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

In most patients with primary gout hyperuricaemia results from a renal defect in tubular uric acid secretion. An increased endogenous purine biosynthesis is observed in only 2% of all patients with gout. Secondary hyperuricaemai results either from an increased breakdown of endogenous nucleic acids as in polycythaemia or from a decreased renal excretion of uric acid due to drug treatment, renal insufficiency or metabolic disturbances. Hyperuricaemia may be defined either in statistical terms from epidemiological studies of normal and gouty populations or from physicochemical properties of urate. Monosodium urate and uric acid are soluble in water to the extent of 6.32 mmol/l and 0.39 mmol/l respectively. In human plasma saturation of monosodium urate occurs at a concentration of about 0.42 mmol/l. The solubility of uric acid and urate in urine is more complicated as it is affected by changes in pH and salt concentration. Uricosuric drugs decrease serum uric acid concentration by enhancing the renal excretion of uric acid. Effects and side effects of uricosuric therapy are discussed.
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PMID:Uricosuric therapy and urate solubility in blood and urine. 50 37

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

Ticrynafen is an orally administered diuretic that is similar to the thiazides in its therapeutic actions, but unlike the thiazides, it increases urate excretion and lowers serum uric acid levels. Ticrynafen is useful in the treatment of hypertension and in selected cases of chronic congestive heart failure. At present, it appears to be indicated primarily in patients with these disorders who have a history of gout. Patients who are currently receiving a thiazide should not have their therapy arbitrarily changed to ticrynafen because of asymptomatic hyperuricemia.
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PMID:Evaluation of a new uricosuric diuretic--ticrynafen. 51 60

Although patients with hemolytic hemoglobinopathies characteristically are over-producers of urate, and hyperuricemia is frequently recognized, clinical gout has rarely been reported in such patients. Our evaluation of 2 premenopausal women with gout led to the diagnosis of previously unrecognized hemoglobinopathies (SC disease and CC disease). Investigation of these 2 patients and review of the reported cases of gout in patients with hemoglobin S or C disorders suggest that relatively minor abnormalities of renal function in these patients may lead to early development of significant hyperuricemia. With increasing lifespan of patients with hemolytic hemoglobinopathies and the likelihood of increased occurrence of renal function abnormalities, it is anticipated that gout will more frequently be responsible for joint symptoms in such patients.
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PMID:Secondary gout in hemoglobinopathies: report of two cases and review of the literature. 60 29

The importance of the gout is growing in the GDR as its frequency has been increasing since the sixties. The gout is a disease of metabolism with the following accompanying phenomena: renal lesion in gout, hypertension, cardiac diseases and peripheral arterial diseases. Besides, there are proved relations between hyperuricemia and obesity, hyperlipoproteinemia, diabetes mellitus as well as steatosis hepatis. In describing the nature of the gout the peculiarities of age are stressed. The treatment of the gout depends on the clinical state.
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PMID:[Gout in the age (author's transl)]. 61 69

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

The uptake of 2-C14 urate by erythrocytes was measured in 19 patients with primary hyperuricemia, 6 patients with secondary hyperuricemia, 17 patients with primary gout and 30 controls. The uptake of urate in patients with primary gout was significantly lower than in the controls. In contrast no such difference could be observed in patients with primary and secondary hyperuricemia. The uptake of labeled urate by erythrocytes from gouty patients is especially diminished in the early phase of the uptake kinetics. The possible relevance of this finding for the pathogenesis of urate precipitation in gout is discussed. Further, we consider the application of the tracer urate uptake by erythrocytes as an aid in the early diagnosis of gout.
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PMID:[Uptake of 2-C14 urate by erythrocytes in hyperuricemia and in gout (author's transl)]. 68 21

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 investigated the prognosis of 153 hypertensive patients, whose initial concentration of serum uric acid had been evaluated. One hundred and seventeen subjects could be followed up after 4 years and 16 of them died during the follow-up period. Cerebrovascular disease was seen in 6 subjects, 4 of whom died from the disease. Myocardial infarction and heart failure occurred in 9 and 7 of them died as a result. The frequency of these diseases was greater among the hyperuricemic group and 8 of the 11 who died belonged to this group. Four men were struck by gouty attacks. They were all hyperuricemic and had been proven to have at least one family member with asymptomatic hyperuricemia and/or gout. It is reasonable to regard the presence of hyperuricemia as one of the poor risk factors for vascular diseases. I addition, we must investigate more closely personal and family histories of gout when we see hyperuricemic subjects, regardless of absence of gouty symptoms.
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PMID:Hyperuricemia associated with hypertension. A 4-year follow-up study of hyperuricemic hypertensives. 71 25


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