuricemia has long been associated with renal disease, uric acid has not been considered as a true mediator of progression of renal disease. The observation that hyperuricemia commonly is associated with other risk factors of cardiovascular and renal disease, especially hypertension, has made it difficult to dissect the effect of uric acid itself. However, recent epidemiologic evidence suggests a significant and independent association between the level of serum uric acid and renal disease progression with beneficial effect of decreasing uric acid levels. Furthermore, our experimental data using hyperuricemic animals and cultured cells have provided robust evidence regarding the role of uric acid on progression of renal disease. Hyperuricemia increased systemic blood pressure, proteinuria, renal dysfunction, vascular disease, and progressive renal scarring in rats. Recent data also suggest hyperuricemia may be one of the key and previously unknown mechanisms for the activation of the renin-angiotensin and cyclooxygenase-2 (COX-2) systems in progressive renal disease. Although we must be cautious in the interpretation of animal models to human disease, these studies provide a mechanism to explain epidemiologic data that show uric acid is an independent risk factor for renal progression. Although there is no concrete evidence yet that uric acid bears a causal or reversible relationship to progressive renal disease in humans, it is time to reevaluate the implication of hyperuricemia as an important player for progression of renal disease and to try to find safe and reasonable therapeutic modalities in individual patients based on their clinical data, medication history, and the presence of cardiovascular complications.

Animals↗
PubMed2006

Is hyperuricemia another facet of the metabolic syndrome?

BACKGROUND: Hyperuricemia is commonly associated with obesity, glucose intolerance, hypertension, dyslipidemia, and atherosclerotic cardiovascular disease. The resemblance of the metabolic syndrome and hyperuricemia has led to the suggestion that hyperuricemia is a part of the metabolic syndrome. The purpose of this study is to examine the contribution of uric acid (UA) as an additional component of the metabolic syndrome in middle-aged men. METHODS: In total, 393 male participants, aged 45-60 years, were recruited from a professional health evaluation program. Anthropometric measurements and blood pressure (BP) were taken after an overnight fast. Fasting blood samples were collected for the measurements of glucose, UA, and lipid profile. Logistic regression models were fitted to examine the relationship between UA and the diagnosis of metabolic syndrome. Factor analysis was performed to explore the relationship between UA and the components of the metabolic syndrome. RESULTS: The diagnosis of the metabolic syndrome was significantly associated with waist circumference (WC), glucose, triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), systolic BP, and liver enzyme levels, but not associated with UA levels. The sensitivity of hyperuricemia (serum UA > or = 7.0 mg/dL) for the diagnosis of the metabolic syndrome was 58.0% and the specificity was 55.3%. In factor analysis, UA aggregated with body mass index, WC, glucose, log TG, and HDL-C as a metabolic factor. Systolic and diastolic BP were loaded on a second factor separately. The model loaded with UA explained a similar proportion of the total variance (56.9%), as did the model loaded without UA (62.5%). CONCLUSION: Our results suggest that the contribution of UA as an additional component of the syndrome seems to be insignificant. We propose that hyperuricemia might not be an important facet for the understanding of the underlying structure of the metabolic syndrome.

Alanine Transaminase↗
PubMed2004

Prevalence of hyperuricemia and relation of serum uric acid with cardiovascular risk factors in a developing country.

BACKGROUND: The prevalence of hyperuricemia has rarely been investigated in developing countries. The purpose of the present study was to investigate the prevalence of hyperuricemia and the association between uric acid levels and the various cardiovascular risk factors in a developing country with high average blood pressures (the Seychelles, Indian Ocean, population mainly of African origin). METHODS: This cross-sectional health examination survey was based on a population random sample from the Seychelles. It included 1011 subjects aged 25 to 64 years. Blood pressure (BP), body mass index (BMI), waist circumference, waist-to-hip ratio, total and HDL cholesterol, serum triglycerides and serum uric acid were measured. Data were analyzed using scatterplot smoothing techniques and gender-specific linear regression models. RESULTS: The prevalence of a serum uric acid level >420 micromol/L in men was 35.2% and the prevalence of a serum uric acid level >360 micromol/L was 8.7% in women. Serum uric acid was strongly related to serum triglycerides in men as well as in women (r = 0.73 in men and r = 0.59 in women, p < 0.001). Uric acid levels were also significantly associated but to a lesser degree with age, BMI, blood pressure, alcohol and the use of antihypertensive therapy. In a regression model, triglycerides, age, BMI, antihypertensive therapy and alcohol consumption accounted for about 50% (R2) of the serum uric acid variations in men as well as in women. CONCLUSIONS: This study shows that the prevalence of hyperuricemia can be high in a developing country such as the Seychelles. Besides alcohol consumption and the use of antihypertensive therapy, mainly diuretics, serum uric acid is markedly associated with parameters of the metabolic syndrome, in particular serum triglycerides. Considering the growing incidence of obesity and metabolic syndrome worldwide and the potential link between hyperuricemia and cardiovascular complications, more emphasis should be put on the evolving prevalence of hyperuricemia in developing countries.

Adult↗
PubMed2005

The effect of alcoholic beverage type on hyperuricemia in Japanese male office workers.

BACKGROUND: The association between alcohol consumption and risk of hyperuricemia has been pointed out. However, the potential difference in the risk of hyperuricemia according to types of alcoholic beverage has not been assessed. METHODS: A cross-sectional survey was performed using data from 715 men who had regular medical examinations in their workplace in 2001. Subjects were interviewed using a questionnaire about their lifestyle including types of alcoholic beverages and quantity of alcohol consumed per day. Logistic regression analysis was performed to assess the relationship between the types of alcoholic beverage and high serum uric acid level. RESULTS: Compared with subjects who did not drink alcohol, the odds ratio (OR) of hyperuricemia (serum uric acid = 7.0+ mg/dL) was 2.89 (95% confidence interval [CI]: 1.46-5.71) for subjects who consumed 50+ g/day of ethanol, and 2.64 (95% CI: 1.33-5.24) for subjects who consumed 25-49g/day. Compared with subjects who drank Japanese sake, subjects who drank beer (OR=1.24, 95% CI: 0.55-2.80) or shochu (OR=1.06, 95% CI: 0.44-2.51) did not have a statistically significant difference in risk for hyperuricemia. CONCLUSION: These findings from a cross-sectional study of Japanese male office workers suggested that alcohol consumption is associated with an increased risk of hyperuricemia and that this increased risk does not vary according to the types of alcoholic beverage.

Adult↗