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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Uric acid is the end-product of purine nucleotide metabolism in man. The renal handling of urate is a complicated process, resulting in a fractional clearance of 8.2-10.3%. The anhydrous form is thermodynamically the most stable uric acid crystal. Uric acid is a weak acid that ionizes with a Pka at pH 5.75. At the normal acidic region, uric acid solubility is strongly increased by urinary pH. The prevalence of uric acid stones varies between countries, reflecting climatic, dietary, and ethnical differences, ranging from 2.1% (in Texas) to 37.7% (in Iran). The risk for uric acid stone formation correlates with the degree of uric acid supersaturation in the urine, depending on uric acid concentration and urinary pH. Hyperuricosuria is the major risk factor, the most common cause being increased purine intake in the diet. Acquired and hereditary diseases accompanied by hyperuricosuria and stone disease include: gout, in strong correlation with the amount of uric acid excreted, myelo- and lymphoproliferative disorders, multiple myeloma, secondary polycythemia, pernicious anemia and hemolytic disorders, hemoglobinopathies and thalassemia, the complete or partial deficiency of HGPRT, superactivity of PRPP synthetase, and hereditary renal hypouricemia. A common denominator in patients with idiopathic and gouty stone formers is a low urinary pH. Uric acid nephrolithiasis is indicated in the presence of a radiolucent stone, a persistent undue urine acidity and uric acid crystals in fresh urine samples. A radiolucent stone in combination with normal or acidic pH should raise the possibility of urate stones.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Uric acid nephrolithiasis. 778 6

Although catabolic events are known to precipitate gout, postsurgical gout has rarely been reported. We identified the charts of 302 patients treated over a 10-year period in a university center who carried the diagnosis of gout and who also had a surgical procedure. Fifty-two patients (42 male, 10 female) were found to have had a postsurgical episode of gouty arthritis. Ages ranged from 20 to 82 years (mean 60.1 +/- 2.1). Forty-five patients had a history of gout, 22 of whom were receiving medication and 23 who were not receiving chronic therapy. In seven patients the postsurgical event was their first attack. Attacks occurred 1-17 days (mean 4.2 +/- 0.5 [SE]) after surgical admission. Most attacks were in the lower extremity, but classic podagra was uncommon. Essentially all patients were febrile (100.7 +/- 0.2 degrees F) compared with admission (99.0 +/- 0.1 degree) (P < 0.001). There was a trend toward leukocytosis in the group as a whole, but the relationship of leukocytosis to the gout attack was most clearly seen in patients admitted for noninflammatory conditions (9.4 +/- 0.7 versus 12.8 +/- 0.8 x 1000 WBC/mm3, P < 0.001). Uric acid levels were elevated but did not follow the course of the attack. Most patients underwent a variety of tests and consultative evaluations because of their undiagnosed febrile episode. Once the diagnosis was established, all patients responded quickly to nonsteroidal anti-inflammatory drugs or colchicine. Despite evidence of a significant inflammatory response, no patient proved to have a suppurative focus as the source of their febrile episode.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Postsurgical gout. 783 83

Purine metabolism disturbances which may be responsible for urate nephropathy were revealed in 35% of the examinees with arterial hypertension. Gout manifestations occurred in many of the above patients. Purine metabolism disturbances contribute much to progression of renal disorders and arterial hypertension, require early diagnosis and treatment. Urate symptoms may serve a primary diagnostic indication.
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PMID:[Urate nephropathy in patients with arterial hypertension]. 794 Mar 61

Uric acid is formed by catabolism of purine nucleotides. Approximately 25% is excreted through the intestines and the rest through the kidneys. A little less than 5% of the population in western industrialised countries have hyperuricaemia, primarily men and postmenopausal women. Hyperuricaemia is in most cases caused by reduced renal excretion, which may be idiopathic with otherwise normal renal function. But the condition is often associated with hypertension, nephropathy and treatment with diuretics and certain other drugs. Hyperuricaemia due to increased purine metabolism is seen in malignant haematological diseases, other conditions with increased cellular turnover and during initiation of chemotherapy in malignant diseases. Moreover hyperuricaemia is associated with some metabolic disturbances and risk factors of atherosclerotic cardiovascular disease including hypertension, overweight, insulin resistance and hyperlipidaemia. Hyperuricaemia is rarely caused by constitutional enzymatic abnormalities influencing purine metabolism. In most cases hyperuricaemia is asymptomatic. It may though be complicated by gout, urolithiasis and possibly gouty nephropathy. The risk of complications is correlated to the degree and duration of hyperuricemia. Consequently, measures to affect predisposing and associated conditions should be taken including weight reduction, physical exercise and diet guidance, treatment of hypertension and possibly changes in medication. Urate lowering drug treatment is normally not indicated in asymptomatic hyperuricaemic individuals.
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PMID:[Hyperuricemia]. 800 1

Several plant hormones and analogues were tested for their inhibitory effects on xanthine oxidase. The flavoprotein enzyme, xanthine oxidase, catalyses the oxidation of hypoxanthine to xanthine and then xanthine to uric acid which has lambda max 295 nm. Uric acid was thus the basis for a spectrophotometric assay of the activity of xanthine oxidase. The results showed that trans-zeatin displayed the strongest activity (IC50 = 23.5 muM) on xanthine oxidase inhibition, followed by indole-3-acrylic acid (IC50 = 136.0 muM) and then by the mixed isomers of zeatin (trans-zeatin and cis-zeatin) (IC50 = 198.65 muM). Trans-zeatin induced an uncompetitive inhibition of the enzyme with respect to the substrate xanthine and the apparent inhibition constant (Ki) was 5.09 muM. However, zeatin riboside was inactive. Since xanthine oxidase serum levels are increased in hepatitis, mild hepatic intoxication, tumours brain tissues, and DNA damage induced by cytotoxic agents, it is expected that trans-zeatin may be useful for the treatment of these diseases as well as gout which is caused by deposition of uric acid in the joints and oxidative damage of tissue caused by generation of superoxide anion radical.
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PMID:Inhibitory effects of plant growth regulators on xanthine oxidase. 861 27

Important observations have continued to expand our understanding of gout. The increased risk of gout in black Americans has been linked more closely with the development of hypertension, and an increasing prevalence in African blacks and in England may have a similar association, possibly through the use of diuretics. The association of gout and insulin resistance appears to be related to fat distribution, and the link with hyperlipidemia may be related to genetic factors. The relationship between gout and renal disease and the frequency of gout in patients with renal failure continue to be areas of controversy. The mechanism and a possible therapeutic approach to the hyperuricemia associated with cyclosporine therapy are better understood. The potential for antibodies against urate crystals to potentiate further crystallization may explain some of the uncertainties about gouty attacks. Unusual manifestations of gout, including more cases of spinal involvement, were reported. The role of formalin in dissolving urate crystals in pathologic specimens was further clarified, and the use of atomic force microscopy to detect crystals was reported. Corticosteroids are increasingly accepted in treating acute gout, and the role of colchicine in acute and intercritical gout has come under increasing scrutiny. Urate-lowering drugs appear to be cost effective in patients with more than one or two attacks per year.
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PMID:Gouty arthritis and uric acid metabolism. 879 84

Uric acid is the end product of purine metabolism in man. The findings of human pathological levels of uric acid in serum and urine have in most patients serious clinical implications. This paper summarizes aspects of uric acid examination in clinical biochemistry laboratory. The clinical consequences of pathological levels of uric acid are shown. Uric acid is a useful diagnostic tool as screening for most of purine metabolic disorders. The importance of uric acid measurement in plasma and urine with respect of metabolic disorders is highlighted. Not only gout and renal stones are indications to send blood to the laboratory for uric acid examination. Also familial nephritis, neurological abnormalities with mental retardation are reasons to know uric acid levels in blood and urine. The results underline the importance of urinary uric acid investigation, which is often quite overlooked, and is helpful in differential diagnosis of gout. This work is dedicated to Professor Jan Horbaczewsky and his 110th anniversary of the opening of lessons in medical chemistry at the Czech medical faculty of Charles University in Prague.
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PMID:The importance of uric acid examination. 886 10

Uric acid is the end product of purine degradation in humans. It is a weak acid with a pK of 5.35 in urine. In acidic urine the undissociated form of uric acid predominates and is poorly soluble, leading to crystalluria and stone formation. Uric acid stones account for 5% to 10% of all stones in the United States. Acidic urine, hyperuricosuria, and low urine volume are the risk factors for uric acid stone formation. Uric acid stones may be idiopathic or secondary to a systemic disease such as gout. Treatment includes alkalinization of the urine, high fluid intake, and reduction of uric acid excretion if it is abnormal.
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PMID:Uric acid stones. 889 Mar 97

We describe a patient with no history of gout and persistently normal serum uric acid concentrations in whom septic acute prepatellar bursitis was diagnosed initially, but empiric antibiotic therapy failed. Urate crystals were detected when the prepatellar bursa was aspirated for the 3rd time, and the diagnosis was changed to gouty bursitis. The case illustrates the importance of repeatedly aspirating suspicious sites to establish the diagnosis in elusive cases of crystal deposition disease.
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PMID:Prepatellar bursitis: a unique presentation of tophaceous gout in an normouricemic patient. 997 97

We evaluated the effect of accumulation of intraabdominal visceral fat on the metabolism of uric acid in 50 healthy male subjects to elucidate any relationship between such obesity and hyperuricemia. The area of abdominal fat (visceral fat and subcutaneous fat) was measured at the level of the umbilicus by abdominal computed tomographic scanning. Serum and urinary concentrations of uric acid and creatinine were determined with an autoanalyzer. Uric acid clearance and the ratio of urinary uric acid to creatinine excreted in urine were calculated. Univariate and multivariate analyses were used to evaluate the relationship between uric acid metabolism and body fat. The size of the area of visceral fat was significantly correlated with the serum concentration of uric acid (r = .37, P < .01), uric acid clearance (r = -.34, P < .05), and the urinary uric acid to creatinine ratio (r = .65, P < .0001). The size of the area of subcutaneous fat was significantly correlated only with the urinary uric acid to creatinine ratio (r = .38, P < .01). Multivariate analyses, including body mass index (BMI), showed that the size of the visceral fat area was the strongest contributor to an elevated serum concentration of uric acid, a decrease in uric acid clearance, and an increase in the urinary uric acid to creatinine ratio. These results suggest that accumulation of visceral fat may have a greater adverse effect on the metabolism of uric acid than BMI or accumulation of subcutaneous fat. Clearly, patients with hyperuricemia should lose weight to reduce excessive visceral fat stores, to help avoid attacks of gout.
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PMID:Close correlation between visceral fat accumulation and uric acid metabolism in healthy men. 932


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