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PubMed1976

[Occurrence of hyperuricemia in atrioventricular block. (Results of a study of 158 patients with isotopic pacemaker implantations)].

The frequency of hyperuricemia is high in these patients with heart block, whose mean age is 39. 91% have serum uric acid levels above the normal range and 61% present "hyperuricemia," according to "gouty risk" criteria. The mean uric acid level, before surgery, of the patients whose total heart block follows "open-heart" is the highest in our statistics.

Adolescent↗

PubMed1993

[Hyperuricemia and atherosclerosis].

To clearly determine whether hyperuricemia participates directly in atherosclerotic disease or not, the prognosis and associated factors were studied, based on data from 104 patients whose serum uric acid had been completely maintained at normal levels with prolonged medication. The mean age at death was 65.8 +/- 10.5 years. The causes of death were as follows: cardiovascular disease (26.9%), cerebral disease (26.2%), malignant neoplasms (26.0%), uremia (7.6%), and miscellaneous disease (18.3%). Serum lipids especially triglycerides, body weight and influenced on the prognosis of the patients FBS. Most common complications were in the cardiovascular disease group; hypertension and hyperlipidemia. These data suggested that the apparent increased incidence of cardiovascular disease in gout rather than renal failure bore a relationship to such complications as hypertension or hypertriglycemia. Hyperuricemia alone may not be an atherosclerotic risk factors. There was no correlation between treatment with allopurinol and probenecid and cardiovascular complications.

Aged↗

PubMedDate not supplied

[Uric acid in blood serum and incidence of hyperuricemia in irradiated people. Connection with radioactive and nonradioactive factors].

A total of 1,002 workers aged 36 to 72 years who were engaged in atomic industry and exposed to external gamma-irradiation and incorporated plutonium 239 in a wide dosage range. The levels of uric acid (UA), the incidence of hyperuricemia and their association with 2 radiation and 12 nonradiation factors were studied in the examinees. There was a positive correlation between the purine metabolic parameters and the total dosage of external gamma-irradiation, sex (UC levels were higher in males than in females), body weight index, essential hypertension, and the type of haptoglobin 1-1. The influence of nonradiation factors on the parameters in question were substantially greater than that of external irradiation. Linear regression equations were derived for the dependence of the levels of UA and hyperuricemia upon the influencing factors.

Adolescent↗

PubMed1996

[Myogenic hyperuricemia].

Myogenic hyperuricemia is caused by over-production of uric acid, which based on the excessive degradation of purine derivatives in exercising muscle. This phenomenon is frequently observed in the patients of muscle glycogen storage disease (GSD) types III, V and VII. In these patients, impairment of muscle ATP production leads to over-production of AMP, followed by excessive release of inosine and hypoxanthine from the muscle. The molecular lesions of muscle GSDs have been well analyzed. Recent repertoire of these mutations were referred in respect of myogenic hyperuricemia.

Adenosine Monophosphate↗

PubMed1996

[Hyperuricemia in hematological disorders].

Hyperuricemia is a common manifestation in various hematological disorders such as hemolytic anemias, megaloblastic anemia malignant lymphomas and leukemias. Tumor lysis syndrome (TLS) is a serious complication consists of hyperuricemia, hyperkalemia, hyperphosphatemia and hypocalcemia due to massive cell lysis, which occurs shortly after the onset of chemotherapy or radiotherapy for acute leukemias and malignant lymphomas. Acute renal failure may develop due to uric acid nephropathy. The risk factors of TLS are heavy tumor cell burden, rapid cell turn over rate and renal involvement of neoplastic cells. To prevent and control TLS, adequate intravenous hydration to keep patient's urine volume, alkalization of urine by sodium bicarbonate and inhibition of uric acid production by high dose allopurinol is recommended.

Bone Marrow↗

PubMed1997

The role of hyperuricemia in the increased cytokine production after lipopolysaccharide challenge in neutropenic mice.

Patients with severe granulocytopenia are more susceptible to severe infections and sepsis. Proinflammatory cytokines such as tumor necrosis factor-alpha (TNF), interleukin-1 alpha (IL-1 alpha), and IL-1 beta play an important role in the pathophysiology of sepsis. The profile of these proinflammatory cytokines after lipopolysaccharide (LPS) challenge in cyclophosphamide-induced neutropenic mice was assessed, and possible mechanisms responsible for the modified cytokine production were studied. After LPS, both circulating concentrations of TNF and IL-1 alpha in neutropenic mice were 50% to 200% higher than those of controls, whereas IL-1 beta concentrations were not modified. The kinetics of cytokine production were similar in neutropenic and control animals. The susceptibility of neutropenic mice to an LPS challenge was increased. The observed overproduction of TNF and IL-1 alpha was not due to a direct effect of cyclophosphamide treatment. Because circulating concentrations of uric acid were increased in the neutropenic mice, the effect of hypouricemic treatment with allopurinol and sodium bicarbonate was investigated; such treatment in neutropenic mice challenged with LPS was followed by an improved survival and a reduced proinflammatory cytokine production towards the concentrations in control mice. Hyperuricemia induced by repeated administrations of uric acid in normal mice led to an increased TNF production after LPS. In conclusion, neutropenic mice respond with enhanced cytokine production and increased susceptibility to an LPS challenge, and hyperuricemia probably plays an important role in this phenomenon.

Agranulocytosis↗

PubMed1977

[Hyperuricemia due to therapeutic measures].

Some therapeutic measures cause hyperuricemia, which may require treatment in certain cases. The following may induce hyperuricemia: cytostatic long-term treatment, weight reduction through fasting, antihypertensive treatment with different chlorothiazides but also furosemide and etacrynic acid, anti-tuberculostatic therapy and Parkinson long-term treatment.

Antihypertensive Agents↗

PubMed1997

[Determination of uric acid in scalp hair for non-invasive estimation of uricemic control in hyperuricemia].

Uric acid in blood has been widely accepted as a reliable indicator of hyperuricemia and gout, and its assay method has been established. In the present study, we developed a simple and non-invasive rapid method for the determination of uric acid in hair. Concentration(nmol/mg hair) of uric acid extracted from 10-20 mg of hair(95% < extractability; 0.1N KOH, 37 degrees C, 2 hr) was determined by an enzymatic method using uricase. The concentration of uric acid(nmol/mg hair, mean +/- SD: 0.489 +/- 0.157, n = 16) in hair from hyperuricemic patients was significantly higher than that(0.258 +/- 0.107, n = 8) from healthy volunteers(p < 0.01). Within-run and between-day precisions(reproducibilities, CVs) for the assay were 9.6-10.3%(n = 10 each) and 11.6-16.3%(n = 7 each), respectively. The concentration(y, nmol/mg hair) of uric acid in hair correlated well with that in blood(x, g/l): y = 8.770x-0.123(r = 0.746, Syx = 0.122, n = 23). Changes in the concentration of uric acid in hair of hyperuricemic patient treated with allopurinol paralleled to those in blood. In conclusion, it was confirmed that the concentration of uric acid in hair reflected that in blood, suggesting that measuring uric acid in hair can be available for the metabolic control in hyperuricemia.

Biomarkers↗

PubMed1998

Disease-specific noncompliance with drug treatment as a cause of persistent hyperuricemia and gout in anorexia nervosa.

A 49 year old female patient with anorexia nervosa was admitted to the hospital because of treatment-refractory hyperuricemia and gout. Medical history and clinical findings were compatible with primary gout and uric acid nephropathy. The patient stated that she regularly took allopurinol. In the hospital she initially received 300 mg allopurinol daily after breakfast. In order to ensure allopurinol ingestion and absorption the plasma concentrations of both allopurinol and its active metabolite oxipurinol were determined in addition to serum uric acid and further clinical chemistry data. Despite allopurinol treatment no decrease of serum uric acid was observed for three days. Therefore the head nurse was instructed to supervise the intake of allopurinol carefully. During the following days serum uric acid decreased and plasma oxipurinol concentrations rose. On day 9 of treatment serum uric acid fell into the upper normal range. Therefore the patient was allowed to leave the hospital within a few days. However serum uric acid thereafter increased again while plasma oxipurinol declined. Later on it became evident that the patient had vomited self-induced approximately 15 minutes after allopurinol intake. In the meantime her husband had urged her to return home. Starting with day 18 benzbromarone treatment was added. Combined therapy with 400 mg allopurinol and 50 mg benzbromarone daily finally resulted in a serum uric acid concentration of 4.5 mg/dl at discharge from the hospital. About three weeks later the private physician again diagnosed hyperuricemia with serum uric acid values between 10 and 12 mg/dl. Meanwhile the patient needs to be dialysed due to end stage renal disease. Our observations show that self-induced vomiting to prevent effective treatment may be a disease-specific pattern of noncompliance with drug therapy in anorexia nervosa.

Allopurinol↗

PubMed2026

Associations between multiple essential trace metal concentrations and risk of hyperuricemia: insights from a central Chinese population.

Previous studies have indicated that levels of individual essential trace metals are related to hyperuricemia (HUA), but evidence on their combined effects is limited. To address this gap, the associations of individual and joint levels of 12 essential trace metals (manganese, selenium, nickel, chromium, cobalt, tin, iron, molybdenum, zinc, strontium, vanadium, and copper) with the risk of HUA were investigated in 2,021 adults recruited from Hunan Province, China. Inductively coupled plasma mass spectrometry (ICP-MS) was employed to determine urinary metal concentrations. Logistic regression, Bayesian kernel machine regression (BKMR), and quantile g calculation (Qgcomp) were applied to evaluate the associations of single and mixture metal concentrations with HUA. Of the participants, 516 (25.53%) were diagnosed with HUA. Inverse associations were found between vanadium, chromium, manganese, iron, cobalt, selenium, strontium, and molybdenum levels and HUA, with ORs ranging from 0.63 to 0.91. Conversely, a positive association was observed between zinc concentration and HUA [OR (95% CI): 1.17 (1.01, 1.37)]. Both BKMR and Qgcomp models showed a negative overall effect of essential trace metals on HUA risk, with strontium (- 43.6%) and vanadium (- 27.8%) being the main contributors. In addition, formal interaction tests revealed significant effect modification by age for tin and by BMI for zinc. In conclusion, the levels of essential trace metals were linked to a decreased risk of HUA, and these associations were modified by age and BMI only for specific metals.

Humans↗

PubMed2026

Integrative multi-omics analysis unravels the metabolic landscape and reveals serum biomarkers for early diagnosis of hyperuricemia.

BACKGROUND: Hyperuricemia (HUA) is a major risk factor for gout and multiple metabolic disorders. Although serum uric acid (UA) is the gold standard for HUA diagnosis, it fails to reflect early metabolic disturbances and shows limited predictive value for asymptomatic HUA. This study sought to elucidate the pathological mechanisms underlying HUA and identify novel diagnostic biomarkers beyond UA. METHODS: This study enrolled 195 patients with HUA and 98 healthy controls. Global metabolomics and proteomics profiling were performed to characterize molecular alterations underlying HUA. Based on the biological relevance of the shared dysregulated pathways, a pathway correlation network was constructed to elucidate the pathological mechanisms driving HUA initiation and progression. Furthermore, diagnostic biomarkers for HUA were identified using machine learning algorithms, and were validated with an external cohort. RESULTS: HUA patients exhibited distinct metabolic and proteomic profiles compared with healthy controls. Integrated multi-omics pathway analysis revealed that peroxisome proliferators-activated receptor signaling pathway, arachidonic acid metabolism, purine metabolism, pyrimidine metabolism and sphingolipid signaling pathway were significantly dysregulated in HUA. Among them, arachidonic acid metabolism was identified as a hub pathway involved in HUA progression. Furthermore, a metabolite panel consisting of cysteine-S-sulfate, glycerophosphocholine and 4-hydroxyphenylpyruvic acid was screened by machine learning and validated in an independent cohort, which showed slightly higher diagnostic performance for HUA than UA. CONCLUSIONS: This study reveals the core metabolic and protein regulatory networks of HUA, and identifies a novel serum metabolite panel for the diagnosis of HUA. These findings provide new insights for improved clinical diagnosis and management.

Humans↗

PubMed2004

Effect of hyperuricemia upon endothelial function in patients at increased cardiovascular risk.

The aim of the present study was to evaluate the effect of increased serum uric acid (UA) levels and their therapeutic reduction with allopurinol on endothelium-dependent dilation in subjects with a high cardiovascular (CV) risk but who were free from clinical CV disease. Patients with hyperuricemia had impaired flow-mediated dilation (FMD) compared with matched controls with normal UA levels and elevated CV risk. Three-month therapy with allopurinol improved FMD in hyperuricemic subjects, showing an intrinsic negative effect of elevated UA levels on the arterial wall; conversely, FMD remained unchanged in controls, thus suggesting that the reduction of UA to less than a certain value does not affect endothelial function.

Aged↗

PubMed2004

Primary prevention in rheumatology: the importance of hyperuricemia.

Hyperuricemia (HU) is present in 5-30% of the general population, although the prevalence is higher among some ethnic groups and seems to be increasing worldwide. Classically, chronic HU has been considered a risk factor for gout or lithiasis and is associated with alcoholism, obesity, hypertension, dyslipidemia, hyperglycemia/diabetes mellitus, renal failure and intake of certain drugs. HU is also associated with cardiovascular diseases such as hypertension, vascular disease, pre-eclampsia, pulmonary arterial hypertension, stroke, heart failure, ischemic heart disease and also metabolic syndrome, renal disease and increased mortality. It is uncertain if these associations are dependent or not, especially cardiovascular and renal diseases. Patients with chronic HU and also those with gout require both medical investigation for associated diseases or drugs as well as nutritional counseling and life-style changes. HU should alert physicians to possible complications.

Humans↗

PubMed2004

Identification of a new point mutation in hypoxanthine phosphoribosyl transferase responsible for hyperuricemia in a female patient.

A 29-year-old woman was referred to our department because of gout. Routine laboratory data showed hyperuricemia, a high level of plasma oxypurines, increased urinary uric acid excretion, and increased urinary oxypurine excretion, with decreased hypoxanthine phosphoribosyl transferase (HPRT) activity in the erythrocytes. From these findings, the patient was diagnosed with a partial deficiency of HPRT. To determine its properties, a cDNA sequence encoding HPRT and the androgen receptor AR XIST minimal promoter gene, as well as methylation of the AR gene were investigated. The HPRT cDNA sequence revealed a point mutation of G to A in nucleotide 40, which changed codon 14 from GAA (Glu) to AAA (Lys) in the mutant gene. In addition, the HPRT genomic DNA sequence, including the mutation site, revealed the same point mutation, indicating that the patient was heterozygote. Further analysis of the AR gene on the X chromosome suggested nonrandom X-chromosome inactivation, whereas the AR XIST minimal promoter gene was normal. Such results have not been previously reported in a female with partial HPRT deficiency.

Adenosine↗

PubMed2003

Elitek-rasburicase: an effective means to prevent and treat hyperuricemia associated with tumor lysis syndrome, a Meeting Report, Dallas, Texas, January 2002.

Renal precipitation of uric acid associated with tumor lysis syndrome (TLS) is a major complication in the management of leukemia, lymphoma, and other drug-sensitive cancers. Management of hyperuricema has historically consisted of administration of allopurinol, hydration, alkalinization to maintain pH between 7.0 and 7.3, and in some cases diuresis. Allopurinol, a xanthine analogue, blocks xanthine oxidase and formation of uric acid. Urate oxidase converts uric acid to allantoin, which is 5-10 times more soluble than uric acid. Homo sapiens cannot express urate oxidase because of a nonsense mutation. Urate oxidase was initially purified from Aspergillus flavus fungus. Treatment with this nonrecombinant product had been effective in preventing renal precipitation of uric acid in cancer patients, but was associated with a relatively high frequency of allergic reactions. This enzyme was recently cloned from A. flavus and is now manufactured as a recombinant protein. Clinical trials have shown this drug to be more effective than allopurinol for prevention and treatment of hyperuricemia in leukemia and lymphoma patients. This drug has been approved in Europe as well as the US and several clinical trials are in progress to further determine its clinical utility in other patient subsets. The purpose of this meeting was to discuss usefulness of recombinant urate oxidase, also known as rasburicase, Fasturtec, and Elitek, for the management of TLS in certain cancer patients.

Adolescent↗

PubMed2003

Hyperuricemia as a prognostic factor in pulmonary arterial hypertension.

Pulmonary arterial hypertension is a malignant disease with a median survival of 3 years. Uric acid levels are elevated in severe heart failure and in states of hypoxemia. Early data suggest a correlation between hyperuricemia and severe pulmonary arterial hypertension. We studied 29 patients with pulmonary arterial hypertension diagnosed and treated between 1998 and 2001. Clinical characteristics (6 min walk test and New York Heart Association class) and hemodynamic parameters (pulmonary artery pressure, pulmonary vascular resistance and cardiac output) were evaluated and correlated to uric acid level in a retrospective study. Uric acid levels correlated positively with New York Heart Association class (r=0.66, P<0.001) and negatively with 6 min walk test (r=-0.35, P=0.03). Uric acid levels were higher in patients who died than in patients who survived at the end ofthe follow-up period (8.8 vs. 5.7 mg/dl, P=0.001). This study shows that uric acid levels are elevated in severe pulmonary arterial hypertension and can be used as a prognostic marker of disease severity.

Adolescent↗

PubMed2005

Febuxostat compared with allopurinol in patients with hyperuricemia and gout.

BACKGROUND: Febuxostat, a novel nonpurine selective inhibitor of xanthine oxidase, is a potential alternative to allopurinol for patients with hyperuricemia and gout. METHODS: We randomly assigned 762 patients with gout and with serum urate concentrations of at least 8.0 mg per deciliter (480 micromol per liter) to receive either febuxostat (80 mg or 120 mg) or allopurinol (300 mg) once daily for 52 weeks; 760 received the study drug. Prophylaxis against gout flares with naproxen or colchicine was provided during weeks 1 through 8. The primary end point was a serum urate concentration of less than 6.0 mg per deciliter (360 micromol per liter) at the last three monthly measurements. The secondary end points included reduction in the incidence of gout flares and in tophus area. RESULTS: The primary end point was reached in 53 percent of patients receiving 80 mg of febuxostat, 62 percent of those receiving 120 mg of febuxostat, and 21 percent of those receiving allopurinol (P<0.001 for the comparison of each febuxostat group with the allopurinol group). Although the incidence of gout flares diminished with continued treatment, the overall incidence during weeks 9 through 52 was similar in all groups: 64 percent of patients receiving 80 mg of febuxostat, 70 percent of those receiving 120 mg of febuxostat, and 64 percent of those receiving allopurinol (P=0.99 for 80 mg of febuxostat vs. allopurinol; P=0.23 for 120 mg of febuxostat vs. allopurinol). The median reduction in tophus area was 83 percent in patients receiving 80 mg of febuxostat and 66 percent in those receiving 120 mg of febuxostat, as compared with 50 percent in those receiving allopurinol (P=0.08 for 80 mg of febuxostat vs. allopurinol; P=0.16 for 120 mg of febuxostat vs. allopurinol). More patients in the high-dose febuxostat group than in the allopurinol group (P=0.003) or the low-dose febuxostat group discontinued the study. Four of the 507 patients in the two febuxostat groups (0.8 percent) and none of the 253 patients in the allopurinol group died; all deaths were from causes that the investigators (while still blinded to treatment) judged to be unrelated to the study drugs (P=0.31 for the comparison between the combined febuxostat groups and the allopurinol group). CONCLUSIONS: Febuxostat, at a daily dose of 80 mg or 120 mg, was more effective than allopurinol at the commonly used fixed daily dose of 300 mg in lowering serum urate. Similar reductions in gout flares and tophus area occurred in all treatment groups.

Allopurinol↗

PubMed2003

Incidence, medical resource utilisation and costs of hyperuricemia and tumour lysis syndrome in patients with acute leukaemia and non-Hodgkin's lymphoma in four European countries.

Hyperuricemia (HU) and tumour lysis syndrome (TLS) are complications of acute leukaemia and non-Hodgkin lymphoma (NHL) leading to increased morbidity and mortality. The objective of this study was to define incidence and calculate health care cost associated with HU and TLS. 788 acute leukaemia and NHL patients from Belgium, The Netherlands, Spain and UK were screened retrospectively for HU and TLS. Resource use related to HU and TLS was recorded and costs were calculated applying local unit costs. Results showed that HU occurred in 18.9% of patients, and 27.8% of them fulfilled TLS criteria. The cost of HU without TLS was 672 euros (SE 181), the cost of TLS 7,342 euros (SE 1,412). TLS requiring dialysis incurred an average cost of 17,706 euros. In conclusion, it is noted that the observed incidence rates were lower than earlier reports. In addition, some risk factors for HU and TLS (e.g. paediatric patients versus adults) were not associated with increased rates of HU or TLS as a consequence of higher rates of prevention. TLS cases incurred 11 times higher costs than HU cases in which TLS was absent. The main cost drivers in TLS are interventions requiring intensive care.

Acute Disease↗