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

The clearance of uric acid, hypoxanthine and xanthine has been examined in gouty patients and in normal subjects comparatively to the creatinine clearance. The clearance of the three purine compounds was lower in the gouty patients, while the creatinine clearance showed a normal behavior. These results indicate that either the tubular excretion or the carriers of the considered metabolites probably undergo specific alterations in the gout.
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PMID:[Clearance of oxypurines and uric acid in patients with gout]. 261 6

The mean age of the onset of gout in Taiwan is 49.6 years old. This is very similar to Japan. The female cases made up 5.78% of total cases. This is very similar to the world average of about 5%. As far as laboratory findings are concerned, uric acid had a significant correlation with BUN, creatinine, cholesterol and triglyceride. In our occupation study we found that gout occurs in almost every class of society and no particular group has any immunity.
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PMID:Clinical aspects of gouty patients in Taiwan. 262 89

The clearance of uric acid, hypoxanthine and xanthine has been examined in gout patients and in normal subjects compared to creatinine, after a purine-free diet. The treatment decreased the clearance in normal subjects, but showed an opposite effect in gout patients. The clearances both of uric acid, hypoxanthine and xanthine were enhanced by allopurinol. The interpretation of the observed variations is discussed.
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PMID:[Clearance of oxypurines in normal subjects and in gout patients subjected to a purine-free diet. Effects of allopurinol]. 262 28

To evaluate the frequency and the pathogenesis of hyperuricemia and gout during cyclosporine therapy, we studied renal-transplant recipients who were treated with either cyclosporine and prednisone (n = 129) or azathioprine and prednisone (n = 168). Among the patients with stable allograft function and serum creatinine concentrations below 265 mumol per liter, hyperuricemia was more common in the cyclosporine group than in the azathioprine group (84 percent vs. 30 percent; P = 0.0001). Gout developed in nine patients (7 percent) in the cyclosporine group, but no episodes occurred in the azathioprine group. Serum urate levels became elevated in 90 percent of the patients in the cyclosporine group who were treated with diuretics, as compared with 60 percent of those not treated with diuretics (P = 0.001); in the azathioprine group, the corresponding values were 47 percent and 15 percent (P = 0.0001). Serum urate levels did not correlate with trough blood cyclosporine levels in a selected subgroup (n = 40) of patients from the cyclosporine group, who were studied from 4 to 96 weeks after transplantation. Detailed studies of urate metabolism in six cyclosporine-treated patients revealed normal turnover rates for urate and decreases in creatinine and urate clearance, as compared with seven control subjects. We conclude that hyperuricemia is a common complication of cyclosporine therapy and is caused by decreased renal urate clearance. Gouty arthritis is the cause of considerable morbidity among renal-transplant recipients who receive cyclosporine.
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PMID:Cyclosporine-induced hyperuricemia and gout. 266 17

During a study of clinical and laboratory features in 83 patients with sickle cell disease in the Netherlands, serum creatinine, sodium, potassium, uric acid and osmolality were determined and reported for 65: 39 with homozygous sickle cell (SS) disease, 5 with beta degrees thalassaemia (S beta degrees thal), with sickle cell beta + thalassaemia (S beta degrees + thal) and 17 with sickle cell haemoglobin C (SC) disease. Data on history of hyposthenuria was unreliable. Haematuria was reported in 6 (7%) of the 83 patients. Four of the six patients with a history of haematuria, two of whom had elevated creatinine levels, had SS disease. Lower mean levels of serum sodium and higher levels of serum potassium were observed in SS's than in the other genotypes (p less than 0.001). Hyperkalaemia of greater than 5 mmol/l was seen in 50% of SS disease cases and in 33% of paediatric SC disease cases. Some high potassium levels must be ascribed to in vitro haemolysis. The rate of hyperuricaemia ranged from 24% to 40% among the various genotypes. Clinical gout was not observed.
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PMID:Renal and electrolyte profile in steady state sickle cell disease: observations in patients with sickle cell disease in The Netherlands. 276 58

The use of long-term allopurinol therapy in patients with gout was evaluated. A pharmacy computer printout was used to identify all outpatients for whom allopurinol had been prescribed during a six-month period in 1985 at a large Veterans Administration medical center. Medical records were reviewed to (1) classify patients as either having or not having definite indications for allopurinol treatment, (2) determine whether physicians had ordered roentgenographic and laboratory tests for presence of monosodium urate crystals, uric acid excretion, and renal function, and (3) identify gout-associated risk factors and disease entities that could cause hyperuricemia. A pharmacy record of all allopurinol and probenecid prescriptions for the six-month period was obtained, along with cost data. Of the 286 patients who received allopurinol, 32 received the drug for an indication that could not definitely be established as gout. Of the 254 remaining patients, only 45 (17.7%) had a definite indication for allopurinol use as defined by the pharmacy and therapeutics committee. Although pretreatment measurement of serum creatinine was common, only a few patients underwent joint aspiration, a 24-hour urine collection, or roentgenography of affected joints. Large proportions of the patients were found to have gout-associated risk factors. If the 209 patients without definite indications for allopurinol therapy had been treated with probenecid instead of allopurinol, the annual cost savings would have been about $3700. Most of the patients receiving allopurinol for gout could reasonably have been treated with a uricosuric agent such as probenecid at a lower cost. Generally, physicians did not use diagnostic tests optimally before prescribing allopurinol and did not attempt to modify risk factors for gout.
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PMID:Evaluation of allopurinol use in patients with gout. 280 16

We recently have conducted a cross-sectional survey to determine the prescribing practices of rheumatologists and a random sample of general practitioners in New South Wales and Queensland. While in general there was agreement as to the preferred management of gout, several important differences were noted between the two groups of doctors. In particular, general practitioners were more liberal than were rheumatologists in their use of allopurinol. However, they were less likely to cover the introduction of allopurinol with anti-inflammatory agents, to titrate the dose against the serum uric acid level or to adjust the dose according to the serum creatinine level. A small number of doctors continued to use urate-lowering drugs as a routine in the treatment of entirely asymptomatic hyperuricaemia. The data indicate a continuing need to disseminate information regarding the preferred management of hyperuricaemic states.
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PMID:A survey of current prescribing practices of anti-inflammatory and urate-lowering drugs in gouty arthritis in New South Wales and Queensland. 281 27

Hyperuricemia is common in cyclosporine-treated renal allograft recipients. An increased incidence of gout in patients receiving both diuretics and cyclosporine has been reported, but the effect of hyperuricemia on renal allograft function has not been studied. In a prospective, randomized trial of cyclosporine and prednisone versus azathioprine, prednisone, and antilymphocyte globulin for immunosuppression in renal allograft recipients, 105 of 131 cyclosporine and prednisone-treated patients (80 percent) experienced hyperuricemia (serum uric acid level above 8 mg/dl) and 13 of 131 (10 percent) were severely hyperuricemic (serum uric acid level above 14 mg/dl). In contrast, hyperuricemia developed in 63 of 115 patients (55 percent) treated with azathioprine, prednisone, and antilymphocyte globulin (p less than 0.002). Despite the frequent occurrence of hyperuricemia, gout was rare. Clinical gout developed in six patients in the cyclosporine and prednisone group and in 0 patients in the azathioprine, prednisone, and antilymphocyte globulin group between 1 and 43 months (median 22.5 months) after transplantation. Neither severe hyperuricemia nor diuretic therapy were associated with a significantly increased incidence of gout. The mean serum creatinine concentration of severely hyperuricemic patients (all on cyclosporine and prednisone) was similar to that of normouricemic cyclosporine and prednisone patients (1.8 mg/dl versus 1.6 mg/dl, p greater than 0.2), and the severely hyperuricemic patients had a 4-year graft survival rate of 90 percent. Asymptomatic hyperuricemia after renal transplantation does not adversely affect allograft function, requires no specific therapy, and is not a contraindication to use of diuretics.
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PMID:Hyperuricemia after renal transplantation. 305 57

Gout rarely develops in nephropathy with advanced renal failure unless other risk factors are present. It has recently been demonstrated that gouty patients with renal failure have greater amounts of mobilizable lead. We have used the EDTA lead mobilization test for 12 gouty patients with renal impairment. Only 7 of these had experienced occupational exposure to lead. 12 patients with nephropathy caused by chronic glomerulonephritis, without a history of gout or lead exposure, were selected as controls. The urinary excretion of lead after the mobilization test was significantly higher in gouty patients. Only in gouty patients was lead excretion directly correlated with the serum creatinine level. Thus, renal failure did not induce any increase in mobilizable lead. Since it is not infrequent in Italy to observe patients with a progressively declining renal function due to chronic interstitial nephritis and with a previous history of gout, we think the EDTA test will be useful to look for lead storage in these patients.
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PMID:Chronic lead accumulation as a possible cause of renal failure in gouty patients. 309 21

The presence of crystal proven podagra coincident with a 52% decrease in plasma urate after a 3-day course of total parenteral nutrition (TPN) prompted a study of urate excretion in 9 patients with Crohn's disease. By Day 9 in those receiving TPN, plasma urate decreased 58% (p less than 0.001), while fractional urate excretion increased 94% (p less than 0.005). Twenty-four hour urate excretion and serum creatinine were not significantly altered. These findings persisted for the duration of TPN. In 2 patients with ileocolitis, the addition or deletion of either lipid emulsion or multivitamin infusions during TPN had no effect on urate values. Rather, the amino acid load or a specific constituent appears to be the causal factor. These data suggest that hypouricemia due to extensive net urate excretion is common during TPN therapy. Finally, patients with established gout may be at risk for acute gouty attacks during TPN therapy.
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PMID:Altered fractional excretion of uric acid during total parenteral nutrition. 312 76


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