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PubMed2003

The epidemiology of hyperuricemia in children of Taiwan aborigines.

OBJECTIVE: To explore the factors influencing serum uric acid concentrations and the prevalence of hyperuricemia in aboriginal children from an area in Taiwan with a high prevalence of gouty arthritis. METHODS: A cross sectional study of the Bunun tribe was conducted in central Taiwan from March to May 2001. Children aged 4-13 were requested to fill out a structured questionnaire with the assistance of their parents. A total of 414 children (mean age, 8.9 +/- 2.1 yrs) were recruited. Uric acid was determined by colorimetry using the uricase method. Since no previous study has investigated serum uric acid concentrations in these aboriginal children, hyperuricemia was defined as uric acid > 416.5 micromol/l (7 mg/dl) in boys and > 357 micromol/l (6 mg/dl) in girls. RESULTS: The mean concentration of serum uric acid was 368.9 +/- 83.3 micro mol/l. Ninety of 224 girls (40.2%) and 56 of 190 boys (29.5%) were hyperuricemic. Children with hyperuricemia had significantly higher body mass index (BMI), blood pressure, and triglyceride and creatinine concentrations than those with normal uric acid concentrations. After adjustment for age, sex, lipid profile, and blood pressure, hyperuricemia was found to be significantly associated with serum creatinine (OR 2.40, 95% CI 1.91-3.04), BMI (OR 1.24, 95% CI 1.11-1.40), and a family history of gouty arthritis in parents (OR 2.01, 95% CI 1.02-3.96). CONCLUSION: BMI, a positive family history of gouty arthritis in parents, and creatinine level correlated with hyperuricemia in aboriginal children in Taiwan.

Arthritis, Gouty↗
PubMed2004

Increasing prevalence of gout and hyperuricemia over 10 years among older adults in a managed care population.

OBJECTIVE: To determine whether the prevalence of gout and/or clinically significant hyperuricemia increased in a managed care population over 10 years. METHODS: The study was a descriptive analysis utilizing an administrative claims database to ascertain 10-year trends in prevalence of gout and/or hyperuricemia. Prevalence rates were calculated cross-sectionally for each year (1990-99) and expressed/compared as rates per 1000 enrollees. RESULTS: The prevalence of gout and/or hyperuricemia in the overall population increased by about 2 cases per 1000 enrollees over 10 years. In the > 75 year age group, rates increased from 21 per 1000 persons in 1990 to 41 per 1000 in 1999. In the 65-74 year age group, prevalence increased from between 21 and 24 per 1000 persons in the years 1990-92 to over 31 per 1000 during the years 1997-99. Prevalence rates in younger age groups (< 65 years) stayed consistently low during the years under study. There were sex differences in most age groups, with men having the greater burden of disease at every time point. CONCLUSION: Prevalence of gout and/or hyperuricemia in the overall study population increased during the 10-year period. When stratified by age, there were increases in prevalence among groups over age 65 in both sexes. Although gout prevalence increased in both sexes over the 10-year period, men still had most of the burden of disease. In ages younger than 65, men had 4 times higher prevalence than women (4:1 ratio), but in the older age groups (> 65), the gender gap narrowed to 1 woman to every 3 men with gout and/or hyperuricemia (3:1 ratio).

Adolescent↗
PubMed2005

[Hyperuricemia].

The association of elevated serum uric acid (hyperuricemia, gout) with the presence of classical coronary risk factors and coronary artery disease or myocardial infarction has been analysed in many epidemiological studies. In this paper the urid acid metabolism, the factors influancing on this metabolism, the laboratory hyperurycemia criteria and the mode of hyperuricemia treatment are presented. The hyperuricemia and it's collaboration with the other coronary risk factors are analysed as an independent risk factors. Hyperuricemia is described as an increased concentration of uric acid in blood. The urate concentration is elevated when the upper level of arbitrary accepted value is exceeded. That corresponds to the mean value of urate concentration of particular sex and age plus two standard deviations. In most cases of epidemiologic investigations the upper normal range of concentration equals 6 mg/dl for women and 7 mg/dl for men. An increased level of uric acid leads to urate gout (diathesis urica). An increased level of urate in serum is connected with numerous cardiovascular risk factors such as: arterial hypertension, hyperglycemia, diabetes and male sex. But up today, hyperuricemia is not used as independent direct risk factor, so the reduction of uric acid is not obligatory recommended in guidelines for prevention of cardiovascular diseases and stroke.

Allopurinol↗
PubMed2006

[Is hyperuricemia a cardiovascular risk factor?].

The association of elevated serum uric acid (hyperuricemia, gout) with the presence of classical coronary risk factors and coronary artery disease (CAD) or myocardial infarction (MI) has been analysed in many epidemiological studies. Numerous studies have revealed that hypertension, high body mass index (BMI), lipid disorders (especially raised triglycerides--TG level and low high dense lipoprotein cholesterol HDL-C level), increased creatinine or insulin levels have caused hyperuricemia. No association has been observed between hyperuricemia and diabetes type 2 and uricemia and glicemia. But in some studies the relationship between cholesterol and uric acid levels has been not confirmed. Hyperuricemia has been observed in patients with non-treated hypertension. Gout has often occurred with typical disorders for the metabolic syndrome X. Significant correlation of the serum uric level and the CAD presence and severity of coronary atherosclerosis confirmed by coronary angiography has been observed in women. Hyperuricemia has also indirect influence on progress of CAD by physical activity restriction, what causes sedentary mode of life and lead to obesity. Obesity is a known risk factor diabetes, lipid disorders and hypertension. To recapitulate, it is a matter of controversy as to whether uric acid is an independent cardiovascular risk factor or rather it only represents reinforcement of typical risk factor.

Cardiovascular Diseases↗
PubMed1995

Natural history and etiology of hyperuricemia following pediatric renal transplantation.

A retrospective review was conducted to determine the incidence, etiology, natural history and complications of hyperuricemia after pediatric renal transplantation. Of 81 active transplant recipients aged 10.1 +/- 4.8 (mean +/- SD) years being followed by St. Christopher's Hospital for Children, 57 (70%) were males and 59 (73%) Caucasian. Their immunosuppression consisted of azathioprine, cyclosporine A and prednisone. Mean serum uric acid concentrations peaked at 6 months post transplantation (6.2 +/- 2.6 mg/dl), when 39% of the patients had hyperuricemia and 60% were receiving diuretics, and decreased thereafter. At 30 months, 23% of the patients had hyperuricemia and 17% required diuretics. When we compared 42 normouricemic (group A) with 24 hyperuricemic (group B) patients at 18 months post transplantation, we found that patients in group B were older (11.6 +/- 4.2 vs. 8.6 +/- 5.2 years, P = 0.01), had worse renal function (77 +/- 25 vs. 96 +/- 36 ml/min per 1.73 m2, P = 0.03) and required diuretics more frequently (63% vs. 21%, P = 0.001), but had identical blood levels of cyclosporine A (82 +/- 28 vs. 84 +/- 35 ng/ml, P = 0.78). A family history of gout did not affect the prevalence of hyperuricemia after transplantation. Asymptomatic hyperuricemia is common following pediatric renal transplantation and is more likely attributable to reduced renal function and diuretic therapy than to the known hyperuricemic effect of cyclosporine A. Of these variables, only diuretic therapy is readily controllable and should be closely regulated following pediatric renal transplantation.

Aging↗
PubMed2001

[Relationship between severity of essential arterial hypertension and the prevalence hyperuricemia].

BACKGROUND: Hyperuricemia has been associated with an increased risk of cardiovascular disease in hypertensive patients. However, the relation between serum urate and severity of hypertension has not been conclusively defined as yet. We aimed at finding out whether there exists an independent relationship between changes in the prevalence of hyperuricemia and severity of hypertension. PATIENTS AND METHOD: We studied 3 cohorts of patients aged 35 to 60 years with essential hypertension diagnosed at a university hospital in Madrid, Spain. The first cohort (before 1981) included 325 patients, the second (from 1981 to 1989) comprised 271 patients and the third cohort (from 1990 to 1999) included 545 patients. Disease severity ranged from 1 to 6 according to blood pressure levels at diagnosis (WHO/ISH grades 1, 2 or 3 were assigned 1, 2 or 3 points, respectively) and target organ damage (left ventricular hypertrophy, hypertensive retinal vascular changes, and proteinuria above 300 mg/day; one point each). RESULTS: Mean serum urate concentrations in the 3 cohorts were 6.6, 5.8 and 5.5 mg/dL, respectively (p < 0.05 for all comparisons). 39% of patients in the first cohort had a serum urate concentration > 7.0 mg/dL whereas only 18.1% patients in the third group showed hyperuricemia (difference: 20.9%; 95% CI, 10.1 to 32.3; p < 0.05). Severity of hypertension was higher in the first cohort (mean SD, 2.50 1.31 points) than in the third group (1.96 1.06 points; p < 0.05), with the second cohort showing an intermediate severity (2.23 1.01 points). Serum urate levels were directly related to the severity of hypertension in the 3 groups (r = 0.08, p < 0.05). In a multivariate analysis, after adjustment for confounding variables, serum urate had no significant association with severity of hypertension. However, target organ damage, systolic blood pressure and serum creatinine were all independent predictors of severity. CONCLUSIONS: Favourable changes in the severity of hypertension for a time period significantly correlate with decreases in hyperuricemia prevalence in the same period. On the other hand, hyperuricemia appears to be an indirect marker of hypertensive renal damage.

Adult↗
PubMed1999

Is hyperuricemia a risk factor of stroke and coronary heart disease among Africans?

BACKGROUND: Uric acid stabilizes platelet aggregation and enhances thrombotic tendency. OBJECTIVE: To examine the relationship between raised serum uric acid and subsequent cardiovascular events (mortality, myocardial infarction, stroke). METHODS: This is a longitudinal study in a small random number (418) of patients in Kinshasa, Congo. In this hospital-based study, uricemia was determined with respect to gender, obesity and hypertension as well correlated with traditional cardiovascular risk factors. A univariate regression model was used to investigate the association of serum uric acid with the incidence of mortality, stroke and myocardial infarction. RESULTS: Serum uric acid was higher (P<0.05) in obese women and men as well in hypertensives, than in their controls. The significant (P<0.05 and 0.001) highest frequency of hyperuricemia was observed in both diabetic and hypertensive patients. Blood pressure (BP) was higher (P<0.001) in patients with hyperuricemia than in those with normal serum uric acid. Serum uric acid was significantly correlated with body weight, BP, glucose, fibrinogen, urea, creatinin and total cholesterol. In men, hyperuricemia was significantly (P<0.01) associated with a twofold increased risk of both myocardial infarction and stroke incidence. However, hyperuricemia was significantly related to a double risk of all mortality and stroke onset. CONCLUSION: Our results indicate that hyperuricemia among african patients is a strong predictor of myocardial infarction in men, stroke in both sexes and all causes of mortality in women.

Black People↗
PubMed1999

Hyperuricemia and renal insufficiency associated with malignant disease: urate oxidase as an efficient therapy?

Hyperuricemia is a common finding in patients with malignant diseases. Chemotherapy can induce life-threatening tumor lysis syndrome with severe hyperuricemia, other metabolic abnormalities, and acute renal failure. Intrarenal precipitation of uric acid contributes to renal insufficiency in this situation. Allopurinol, by preventing the conversion of hypoxanthine and xanthine to uric acid, has been long considered the standard pharmacological approach to hyperuricemia and prevention of tumor lysis syndrome. However, allopurinol itself may facilitate precipitation of xanthine crystals and has little influence on already-formed uric acid crystals deposited in the kidney. Urate oxidase further oxidizes uric acid to the highly water-soluble allantoin in mammals, except humans, who lack this enzyme. We report four cases of hyperuricemia (initial serum uric acid concentrations, 14.0 to 25.0 mg/dL) associated with malignant diseases treated with exogenous urate oxidase. Two of the patients showed full-blown tumor lysis syndrome. A single urate oxidase infusion (1,000 U) readily reduced serum uric acid levels in all patients. Furthermore, renal insufficiency, determined by serum creatinine concentrations, improved in three of the four patients. No adverse effects were observed. Currently, a recombinant urate oxidase is undergoing clinical testing and may make this efficient therapy more widely available. We believe that treatment with urate oxidase is a safe and efficient therapy for patients with cancer-associated hyperuricemia and may be effective even in individuals with only moderately elevated serum uric acid concentrations.

Journal Article↗
PubMed1999

Influence of hyperglycemia and hyperuricemia on long-term transplant survival in kidney transplant recipients.

Long-term prognosis in kidney transplant recipients depends on multiple factors. The purpose of this study was to quantify the influence of hyperuricemia and hyperglycemia (elements of the so-called 'syndrome X', i.e., a combination of metabolic disorders like hyperuricemia, diabetes mellitus, hyperlipidemia, and hypertension) on organ function in 350 kidney transplant recipients who had received 375 kidney transplants up to 1990 and in whom sex, age of recipient and donor, nephrologic disease, duration of dialysis, human leukocyte antigen (HLA) classification, and duration of transplant ischemia had been well matched. We found the influence of hyperuricemia on graft survival to be statistically significant (p < or = 0.05), while a statistically significant correlation between hyperglycemia and graft survival could not be detected in the present study. The transplant survival rates 2, 4, and 5 yr post-kidney-transplantation were 96.7, 80.7, and 78.7 in normogylcemic patients vs. 96.9, 85, and 82.7% in hyperglycemic ( > 100 mg,dL) kidney transplant recipients (p > 0.05). Transplant survival in hyperuricemic patients (male, > 8 mg dL; female, > 6.2 mg/dL) 2, 4, and 5 yr post-transplantation was significantly reduced (92.2, 70.6, and 68.8% vs. 98.1, 85.6, and 83.3%), as compared to normouricemic recipients. A combined presence of both hyperuricemia and hyperglycemia probably influencing the prognosis post-kidney-transplantation failed to reach the level of statistical significance. We found a significant correlation between age of recipients and plasma glucose (p < or = 0.01) and between serum uric acid concentrations and diuretic therapy (p < or = 0.05) and gender (p < or = 0.(5). In conclusion, hyperuricemia after kidney transplantation seems to reduce graft survival, whereas an influence of the carbohydrate metabolism has to be denied.

Adult↗
PubMed2001

Hyperuricemia exacerbates chronic cyclosporine nephropathy.

BACKGROUND: Hyperuricemia frequently complicates cyclosporine (CSA) therapy. The observation that longstanding hyperuricemia is associated with chronic tubulointerstitial disease and intrarenal vasoconstriction raised the hypothesis that hyperuricemia might contribute to chronic CSA nephropathy. METHODS: CSA nephropathy was induced by the administration of CSA (15 mg/kg/day) for 5 and 7 weeks to rats on a low salt diet (CSA group). The effect of hyperuricemia on CSA nephropathy was determined by blocking the hepatic enzyme uricase with oxonic acid (CSA-OA). Control groups included rats treated with vehicle (VEH) and oxonic acid alone (OA). Histological and functional studies were determined at sacrifice. RESULTS: CSA treated rats developed mild hyperuricemia with arteriolar hyalinosis, tubular injury and striped interstitial fibrosis. CSA-OA treated rats had higher uric acid levels in association with more severe arteriolar hyalinosis and tubulointerstitial damage. Intrarenal urate crystal deposition was absent in all groups. Both CSA and CSA-OA treated rats had increased renin and decreased NOS1 and NOS3 in their kidneys, and these changes are more evident in CSA-OA treated rats. CONCLUSION: An increase in uric acid exacerbates CSA nephropathy in the rat. The mechanism does not involve intrarenal uric acid crystal deposition and appears to involve activation of the renin angiotensin system and inhibition of intrarenal nitric oxide production.

Animals↗
PubMed2001

Recombinant urate oxidase for the prophylaxis or treatment of hyperuricemia in patients With leukemia or lymphoma.

PURPOSE: To improve the control of hyperuricemia in patients with leukemia or lymphoma, we tested a newly developed uricolytic agent, recombinant urate oxidase (SR29142; Rasburicase; Sanofi-Synthelabo, Inc, Paris, France), which catalyzes the oxidation of uric acid to allantoin, a highly water-soluble metabolite readily excreted by the kidneys. PATIENTS AND METHODS: We administered Rasburicase intravenously, at 0.15 or 0.20 mg/kg, for 5 to 7 consecutive days to 131 children, adolescents, and young adults with newly diagnosed leukemia or lymphoma, who either presented with abnormally high plasma uric acid concentrations or had large tumor cell burdens. Blood levels of uric acid, creatinine, phosphorus, and potassium were measured daily. The pharmacokinetics of Rasburicase, the urinary excretion rate of allantoin, and antibodies to Rasburicase were also studied. RESULTS: At either dosage, the recombinant enzyme produced a rapid and sharp decrease in plasma uric acid concentrations in all patients. The median level decreased by 4 hours after treatment, from 9.7 to 1 mg/dL (P =.0001), in the 65 patients who presented with hyperuricemia, and from 4.3 to 0.5 mg/dL (P =.0001) in the remaining 66 patients. Despite cytoreductive chemotherapy, plasma uric acid concentrations remained low throughout the treatment (daily median level, 0.5 mg/dL). The urinary excretion rate of allantoin increased during Rasburicase treatment, peaking on day 3. Serum phosphorus concentrations did not change significantly during the first 3 days of treatment, decreased significantly by day 4 in patients presenting with hyperuricemia (P =.0003), and fell within the normal range in all patients by 48 hours after treatment. Serum creatinine levels decreased significantly after 1 day of treatment in patients with or without hyperuricemia at diagnosis (P =.0003 and P =.02, respectively) and returned to normal range in all patients by day 6 of treatment. Toxicity was negligible, and none of the patients required dialysis. The mean plasma half-lives of the agent were 16.0 +/- 6.3 (SD) hours and 21.1 +/- 12.0 hours, respectively, in patients treated at dosages of 0.15 or 0.20 mg/kg. Seventeen of the 121 assessable patients developed antibodies to the enzyme. CONCLUSION: Rasburicase is safe and highly effective for the prophylaxis or treatment of hyperuricemia in patients with leukemia or lymphoma.

Adolescent↗
PubMed1981

Catecholamine-induced hyperuricemia in eviscerated rats with functional hepatectomy.

The presence of extra-hepatic systems for uric acid production and their role in catecholamine-induced hyperuricemia were studied in eviscerated rats with functional hepatectomy. In these animals, the plasma uric acid level progressively increased with a decrease of allantoin, and isoproterenol subcutaneously administered in low doses produced an evident hyperuricemia. The effect of isoproterenol was seen even in nephrectomized animals, but all effects were abolished by pretreatment with allopurinol. Epinephrine and norepinephrine also produced hyperuricemia, though to a lesser extent than isoproterenol. Propranolol inhibited the hyperuricemic effects of isoproterenol and epinephrine, while phentolamine potentiated the effects of epinephrine. Electrical stimulation of the splanchnic nerve also produced hyperuricemia in eviscerated rats with functional hepatectomy, and this state was abolished by pretreatment with propranolol and by adrenalectomy but was not affected by pretreatment with phentolamine. Thus, beta adrenoceptor agonists stimulate production of uric acid in tissues other than the liver and the viscera, and hyperuricemia results. An effect similar to that on the uric acid level was also observed for the levels of plasma lactate, creatinine and glutamic oxalacetic transaminase in rats given isoproterenol.

Animals↗
PubMedDate not supplied

[Hyperuricemia as a risk factor for cerebrovascular accident: a case-control study].

INTRODUCTION: Although several collateral studies have been made of the relationship between hyperuricemia and cerebral vascular accidents (CVA), no definite conclusion has been reached. OBJECTIVE: To analyze the possible relationship between hyperuricemia and CVA. PATIENTS AND METHODS: We studied the cases and controls paired for age, sex and hospital. They included patients with CVA (125) and controls (250 ophthalmological patients). Both groups contained 50.4% men and 49.6% women with an average age of 70 +/- 11 years. Data regarding vascular risk factors, a known personal history of hyperuricemia were recorded and serum uric acid levels determined in both groups. The relative risks were calculated using the Odds Ratio (OR) with a confidence interval of 95% (CI 95) and a conditional logistic regression study made. RESULTS: A statistically significant relationship was found between CVA and: arterial hypertension (OR: 6.32; CI 95: 3.43, 11.65); smoking (OR: 3.79; CI 95: 1.36, 10.58); alcoholism (OR: 2.54; CI 95: 1.11, 5.41); ischemic cardiopathy (OR: 2.37; CI 95: 1.2, 4.70) and previous CVA (OR: 5.93; CI 95: 3.17, 11.09). No relation was found with: a history of hyperuricemia (OR: 1.53; CI 95: 0.63, 3.73), serum uric acid levels (OR: 0.86, CI 95: 0.36, 2.00 when the uricemia was between 5 and 5.99 mg/dl and OR: 0.46, CI 95: 0.21, 1.02, when the uricemia was over 6 mg/dl). CONCLUSION: Our results suggest that hyperuricemia is not an independent risk factor for CVA.

Adult↗
PubMed1992

[First indications of decrease in the incidence of hyperuricemia in North Germany].

For the first time after onset of the economic miracle since 1948/49 the continuous considerable upward trend of the prevalence of hyperuricemia among the adult population in northern Germany seems to be stopped. In a comparative study of a total of 7169 unselected patients of both sexes, that has been admitted as inpatients for rehabilitation reasons predominantly concerning rheumatic diseases, has been examined which differences result between 1988 and 1990 with respect to the prevalence of hyperuricemia in relation to overweight. Age structure, professions and social levels were comparable in both populations. In comparison with the large upward trend of the risk factor profile between 1976 and 1988 the prevalence of hyperuricemia in males decreased significantly from an average of 17.9 per cent to 15.2 per cent. For females only an insignificant trend to a decrease of the prevalence of hyperuricemia (4.5 per cent vs. 4.2 per cent) was noted. In hyperuricemic males the prevalence of overweight of more than 20 per cent in relation to the individual ideal weight was significantly more frequent than in the whole male population (70.1 per cent vs. 57.7 per cent). Just as for obesity and diabetes mellitus the prevalence of hyperuricemia among the adult population in northern Germany appears to have culminated or crossed its summit. There is further evidence for a small success of public and medical efforts to improve public health. Of a total of 3584 patients who were investigated in 1990 1977 males showed a mean serum uric acid level of 5.71 +/- 1.62 mg/dl whereas in females the corresponding mean value was highly significantly less (4.22 +/- 1.06 mg/dl).

Adult↗
PubMed1993

Hereditary nephropathy associated with hyperuricemia and gout.

BACKGROUND: The clinical characteristics of hereditary nephropathy associated with hyperuricemia or gout have not been fully described, and the pathogenetic role of increased serum urate concentration is controversial. METHODS: We examined the clinical characteristics of 14 patients and purine metabolism of seven patients, while they were on a purine-restricted diet, in two families with hereditary nephropathy associated with asymptomatic hyperuricemia or gout. Results of plasma and urinary purine measurements were compared with those obtained in 25 patients with gout and renal insufficiency and in 25 normal subjects. Eight subjects in both families were followed up for a mean of 44 months. Allopurinol was given to all patients and enalapril maleate to hypertensive subjects. RESULTS: All patients had some combination of hyperuricemia, gout, renal insufficiency, arterial hypertension, and reduced kidney size. Decreased glomerular filtration rate was proportional to the decreased renal plasma flow. Renal vascular resistance was markedly increased in the patients with diminished renal plasma flow. All patients with familial nephropathy showed diminished urinary uric acid, hypoxanthine, and xanthine excretion rates. Purine under-excretion was more severe in affected patients with familial nephropathy than in patients with gout and renal insufficiency. Kidney biopsy specimens from three patients with familial nephropathy showed tubulointerstitial lesions and ischemic changes in glomeruli but no uric acid crystals. The kidney uric acid content was normal. Allopurinol treatment normalized serum urate levels, but serum creatinine concentrations increased and creatinine clearance decreased in all patients with familial nephropathy. One patient with gout only at initial evaluation developed renal failure during the follow-up period. CONCLUSIONS: Increased serum urate concentrations in hereditary nephropathy associated with hyperuricemia and gout are due to severe impairment of uric acid excretion. Hyperuricemia does not appear, however, to be of pathogenetic relevance and may be a consequence of a primary disruption of renal hemodynamics.

Adolescent↗
PubMed1996

[Dynamics of uric acid metabolism in hyperuricemia].

This paper is a review of the studies on urate metabolism of gouty patients with hyperuricemia and normal healthy subjects, performed mainly in our laboratory. The pathogenesis of hyperuricemia consisted of overproduction and underexcretion, which can be estimated using the urate clearance test. Overproduction was defined as urinary urate excretion (Uua) higher than [0.030 Cua + 0.325] mg/kg/hr and underexcretion as urate clearance (Cua) lower than 6.1 ml/min. According to those criteria, hyperuricemia was classified into the 4 types of overproduction (12%), underexcretion (60%), combined (25%) and normal type (3%). Patients with overproduction had a tendency of lower serum urate level (Sua) than those with underexcretion, higher Uua than those with the normal control and lower Cua and creatinine clearance (Ccr) than those with the normal control. Patients with underexcretion had a tendency of higher Sua and lower Cua, Ccr and Cua/Ccr ratio than those with overproduction or normal control. Patients with the combined type had the highest Sua among the 4 types, and those with the normal type had the lowest Sua. These findings indicate that each subtype of hyperuricemia has characteristic features in the urate metabolism, which are valuable for better understanding and treatment of hyperuricemia in gouty patients.

Blood Proteins↗
PubMed2007

The association between hyperuricemia and the Trp64Arg polymorphism of the beta-3 adrenergic receptor.

The object of this study was to determine the association of Trp64Arg polymorphism with hyperuricemia. This study is an age-matched, case-controlled study of 203 hyperuricemic and 203 normouricemic men. The frequency of genotypes was compared between the two groups. Possible confounding metabolic variables were included in a multiple logistic regression model for multivariate adjustment. The genotype frequencies of Trp64Trp, Trp64Arg, and Arg64Arg in hyperuricemic and normouricemic groups are respectively 130, 69, and 4 (64.0%, 34.0%, 2.0%) and 154, 45, and 4 (75.9%, 22.2%, 2.0%) (P = 0.029, Chi-square test). Simple logistic regression analysis indicated that the Trp64Arg genotype is significantly associated with hyperuricemia (OR = 1.816, 95% CI (1.167-2.827), P = 0.008). Multivariate analysis for controlling metabolic effects also showed a significant association with the occurrence of hyperuricemia (OR = 1.937, 95% CI (1.149-3.266), P = 0.013). Trp64Arg polymorphism of the beta-3 adrenergic receptor may be independently associated with hyperuricemia in males.

Adult↗
PubMed2003

Hyperuricemia and gout.

Gout is not a new disease for clinicians; nevertheless, there are still many secrets awaiting discovery for improving knowledge with respect to uric acid metabolism and monosodium urate crystal-induced inflammation. This review of the literature will focus on new insights on the pathogenesis of idiopathic hyperuricemia, and on secondary hyperuricemia and gout. There are also important advances on the pathophysiology of acute gout, especially as a self-limited process (switch from monocyte to macrophage, peroxisome proliferator activated receptor-gamma, and nitric oxide), but also of chronic gouty arthropathy. Armaments for treating hyperuricemia and gout may be already improved by losartan or fenofibrate and, in the future, by urate oxydase-polyethylene glycol 20 and renal handling regulatory molecules. Finally, control of hyperuricemia may also be considered in the prevention and treatment of cardiovascular disease.

Gout↗