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

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

A study of the clinical profile of gout-diagnosed patients was undertaken within general practice in Great Britain. At the time of the first attack of acute gouty arthritis, the mean age was 52.3 years and 15.6% of the total 1077 patients were female. Males had an earlier clinical onset than females and the average frequency of attacks of acute gouty arthritis was 0.91 per patient year. Ten per cent of the cases were believed to be secondary gout, with diuretic therapy the most frequent cause. The sample showed a highly significant association between gout and the higher social classes, a family history among blood relatives in 23% of cases, tophi were noted in 4.6% of cases where sought and 38.2% of cases were 10% or more overweight and significantly heavier than a non-gouty population. The great toe joint was most frequently involved, both in the first episode and in all acute episodes combined. The most frequently occurring associated chronic condition was hypertension which was present in 27.8% of cases. Renal stones occurred in 6.1% and renal impairment in 2.2%. Only 20.4% of the patients were referred to hospital, with the younger being referred more frequently than the older. Those with joint involvement other than the great toe had a greater chance of being referred, as did those who also had angina pectoris, myocardial infarction and hypertension. Allopurinol appeared to be the drug of choice for long-term control therapy and phenylbutazone for the acute attack.
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PMID:The gout patient in general practice. 73 15

1. Erythrocyte adenosine deaminase (EC 3.5.4.4) and purine nucleoside (inosine) phosphorylase (EC 2.4.1.1) were measured in 33 healthy controls and 43 primary gouty subjects. Adenosine deaminase activity in controls and gouty subjects was 0.373 plus or minus 0.108 and 0.457 plus or minus 0.140 A unit per 5-10-3 ml packed red cells per h, respectively. The difference was statistically significant (P less than 0.01). Mean adenosine deaminase: inosine phosphorylase (X10) in primary gout was also significantly higher than in controls (P less than 0.05). Inosine phosphorylase activities in the two groups were not significantly different. 2. When gouty patients were divided into two groups according to weight, normal weight gouty subjects had a higher adenosine deaminase activity and an increased ration of adenosine deaminase to inosine phosphorylase when compared with overweight patients (P less than 0.10). In two control groups divided according to the percentage overweight, such differences were not found. In the case of two gouty groups divided according to the existence of gouty heredity, tophi or renal impairment, adenosine deaminase and inosine phosphorylase activity in the two groups were not significantly different. The possible biochemical role of adenosine deaminase activity in primary gout is discussed.
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PMID:Erythrocyte adenosine deaminase and purine nucleoside phosphorylase activity in gout. 111 66

Our data demonstrate that adequate control of uric acid production and serum acid concentration in primary gout arrests further deterioration of renal function and in some instances permits subsequent improvement in renal hemodynamic function even when renal impairment is clearly established. In considering the nature of the lesions of urate nephropathy, our study suggests that control of serum uric acid with drug therapy before renal involvement is apparent might prevent or significantly delay the morbidity and mortality of this complication of primary gout.
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PMID:The influence of allopurinol on renal function in gout. 120 Nov 33

Chronic lead nephropathy has recently been rediscovered. Its usual manifestations are hypertension, gout and renal impairment. Retrospective epidemiological data suggest that prolonged exposure to lead increases the risk of hypertension and nephropathy. An increase in EDTA-induced urinary lead concentration (above 600 micrograms/72 hours), perfectly representative of lead concentration in bone, has been found with a 5 to 12 percent prevalence in chronic renal impairment irrespective of its cause. The origin of lead impregnation and its influence on the course of the renal disease have not yet been elucidated.
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PMID:[Chronic lead nephropathy. Epidemiology and diagnosis]. 153 33

From 120 patients attending a referral gout clinic, 12 patients were found to have primary renal disease at the time of, or prior to, their first attack of acute gouty arthritis. This number excluded those with chronic lead nephropathy, polycystic kidneys or who were receiving diuretics. The nature of the renal disease was usually of the tubulointerstitial variety rather than of glomerular origin. The renal clearance of urate per unit of glomerular filtration rate, which usually increases with renal disease, was generally reduced, suggesting impairment of renal excretion of urate. Nine of the patients were female (four premenopausal) and only three were males. The degree of renal impairment was only mild to moderate. Other common associations with gout, such as obesity, hypertension and regular alcohol consumption, were not prominent. The intrinsic renal disease in these patients was considered to be the major contributor to their development of hyperuricaemia and gout.
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PMID:Gout due to renal disease. 173 Jan 9

Between December 15, 1988 and November 30, 1990, the application of Rome and New York criteria enabled the diagnosis of 60 cases of gout among patients with arthritis or hyperuricemia seen as out-patients or hospitalised in the Department of Rheumatology of the Brazzavile T.H.G. There were 57 men and 3 women, with a mean age of 51. Gout is the primary form of inflammatory arthropathy in adults in the Congo. Affecting all socio-professional groups, it is diversely associated with obesity, alcoholism, hypertension and diabetes. Initial involvement affects the big toe. Oligo and polyarticular forms predominate because of the absence or delay in specific treatment. This series included 30 per cent of cases of chronic gout. Evidence of renal impairment was found in one third of patients. However, urate lithiasis was absent. Tophi were found preferentially over the elbows. Sickle cell disease was responsible for one case of tophaceous gout. In contrast with the results of studies undertaken before the 1980s, gout is seen to be a common condition in equatorial Africa.
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PMID:[Epidemiological and clinical aspects of gout in equatorial Africa. Apropos of 60 cases followed in the Department of Rheumatology of the Teaching Hospital Center in Brazzaville]. 178 Jun 67

Hyperuricemic nephropathy can progress to the permanent renal damage even in infancy in partial hypoxanthine-guanine phosphoribosyltransferase (HPRT) deficiency. We have encountered two unrelated patients with partial HPRT deficiency, and found that early detection of the disease and long-term management for hyperuricemia were necessary to prevent renal impairment. The HPRT gene is situated in the q26-27 region of the long arm of the X-chromosome, and females with mutant HPRT alleles are heterozygous for the disease, and they develop gout after menopause. We undertook the investigation of carriers in the two patients' families, using BamHI restriction fragment length polymorphisms and oligonucleotide probes that recognized the specific mutations within the HPRT gene. We also demonstrated that the allele frequencies of BamHI restriction fragment length polymorphisms in 62 Japanese females were 0.36 for the 22-kb/25-kb allele, 0.41 for the 12-kb/25-kb allele, and 0.23 for the 22-kb/18-kb allele, resulting in a heterozygous state in 66% of females.
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PMID:Carrier detection of partial hypoxanthine-guanine phosphoribosyltransferase deficiency by analysis with BamHI restriction fragment length polymorphisms and oligonucleotide probes. 197 37

The drug treatment of mild hypertension has been shown to afford protection against fatal and nonfatal strokes, congestive heart failure, progression to more severe levels of hypertension, and all-cause mortality, but not against the complications of coronary artery disease. The lack of benefit against coronary artery disease may result from failure to reduce other risk factors or because the drugs employed increased coronary risk. It can be taken as axiomatic that effective preventive antihypertensive therapy is more likely with drugs with mechanisms and sites of action that are focused on the underlying pathophysiology than with drugs that lower blood pressure by means unrelated to the hypertensive process. Adrenergic predominance plays a major role in the initiation and maintenance of essential hypertension and, consequently, the alpha-adrenergic receptor inhibitors were among the first substances to receive serious consideration as antihypertensive agents. However, since these drugs are nonselective, feedback control of transmitter norepinephrine was lost and, consequently, the clinical expectations of the early alpha-adrenergic receptor inhibitors in the treatment of high blood pressure were not fulfilled. The discovery of selective postjunctional alpha 1-adrenergic-receptor inhibitors, such as prazosin and doxazosin, which preserve feedback control of transmitter norepinephrine release, was the crucially important step in the development of specific drugs to combat the hyperactivity of adrenergic vasoconstrictor nerves in hypertension. These drugs have been shown to normalize hemodynamics in hypertensive patients. They lower blood pressure through a reduction in peripheral resistance at rest and during exercise, independent of changes in heart rate and blood pressure, with minimal reflex activation or tolerance development. Alpha 1-adrenergic-receptor inhibitors, such as prazosin and doxazosin, represent an attractive choice for initial therapy in all grades of hypertension and are especially appropriate in hypertensive patients with congestive heart failure, asthma and chronic obstructive airways disease, renal impairment, diabetes mellitus, hyperlipidemia, benign prostatic hyperplasia, or gout, and in those involved in vigorous work, sports, or exercise. There are no known contraindications to these drugs, except in patients who are sensitive to quinazolines.
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PMID:Pharmacologic basis for the use of doxazosin in the treatment of essential hypertension. 256 23

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


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