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

This study attempted to simulate the drinking habits of gout patients. Beer or squash was drunk over a 4-hour period on two successive days by five gouty and five normouricaemic men. Serum lactate increased with beer and squash, but elevation of plasma uric acid was confined to beer drinking. Urate clearance increased with both beverages, but 24-hour uric acid excretion was accentuated only by beer. The purine content of several beers was measured and the principal constituent found to be guanosine, which is probably the most readily absorbed dietary purine. It was concluded that the hyperuricaemic effect of beer was mediated by the digestion of purines contained by the beer and by an effect of ethanol on uric acid synthesis. There was no evidence that beer taken in usual quantities reduced the renal excretion of uric acid.
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PMID:Beer drinking and its effect on uric acid. 674 68

Fifty-nine patients with primary gout were treated with either a combination of colchicine and allopurinol or colchicine alone. Assessments of renal function over 2 years revealed a statistically significant fall of glomerular filtration rate an urine concentrating ability in those receiving only colchicine. The renal function of patients given allopurinol did not change. Treatment with allopurinol resulted ina significant reduction of ammonium excretion, a phenomenon which could not be readily explained. Urate clearance also declined during allopurinol treatment, and the impaired urate clearance associated with gout became more evident. The most important observation was that allopurinol retarded an apparent decline of renal function. Presumably this was achieved through its hypouricaemic effect and implies that the hyperuricaemia of gouty patients is deleterious to the kidneys.
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PMID:Allopurinol treatment and its effect on renal function in gout: a controlled study. 703 23

Uric acid metabolism was investigated in 69 insulin-treated male diabetic outpatients and in 23 healthy male subjects, because of a reported coincidence between diabetes and gout. All subjects had normal serum creatinine concentrations and none received diuretic treatments. Compared with normal, the diabetics had significantly lower mean serum uric acid concentrations (0.34 +/- 0.08 (SD) mmol/l versus 0.23 +/- 0.06 mmol/l, p less than 0.001). 17% of the diabetic patients had serum concentrations below the normal mean--2 SD. In contrast, the diabetic patients had a 42% increase in renal uric acid excretion rate (p less than 0.01), and an 83% increase in the ratio of uric acid clearance/creatinine clearance (p less than 0.001). These indices of renal uric acid excretion were both positively correlated to fasting blood glucose levels (r=0.57, p less than 0.001, and r=0.50, p less than 0.001, respectively), to the degree of glycosuria (r=0.73, p less than 0.001, and r=0.63, p less than 0.001, respectively), and to the magnitude of water diuresis (r=0.60, p less than 0.001, and r=0.39, p less than 0.01, respectively). The hypouricaemia observed in these insulin-dependent diabetic male subjects may probably be caused by the increased renal excretion of uric acid in the presence of hyperglycaemia. The study gave no evidence of increased serum uric acid concentrations in insulin-dependent diabetics. It is therefore likely that any coincidence between gout and diabetes derives from other coexisting serum uric acid raising factors.
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PMID:Renal hypouricaemia in insulin treated diabetes mellitus. 704 28

Consumption of alcoholic beverages is associated with hyperuricemia and gout. To determine the contributions to this process of increased production and decreased excretion of uric acid, we gave oral ethanol (1.8 g per kilogram of body weight every 24 hours) for eight days or intravenous ethanol (0.25 to 0.35 g per kilogram per hour) for two hours to six patients with gout. During the long-term oral study we observed the following: serum urate levels increased from 8.4 +/- 0.4 (mean +/- S.E.) to 10.1 +/- 0.9 mg per deciliter; whole blood lactate reached a peak of 3.1 +/- 0.7 mM from a base line of 1.3 +/- 0.3 mM; and urinary oxypurines increased to 641 +/- 397 per cent of the base-line value. Urate clearance increased to 145 +/- 25 per cent of the base-line value. Daily uric acid turnover increased from 1010 mg per deciliter to 170 +/- 17 per cent of the base-line value. During short-term intravenous ethanol administration, serum urate levels, urate clearance, and urinary uric acid excretion were not substantially altered from the base-line period. Urinary oxypurine levels increased to 341 to 415 per cent of base-line values. Urinary radioactivity, originating from the adenine nucleotide pool labeled by [8-(14)C]adenine, increased to 127 to 149 per cent of base-line values. These data indicate that ethanol increases urate synthesis by enhancing the turnover of adenine nucleotides.
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PMID:Ethanol-induced hyperuricemia: evidence for increased urate production by activation of adenine nucleotide turnover. 714 47

Forty-nine patients with gout, many with hypertension and/or renal calculi, were given hydrochlorothiazide, furosemide, or ticrynafen. Diuresis and increased clearances of sodium (Na), potassium (K), chloride (Cl), and calcium (Ca) occurred after a single dose of hydrochlorothiazide, 100 mg, or furosemide, 40 mg, orally. There was very slight change in urate and phosphorus clearances. With prolonged use of hydrochloride or furosemide, diuresis and increased electrolyte excretion disappeared. Urate and Ca excretion fell with hydrochlorothiazide. With long-term use of furosemide, urate excretion was suppressed, but Ca excretion was sustained. Ticrynafen produced diuresis and increased clearances of Na, K, and Cl. Calcium excretion was increased after a single dose and minimally decreased after long-term use. Most striking was the severe and rather sustained uricosuria. Though ticrynafen is an effective uricosuric, natriuretic, and antihypertensive agent, its hepatotoxicity and nephrotoxicity mitigate against its clinical use.
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PMID:Effects of diuretics on urate and calcium excretion. 723 11

The contribution of enhanced purine salvage to the decreased total purine excretion associated with allopurinol therapy was measured by the intravenous administration of tracer doses of [8-(14)C] adenine to four patients with gout and normal purine salvage enzyme activity and four patients with the Lesch-Nyhan syndrome and absent purine salvage activity. The mean cumulative excretion of radioactivity 5 days after the adenine administration to patients not receiving and receiving (off and on) allopurinol therapy was 6.1% and 3.6% of infused radioactivity for gouty subjects and 15.9% and 20.8% for the Lesch-Nyhan patients. Urate pool size and urate turnover, as measured by pool labeling with [2-(14)C]uric acid, were substantially decreased in both groups of patients during allopurinol therapy. The intestinal loss of uric acid was estimated from these pool measurements on and off allopurinol. With a correction for this extrarenal purine loss, the mean cumulative excretions of radioactivity 5 days after adenine administration to patients off and on allopurinol therapy were 11.9% and 4.8% for the gouty subjects and 31.7% and 24.5% for the Lesch-Nyhan patients. In vitro studies demonstrated no alteration of the synthesis or degradation of adenine nucleotides by allopurinol in cultured human diploid fibroblasts. These observations suggest that enhanced purine salvage is an important component leading to decreased purine excretion during allopurinol therapy.
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PMID:Enhanced purine salvage during allopurinol therapy: an important pharmacologic property in humans. 729 39

Urate deposits within microtophi were found in 8% of unselected autopsies in Brisbane, Australia. Significant association were demonstrated with (a) a history of gouty arthritis and (b) the existence of nitrogen retention and renal disease of apparently primary, but not gouty, origin. However, in 26% of the patients, a retrospective survey of their medical records did not reveal any causative factor. The possible aetiological importance of the urine flow rate is stressed. The presence of medullary urate deposits at autopsy was most frequently associated with a history of gout or the presence of pre-existing and non-gouty renal disease, although no aetiological factor could be determined in a quarter of the cases.
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PMID:Urate deposits in the renal medulla. Prevalence and associations. 732 50

Inherited enzyme deficiencies are found in a small proportion of patients with gout who produce an excess of uric acid. The clinical, biochemical and therapeutic aspects of a case of hyperuricaemia caused by an atypical mutant hypoxanthine-guanine phosphoribosyl transferase are presented. Urate overproduction was moderate and controlled by allopurinol therapy.
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PMID:Primary overproduction of urate caused by a partial deficiency of hypoxanthine-guanine phosphoribosyl transferase. 740 61

A study of renal function of 51 patients with gout and an equal number of normouricaemic controls revealed significant differences. A relative impairment of the glomerular filtration rate and urine concentrating ability in the gouty subjects could not be wholly explained on the basis of aging or hypertension. Renal dysfunction was generally mild and was not associated with specific clinical characteristics higher levels of uric acid excretion, or hypertriglyceridaemia. Gout patients excreted urine with a significantly lower pH. This was associated with a relatively high excretion of titratable acid and a deficit of ammonium excretion, which was accentuated by ingestion of an acid load. Urate clearance was significantly reduced in gout, even when expressed as a fraction of the glomerular filtration rate.
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PMID:Renal impairment and gout. 743 72

Gout in heart transplant recipients is common and poses a significant therapeutic challenge. Concomitant administration of azathioprine and allopurinol therapy carries a high risk of leukopenia. Uricosuric agents can cause renal lithiasis and/or acute renal failure in patients with renal failure and/or high urinary levels of uric acid. We report our experience with urate-oxidase in three heart transplant recipients with severe polyarticular and tophaceous gout, a history of leukopenia under allopurinol and unresponsiveness or contraindications to uricosuric agents. Urate-oxidase was given parenterally in a dosage of 1000 units per day, seven days a month. The injections were done intramuscularly in one patient and intravenously in the other two, who were under anticoagulant therapy. Patients 1 and 2 received 12 and 6 courses, respectively. The third patient had had four courses and was still under treatment at the time of this writing. Shrinking of the tophi and improved mobility of the fingers were seen in all three patients after the second course. No adverse effects were recorded. Our experience suggests that urate-oxidase therapy may decrease the urate burden in patients with severe tophaceous gout. Urate-oxidase therapy should be viewed as a phase in the treatment of gout, which must be followed by administration of another agent.
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PMID:Urate-oxidase for the treatment of tophaceous gout in heart transplant recipients. A report of three cases. 765 72


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