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

In order to clarify the mechanism of hyperuricemia and hyperuricosuria resulting from rapid infusion of fructose in man, the effects of an intravenous infusion of 125-200 g of fructose given over 3-4 hr on the rate of purine synthesis de novo was measured in one individual with osteoarthritis and four patients with gout. The incorporation of 1-minus 14C glycine into urinary uric acid was measured, and the pool size and turnover of urate were assessed by renal excretion of simultaneously administered 15-N urate. Fructose caused an expansion of body urate pool in all subjects, while urate turnover was increased in four. The rate of incorporation of 14-C glycine into urinary uric acid corrected for extrarenal disposal was increased in all cases (21%-430%). In two patients, rates of incorporation of 14-C glycine into urinary creatinine were increased by 10% and 11%, while rates of incorporation into uric acid were increased 84% and 159%, respectively, as a result of fructose infusion. Specific enhancement of the rate of purine synthesis de novo was suggested by these findings. The rate of infusion appeared more important than total dose in determining the magnitude of this effect. Whether the increased rate of purine synthesis was a result of direct stimulation by a fructose metabolite or was secondary to fructose-induced purine nucleotide depletion is uncertain, since the kinetics of glycine incorporation were consistent with either mechanism. Erythrocyte PP-ribose-P concentrations, however, were diminished during infusion rather than increased as might be expected if fructose infusion stimulated purine synthesis by increasing availability of this regulatory substrate.
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PMID:Stimulation of human purine synthesis de novo by fructose infusion. 16 70

Tienilic acid, a diuretic agent effective at the cortical diluting segment of the distal tubule, has been found to have equivalent antihypertensive action in a dose of 250 mg twice daily to hydrochlorothiazide in a dose of 50 mg twice daily. Tienilic acid reduced arterial pressure without diminishing renal plasma flow or endogenous creatinine clearance; moreover, it did so whilst achieving hypouricaemia through a uricosuric effect. Hypokalaemia was observed but corrected by supplemental potassium. A transient but reversible, slight elevation in serum creatinine concentration and significant hypertriglyceridaemia were also observed. In conclusion, tienilic acid seems to be a novel diuretic, well-suited for the patient with hypertension, particularly if there is coincidental gout or coexisting hyperuricaemia.
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PMID:Antihypertensive and renal effects of tienilic acid. 50 45

The etiology of hyperuricemia following myocardial infarction was investigated by uric acid kinetic studies carried out on seven male patients following myocardial infarction and on two control subjects. The patients selected had uncomplicated myocardial infarction and were maintained on a low-purine diet. Measurements of uric acid pool size and turnover rates using 2-C14 uric acid were made, commencing on days 2-5 following myocardial infarction. Initial concentration of serum uric acid ranged from 2.9 to 9.8 mg/100 ml. Uric acid pool size was elevated in six of seven patients. Five had a pool size of from 36.9 to 79.6 mg/kg, while the single gouty subject demonstrated 104 mg/kg compared with 12.6 and 16.8 mg/kg for the control subjects. Turnover rates were also increased, ranging from 1036 to 2772 mg/day (controls, 612 and 872 mg/day). Twenty-four-hour urine uric acid excretions ranged from 358 to 623 mg/24 hr. Serum lactic acid concentration was normal (1.03 plus or minus 0.17 muM/ml), and endogenous creatinine clearance in all cases was 77.9 ml/min or greater. These data suggest that following myocardial infarction there is an expansion of the uric acid pool with an increased uric acid turnover rate. Only the patient with a previous history of gout had uric acid excretion outside the normal range.
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PMID:Uric acid kinetic studies in the immediate post-myocardial-infarction period. 111 39

The effect of ascorbic acid on the serum and urinary uric acid was studied in 14 subjects. Two to 6 h after the ingestion of 4.0 g of ascorbic acid, the fractional clearance of uric acid increased to 202% +/- 41% of the control value. This uricosuria was inhibited by pyrazinamide and by low-dose acetylsalicylic acid, but was not accompanied by an increase of the creatinine clearnace. Ascorbic acid did not diminish protein-bound uric acid. In 3 subjects who ingested 8.0 g of ascorbic acid for 3 to 7 days the serum uric acid decreased by 1.2 to 3.1 mg/dl as a result of a sustained uricosuria. These results suggest that ascorbic acid could invalidate studies involving the measurement of uric acid and obscure the diagnosis of gout in some cases. Theoretically it could precipitate attacks of gouty arthritis or renal calculi in predisposed persons. These observations show a pharmacologic effect of megadoses of a simple vitamin.
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PMID:Ascorbic acid-induced uricosuria. A consequency of megavitamin therapy. 125 82

Experience with chemodissolution of uric acid stones in 30 patients is presented. Chemodissolution was achieved either with infusion of 0.16 M i.v. lactate or oral sodium bicarbonate, in addition to liberal fluid intake and allopurinol wherever indicated. In some cases direct chemodissolution by in situ irrigation with sodium bicarbonate solution was done after an initial percutaneous nephrostomy. Seven patients presented with acute obstructive anuria. In this group, 5 of them had bilateral obstructive calculi, while 2 had unilateral obstruction in a solitary kidney. The latter 2 had complete recovery following intravenous lactate therapy. Of the 5 presenting with bilateral obstruction, 2 patients had complete response to chemodissolution, whereas the remaining 3 had only a partial response requiring surgery for ultimate salvage. In this group I, 6 patients are doing well with a normal serum creatinine at 3 months to 4 years follow-up, while 1 patient has a serum creatinine, stabilised at 3.2 mg%. In the second group, 23 patients presented with non-obstructing urinary stones. Flank pain was the commonest complaint and a concomitant history of gout was present in 6 patients. Hyperuricaemia was detected in 12 and hyperuricosuria in 19. All cases were managed by high fluid intake and oral sodium bicarbonate, with self-monitoring of urine pH, which was kept between 6.5 and 7.0. Allopurinol was administered in cases having hyperuricaemia and/or hyperuricosuria. Systemic alkali therapy in the form of intravenous molar lactate or sodium bicarbonate is effective and safe both in obstructive anuria and non-obstructive urinary uric acid stones.
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PMID:Chemodissolution of urinary uric acid stones by alkali therapy. 131 80

Renal dysfunction is a common problem in cardiac transplant recipients who receive the immunosuppressive agent cyclosporine. Elevation in serum creatinine levels and other indicators of renal dysfunction often appear during the first year after transplant. Related problems of hypertension and gout also are common. Specific strategies to minimize the nephrotoxic effects of cyclosporine and other potential insults to renal function can be used by nurses, physicians, and other health team members. Preservation of renal function enhances a patient's overall functional status and improves survival and quality of life for cardiac transplant recipients.
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PMID:Monitoring and prevention of renal dysfunction in cardiac transplant recipients. 152 34

The relation between creatinine and uric acid metabolism was analysed in 77 male patients with primary gout and 62 healthy male subjects. Significant positive correlations between 24 hour urinary creatinine and uric acid excretion were shown in both groups. The mean urinary creatinine and uric acid excretions in the patients with gout were significantly increased as compared with those of normal male controls. These results suggest that there is a close correlation between creatinine and uric acid synthesis. In addition, it seems that accelerated uric acid synthesis seen in some patients with gout is due to increased creatinine synthesis.
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PMID:Relation between creatinine and uric acid excretion. 154 11

Fifteen patients with clinical gout occurring after long term treatment with diuretics were studied retrospectively. In all 15 patients one or more additional factors were present which might have contributed to the hyperuricaemia and gout. The most common of these was the impairment of the glomerular filtration rate. Twenty five other patients receiving long term treatment with diuretics who did not have gout were also studied. The concentrations of uric acid, urea, and creatinine were, in general, markedly lower in these patients than in those who had developed gout. It is concluded that diuretic induced gout occurs in patients in whom there is an additional cause of hyperuricaemia, usually impaired renal function.
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PMID:Diuretic induced gout: a multifactorial condition. 155 Apr 14

The effect of ingesting some purine-rich foods (beef liver, haddock fillets and soybeans) on uric acid metabolism was investigated in 18 male subjects with no history of gout or kidney disorder. In a crossover design, three isoenergetic and isonitrogenous meals were fed to volunteers during a 3-week period. Only the content of uricogenic bases (adenine and hypoxanthine) varied among the test meals. Ingestion of all experimental meals caused an increase in serum uric acid levels at 120 minutes and this increase was more marked (about twofold) with haddock and soybean ingestion. In all groups, the postprandial serum uric acid levels at 240 minutes were lower than those obtained at 120 minutes, but still remained elevated in comparison to the fasting level. The test foods had little or no effect on serum and urinary creatinine values. As expected, 24-hour urinary uric acid excretion was similar for the three test meals due to the isonitrogenous load of proteins and purines. Assessment of each purine base content rather than the total purine content of foods should be considered in future recommendations for hyperuricemic individuals.
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PMID:Changes in serum and urinary uric acid levels in normal human subjects fed purine-rich foods containing different amounts of adenine and hypoxanthine. 161 89

During Ramadan, Moslems are required strictly to avoid fluids and nourishment from dawn to sunset. Heat stress during such abstinence represents a substantial health hazard. In the Federal Republic of Germany (FRG) where numerous Moslems, particularly of Turkish origin, perform heat work and other heavy labour, we observed moderate to severe health disturbances in such labourers during Ramadan, e.g.: tachycardia, severe headaches, dizziness, nausea, vomiting and circulatory collapse. The severe dehydration of these workers was demonstrated by substantial increases in their hematocrit, serum protein, urea, creatinine, uric acid and electrolyte imbalance. Because of the evidence of the substantial health hazard to Islamic workers in such situations, we have strongly urged employers to refrain from assigning Islamic workers to heat work or heavy daytime work during Ramadan; we have therefore limited systematic studies of health problems during Ramadan to persons performing only moderate work. Even under these conditions signs of dehydration were found in the 32 labourers monitored. Some of these labourers also had to interrupt their observance of Ramadan due to health problems, e.g.: acute gout due to serum uric acid increase, or circulatory insufficiency. In light of the observed potentially harmful pathophysiological effects, the danger of dehydration of Islamic workers due to heat work during Ramadan should be taken very seriously.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The health risks of occupational stress in islamic industrial workers during the Ramadan fasting period. 181 40


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