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

A 25-year-old white man with gout and nephropathy and with a previous reaction to allopurinol was given a trial dose of oxypurinol. He developed malaise, a generalized erythematous reaction with edema, pruritus, and emesis; this was clinically identical to the reaction he experienced with allopurinol. When the patient's lymphocytes were exposed in vitro to oxypurinol and allopurinol, increased DNA synthesis was observed, suggesting an immunologic basis for the reaction. This patient indicates that clinical cross reactivity to allopurinol and oxypurinol does occur and may be of an immunologic basis. There is a need for additional xanthine oxidase inhibitors for such patients.
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PMID:Allergic reaction to allopurinol with cross-reactivity to oxypurinol. 13 55

Patients with hepatic glucose-6-phosphatase deficiency usually have a striking clinical syndrome during childhood and are readily diagnosed by the pediatrician. An adult patient had childhood manifestations of glucose-6-phosphatase deficiency that were mild and unrecognized; symptoms of tophaceous gout, urate nephropathy and characteristic blood chemical studies suggested the diagnosis at age 39. Subsequent epinephrine and galactose tolerance tests were characteristic of hepatic glucose-6-phosphatase deficiency and direct assay of hepatic glucose-6-phosphatase confirmed a partial deficiency of the enzyme. The case emphasized that patients with this deficiency may escape diagnosis during childhood and that internists should consider the diagnosis in adolescents or young adults with acute gouty arthritis or tophaceous gout.
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PMID:Partial deficiency of hepatic glucose-6-phosphatase in an adult patient. 16 24

Renal hemodynamics as measured by inulin clearance (Cinulin) and para-aminohippurate clearance (CPAH) was evaluated in 149 patients with primary gout over intervals of two to 22 years. In over 30 per cent of the patients plasma urate was greater than 10 mg/dl and urinary uric acid greater than 800 mg/min. A linear trend in decreasing frequency of hyperuricemia and excessive uricosuria is significantly related to the patient's age at the onset of gout. Group I consisted of 84 patients with uncomplicated gout in both clearance studies. Cinulin and CPAH were somewhat lower in patients larger than or equal to 50 years of age with longer duration of gout. Further reduction in clearances was minimal at the second clearance study in intervals of approximately 10 years. Group II included 27 patients who had no associated disease at the time of the first clearance study but in whom associated disease had developed by the time of the second clearance study. A striking reduction in Cinulin and CPAH was noted, especially in those 50 years old or above. There were 38 patients in group III with associated diseases at the time of both clearance studies. They had lower Cinulin and CPAH at the time of the first study, particularly the older patients. Further reduction during the second study was less striking than that in group II. Analyses of variance suggest that various coexisting vascular diseases with associated nephropathy have the most significant impact on the status of renal function in gout, with aging the second most important and duration of gout, the third.
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PMID:Renal function in gout. V. Factors influencing the renal hemodynamics. 50 87

After a short survey of the purine metabolism, excretion of uric acid, theories of gout and urate nephropathy methodical references are given for the estimation of excretion of uric acid, a normal region on test persons was established and compared with other authors. The quantities of excretion and concentrations of uric acid from the 24 hours urine found on patients with asymptomatic hyperuricemia and manifest gout are the basis of the discussion of the diagnostic and therapeutic value of these examinations. In patients with gout and asymptomatic hyperuricemia the excretions of uric acid are a little higher than in healthy persons. A treatment with uricosuric remedies might not reduce the factor of risk hyperuricemia, since this does not lead to a prevention of the gout nephrophathy, on the contrary it furthers it.
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PMID:[Diagnostic value of renal urate excretion]. 64 53

The management of asymptomatic hyperuricemia is controversial. Reported benefits from treatment prevention of acute gouty arthritis, chronic tophaceous gout, urolithiasis, or gouty nephropathy. A review of experimental and clinical data suggests that the risks of asymptomatic hyperuricemia are small or unknown and the efficacy of long-term treatment in preventing gout or renal disease is unproved. The costs and risks of prolonged drug administration and practical considerations such as patient compliance mitigate against long-term therapy in asymptomatic persons. We offer some recommendations for an expectant approach to the management of asymptomatic hyperuricemia.
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PMID:Asymptomatic hyperuricemia: the case for conservative management. 64 60

Gout is rarely noted as a clinical problem in secondary polycythemia-- even if profound polycythemia exists, as in cyanotic congenital heart disease. A retrospective study of 81 patients with congenital heart disease was done to assess the incidence of hyperuricemia. Twenty of 46 patients with cyanotic congenital heart disease had serum levels of uric acid greater than 8 mg/dl. Thirteen of 16 (81%) cyanotic male patients more than 15 years old had serum levels greater than 8 mg/dl. For cyanotic patients, serum levels of uric acid were related directly to the degree of polycythemia (r = .44; P less than .02). Impaired renal function or drug therapy did not seem to account for the hyperuricemia. Because levels of uric acid greater than 10 mg/dl probably are nephropathic, many of these patients may be incurring subclinical uric acid nephropathy.
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PMID:Hyperuricemia in congenital heart disease. 68 9

We studied the prevalence and the risk factor among the patients of gout in Mexico. Research was conducted in the National Institute of Cardiology and in our private practice. Prevalence of hiperuricemia and gout in the Institute of Cardiology was of 1% (970 out of nearly 100,000 patients). We divided those cases of two subgroups: Reumatology patients (333) and Cardiovascular patients (529). In the first group primary gout was (96.3), and (50.32% in the second. Risk factor was quite different too: nephropathy 9.9%, lithiasis 9.3%, pyelonephritis 2.7%, cardioangiosclerosis 12.9%, aortosclerosis 6.6%, coronary insufficiency 6.3%, myocardial infarction 0.9%, arterial hypertension 24.6% obesity 56.1% and diabetes 9.9% in the Reumatology group; in the Cardiovascular one, nephropathy 14.3%, lithiasis 12.2%, pyelonephritis 7.1%, cardioangiosclerosis 62.7%, aortosclerosis 31.7%, coronary insufficiency 24.9%, myocardial infarction 29%, arterial hypertension 51%, obesity 54.8% and diabetes 20.4%. Among the private practice patients prevalence was of 10.1% (961). In an early age (39 years) in men and a later one for women (53 years). Other characteristics of epidemiology and risk factor are: primary gout 89%, atherosclerosis 5%, coronary disease 4.6%, lithiasis 4.7%, nephropathy 2%, pyelonephritis 1%, obesity 43%, and diabetes 4.6%. In an small group of patients of our private practice we made an exhaustive study of risk factor and the metabolic disorder of lipids. We found the following frequency: 9.3 of nephropathy, 31.2% of lithiasis, 18.7% of pyelonephritis, 68.9% of cardioangiosclerosis, 46.8% de coronary insufficiency, 9.3% of myocardial infarction, 68.7% of arterial hypertension, 68.7% of obesity and 18.7% of diabetes. In the lipid profile we found an increase in triglicerids and prebeta lipoprotein. We have amply discussed the relation between hiperuricemia and pathology considered as a risk factor from the genetic point of view as well as the metabolic and circumstancial aspect. From all that we concluded that risk is multifactorial.
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PMID:[Various epidemiological aspects of hyperuricemia and gout in Mexico: incidence and the cardiovascular risk factor]. 72 44

The results of kidney transplantation in a variety of renal diseases have been analyzed. The diseases causing end-stage kidney failure in recipients were Alport syndrome, amyloidosis, cystinosis, diabetes mellitus, Fabry disease, familial nephritis, gout, medullary cystic disease, oxalosis, and systemic lupus erythematosus. The data indicate that renal transplantation is justifiable and parallels functional results for the more common causes of end-stage renal disease in all but Fabry disease and oxalosis. Although Fabry disease did not recur in any grafted kidney, only three patients have a functioning graft one year after transplantation. From a group of ten patients with oxalosis who received a total of 14 kidneys, only one survives. In no other metabolic disease, except one instance of primary amyloidosis, did the metabolic disease notably affect the transplant as it did in oxalosis.
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PMID:Renal transplantation in congenital and metabolic diseases. A report from the ASC/NIH renal transplant registry. 80 49

Chronic lead nephtropathy, secondary gout (lead-gout) and porphyrinuria may develop after long lasting professional exposure to lead. A printer with giant tophi on his hands and feet excreted a significantly higher amount of lead after infusion of calcium EDTA in comparison with a normal control person. This result indicates an increased mobilization of lead from skeletal deposits. Furthermore, the laboratory findings showed renal insufficency and porphyrinuria up to 1316 mug/l (elevation of total porphyrins with slight or no elevation of delta-amino-levulic acid and porphobilinogene). The clinical triad nephropathy, secondary gout and porphyrinuria seems to be a variant of chronic lead poisoning.
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PMID:[Chronic lead poisoning: Lead gout with giant tophi on the skin, nephrophathy and porphyrinopathy]. 81 45

In a three-phase study that began in 1969, prazosin was shown to be especially suitable for use in treatment of hypertensive patients with gout, renal disease, or borderline diabetes, owing to the sparing of organ systems often harmed by other antihypertensive drugs.
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PMID:Experience with prazosin in a clinical setting. 110 82


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