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

Allopurinol is used frequently to treat patients with gout and hyperuricemia. However, adverse effects associated with this agent have been reported occasionally, especially among patients with hyperuricemia complicated with renal diseases. A rise in the blood concentration of oxipurinol, the chief active metabolite of allopurinol, has been noted in patients with renal dysfunctions, pointing to an implication of oxipurinol toxicity. It has been reported that monitoring the serum oxipurinol concentration to maintain in level below 15.2 micrograms/ml (= 100 mumol/l: recommended level) is helpful in avoiding toxicity. At Jikei University Hospital, a survey was conducted on 148 hyperuricemic patients who had been treated with allopurinol at the dosages of 50, 100, 200 and 300 mg daily or 100 mg on alternate days for more than one month. Because oxipurinol is an uricosuric substance, the steady-state serum oxipurinol concentration was determined by HPLC; and creatinine clearance (CCr) was calculated for each patient. 1. In the group composed of patients with normal kidney function (CCr > or = 80 ml/min), increase in the dosage of allopurinol was associated with a linear increase in the serum concentration of oxipurinol. 2. Among the patients with varying renal function who were receiving 100 mg of allopurinol daily, the oxipurinol level increased logarithmically as the creatinine clearance decreased. In some of the patients with renal insufficiency (CCr < 30 ml/min), daily administration of 100 mg of allopurinol resulted in a serum concentration of oxipurinol over 15.2 micrograms/ml. 3. For patients with renal insufficiency (CCr < 30 ml/min), administration of allopurinol at the dosage of 50 mg/day is considered adequate to avoid the accumulation of serum oxipurinol.
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PMID:[A study of serum oxipurinol concentration and renal function in patients administered allopurinol]. 901 85

Primary gout is characterized by increased plasma and decreased urinary concentrations of hypoxanthine, xanthine and uric acid. To examine whether lead could explain the disturbance of purine metabolism in gout, we determined hypoxanthine, xanthine and uric acid metabolism and 5-day cumulative urinary lead excretion rates after an EDTA (calcium disodium edetate) test in 27 patients with primary gout and reduced creatinine clearance (C(cr)) and in 50 patients with gout and normal C(cr). The results were compared to those obtained in 26 normal subjects matched for age. All gout patients evidenced a marked renal underexcretion of hypoxanthine, xanthine and uric acid relative to their increased plasma levels. Purine metabolism was remarkably similar in both gout groups except for a significantly lower uric acid excretion in patients with reduced C(cr). Blood lead levels and cumulative lead excretion rates were significantly higher in gout patients with renal failure as compared to patients with normal C(cr). Fourteen patients (52%) with renal insufficiency and 6 (12%) with normal C(cr) showed increased lead excretion rates (95% Cl for the difference, 29-51%, p < 0.001). Mobilizable lead was not significantly correlated with serum or urinary purine concentrations. Hypoxanthine, xanthine and uric acid underexcretion was similar in gout patients with increased or normal cumulative lead excretion rates. The prevalence of atheromatosis and arterial hypertension together was significantly higher in gout patients with renal failure than in patients with normal C(cr) (81 vs. 60%, 95% Cl for the difference, 11-31%, p < 0.005). These results indicate that lead is not a significant contributor to the renal underexcretion of purines in gout. An increased mobilizable lead is not by itself evidence that lead is the cause of the renal insufficiency in patients with primary gout. Atheromatous nephropathy and/or nephroangiosclerosis may explain impaired renal function in patients with primary gout.
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PMID:Purine metabolism in patients with gout: the role of lead. 906 56

Environmental and industrial lead exposures continue to pose major public health problems in children and in adults. Acute exposure to high concentrations of lead can result in proximal tubular damage with characteristic histologic features and manifested by glycosuria and aminoaciduria. Chronic occupational exposure to lead, or consumption of illicit alcohol adulterated with lead, has also been linked to a high incidence of renal dysfunction, which is characterized by glomerular and tubulointerstitial changes resulting in chronic renal failure, hypertension, hyperuricemia, and gout. A high incidence of nephropathy was reported during the early part of this century from Queensland, Australia, in persons with a history of childhood lead poisoning. No such sequela has been found in studies of three cohorts of lead-poisoned children from the United States. Studies in individuals with low-level lead exposure have shown a correlation between blood lead levels and serum creatinine or creatinine clearance. Chronic low-level exposure to lead is also associated with increased urinary excretion of low molecular weight proteins and lysosomal enzymes. The relationship between renal dysfunction detected by these sensitive tests and the future development of chronic renal disease remains uncertain. Epidemiologic studies have shown an association between blood lead levels and blood pressure, and hypertension is a cardinal feature of lead nephropathy. Evidence for increased body lead burden is a prerequisite for the diagnosis of lead nephropathy. Blood lead levels are a poor indicator of body lead burden and reflect recent exposure. The EDTA lead mobilization test has been used extensively in the past to assess body lead burden. It is now replaced by the less invasive in vivo X-ray fluorescence for determination of bone lead content.
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PMID:Renal effects of environmental and occupational lead exposure. 930 Sep 27

We evaluated the effect of accumulation of intraabdominal visceral fat on the metabolism of uric acid in 50 healthy male subjects to elucidate any relationship between such obesity and hyperuricemia. The area of abdominal fat (visceral fat and subcutaneous fat) was measured at the level of the umbilicus by abdominal computed tomographic scanning. Serum and urinary concentrations of uric acid and creatinine were determined with an autoanalyzer. Uric acid clearance and the ratio of urinary uric acid to creatinine excreted in urine were calculated. Univariate and multivariate analyses were used to evaluate the relationship between uric acid metabolism and body fat. The size of the area of visceral fat was significantly correlated with the serum concentration of uric acid (r = .37, P < .01), uric acid clearance (r = -.34, P < .05), and the urinary uric acid to creatinine ratio (r = .65, P < .0001). The size of the area of subcutaneous fat was significantly correlated only with the urinary uric acid to creatinine ratio (r = .38, P < .01). Multivariate analyses, including body mass index (BMI), showed that the size of the visceral fat area was the strongest contributor to an elevated serum concentration of uric acid, a decrease in uric acid clearance, and an increase in the urinary uric acid to creatinine ratio. These results suggest that accumulation of visceral fat may have a greater adverse effect on the metabolism of uric acid than BMI or accumulation of subcutaneous fat. Clearly, patients with hyperuricemia should lose weight to reduce excessive visceral fat stores, to help avoid attacks of gout.
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PMID:Close correlation between visceral fat accumulation and uric acid metabolism in healthy men. 932

A 59-year-old man with chronic obstructive pulmonary disease (COPD), atrial fibrillation, and gout developed acute dyspnea, cough, and diffuse muscle aches and pains. He had commenced colchicine (0.6 mg b.i.d. p.o.), for the first time, one month earlier for recurrent gout attacks. Clinical examination revealed atrial fibrillation, an exacerbation of his pulmonary disease, tender muscles, especially calves, and diffuse muscle weakness. Laboratory results included creatinine phosphokinase 6961 U/l (1% MB), microscopic hematuria, myoglobinuria, elevated creatinine 1.6 mg/dl, and blood urea nitrogen 17 mg/dl. COPD and atrial fibrillation were treated and colchicine was discontinued. The patient made a full recovery. This 2nd reported case of colchicine induced rhabdomyolysis is the first reported in the treatment of gout.
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PMID:Colchicine induced rhabdomyolysis. 933 Sep 53

We identified 174 cases of chronic severe renal failure (blood creatinine > 650 mumol/l) and/or blood urea > 35 mmol/l) in a retrospective study of patients admitted to hospital between January 1989 and June 1996. Of these patients, 110 were men and 64 were women. The mean age was 36 +/- 15 years. Fifty three patients had a history of hypertension before admission, 3 patients had diabetes and 3 had gout. The most frequent clinical signs were dyspnea (55.2% of all patients), fatigue (78.2%), vomiting (63.2%) and edema (66.1%). The prevalence of hypertension was 64.9%. Glomerulonephritis was found in 42.5% of patients, chronic interstitial nephritis in 16.1%, polycystic kidney disease in 2 cases, congenital renal hypoplasia in 4 cases and unclassified kidney disease in 14.4% of cases. End-stage renal failure was complicated by heart failure in 40.2% of patients, pericarditis in 31.6%, hemorrhage of the gastrointestinal tract in 15% and infections in 22.4%. 47.7% of the patients died following admission.
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PMID:[Epidemiology of severe chronic renal insufficiency in Burkina Faso]. 950 95

To determine the prevalence of hyperuricaemia, gout and gout-related factors in Central Taiwan Atayal aborigines, 342 subjects over 18 yr old were interviewed and examined. A questionnaire was designed to screen for signs and symptoms of gout and gout-related risk factors. Serum uric acid, triglyceride and creatinine were measured in all subjects. The prevalence of hyperuricaemia was 41.4% and that of gout 11.7% in aborigines. The uric acid level was 7.9+/-1.7 mg/dl in males and 5.7+/-1.5 in females, and differed significantly under age 70 yr (P < 0.001). Significantly increased triglyceride, creatinine and alcoholism was found in gouty patients compared with non-gouty patients. In 40 cases with gout, 54% had tophi and 35% of their first-degree relatives had gout. The high prevalence of hyperuricaemia and gout in Taiwan Atayal aborigines, a significant family predisposition, increased creatinine level and alcoholism suggest multiple factors affecting the hyperuricaemia.
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PMID:The epidemiology of hyperuricaemia and gout in Taiwan aborigines. 956 64

The risk of contrast-associated nephrotoxicity (CAN) is increased in the presence of preexisting renal disease. Although routine determination of serum creatinine (Cr) prior to imaging studies is the traditional method of assessing renal function, it is a costly and time-consuming practice. The purpose of this study was to investigate whether a patient survey could identify patients with a high likelihood of having normal Cr values and who, therefore, did not require serum testing. A survey was administered to 673 consecutive adult patients who were scheduled for contrast-enhanced computed tomography. Survey questions were designed to elicit a history of renal disorders as well as additional risk factors for CAN. Each patient had a Cr level determined within 48 hours prior to the injection of iodinated contrast media. Cr levels were assessed in the patients who gave negative responses to all survey questions. The degree to which positive responses to each survey question predicted elevated Cr levels was determined using the odds ratio (OR). Among the 673 respondents, 577 (85%) had normal Cr values (< or =1.3 mg/dL for women and < or =1.4 mg/dL for men). Completely negative responses to the questionnaire occurred in 191 (28%) of 673 of respondents, and 176 (92%) of these 191 had normal Cr values. A Cr cutoff value of 1.7 mg/dL is used in our department, i.e., patients with Cr values >1.7 mg/dL usually do not receive iodinated contrast media. Using this Cr cutoff value, 189 (99%) of 191 patients with negative responses had Cr values less than or equal to the cutoff value. The survey questions most strongly associated with elevated Cr values pertained to preexisting renal disease (OR 13.6), proteinuria (OR 8.7), prior kidney surgery (OR 8.1), hypertension (OR 5.4), gout (OR 4.6), and diabetes (OR 3.2). If the survey had been limited to these six questions, completely negative responses would have occurred in 450 (67%) of 673, 424 (94%) of these 450 would have normal Cr values, and 446 (99%) of 450 would have had Cr values at or below the 1.7 mg/dL cutoff for iodinated contrast. A completely negative response to a simple (six question) patient survey prior to iodinated contrast administration can identify a significant fraction of patients with normal Cr levels. Use of this survey could reduce by 67% the number of patients undergoing routine Cr determinations prior to imaging studies. This could reduce costs, decrease delays, and increase patient satisfaction associated with imaging studies.
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PMID:Determination of serum creatinine prior to iodinated contrast media: is it necessary in all patients? 962 18

Gout in the elderly differs from classical gout found in middle-aged men in several respects: it has a more equal gender distribution, frequent polyarticular presentation with involvement of the joints of the upper extremities, fewer acute gouty episodes, a more indolent chronic clinical course, and an increased incidence of tophi. Long term diuretic use in patients with hypertension or congestive cardiac failure, renal insufficiency, prophylactic low dose aspirin (acetylsalicylic acid), and alcohol (ethanol) abuse (particularly by men) are factors associated with the development of hyperuricaemia and gout in the elderly. Extreme caution is necessary when prescribing nonsteroidal anti-inflammatory drugs (NSAIDs) for the treatment of acute gouty arthritis in the elderly. NSAIDs with short plasma half-life (such as diclofenac and ketoprofen) are preferred, but these drugs are not recommended in patients with peptic ulcer disease, renal failure, uncontrolled hypertension or cardiac failure. Colchicine is poorly tolerated in the elderly and is best avoided. Intra-articular and systemic corticosteroids are increasingly being used for treating acute gouty flares in aged patients with medical disorders contraindicating NSAID therapy. Urate-lowering drugs are indicated for the treatment of hyperuricaemia and chronic gouty arthritis. Uricosuric drugs are poorly tolerated and the frequent presence of renal impairment in the elderly renders these drugs ineffective. Allopurinol is the urate-lowering drug of choice, but its use in the aged is associated with an increased incidence of both cutaneous and severe hypersensitivity reactions. To minimise this risk, allopurinol dose must be kept low. A starting dose of allopurinal 50 to 100mg on alternate days, to a maximum daily dose of about 100 to 300mg, based upon the patient's creatinine clearance and serum urate level, is recommended. Asymptomatic hyperuricaemia is not an indication for long term urate-lowering therapy; the risks of drug toxicity often outweigh any benefit.
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PMID:Gout in the elderly. Clinical presentation and treatment. 978 27

An epidemiologic study to determine lipids and biochemical traits was performed in central Taiwan aborigines with and without gout and in the local Han Chinese. The lipid profile included measurement of serum triglyceride, cholesterol, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), apolipoprotein A-I (apoA-I), and apoB. The results showed no significant difference for body mass index (BMI) and cholesterol between the three groups. Greater alcohol consumption was found in aborigines with gout compared with the other two groups. With univariate analysis, serum triglyceride, uric acid, creatinine, LDL-C, and apoB were significantly higher in aborigines with gout versus aborigines without gout or Han people (P<.001). By contrast, HDL-C and apoA-I were significantly lower in aborigines with gout (P<.001 or .01). However, with multivariate analysis, only serum triglyceride, uric acid, and apoB-1 were significantly different between aborigines with versus without gout. In conclusion, the apparent lipid abnormalities, particularly triglyceride and apoB, in Taiwan aborigines with gout are unlikely secondary to obesity. Instead, excessive alcohol intake or genetic factors may play a role in inducing hyperlipidemia in gout.
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PMID:Lipid abnormalities in Taiwan aborigines with gout. 992 Jan 57


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