Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypertriglyceridemia has been reported frequently in patients with hyperuricemia and gout. The current studies have evaluated this relationship. To examine whether hypertriglyceridemia leads to hyperuricemia, IV intralipid was given to three gouty patients. Triglycerides increased from 169 to 700 mg/dl for three hours but caused no change in serum urate level or urine uric acid and oxypurine excretion. We next examined whether high carbohydrate intake increases serum urate and triglyceride levels. Four obese patients were placed on a 2000 kcal/d sucrose diet for seven days. The serum urate increased from 6.3 +/- 1.7 to 7.9 +/- 2.0 mg/dL. The percent uric acid clearance to creatinine clearance decreased from 5.9 +/- 1.3 to the lowest mean value of 3.7 +/- 1.2, while serum triglycerides increased from 106 +/- 33 to 252 +/- 57 mg/dL and blood lactate from 607 +/- 227 to 1167 +/- 381 mumol/L. A 3000 kcal/d glucose diet in four other obese subjects produced no change in serum urate levels but increased lactate and triglyceride levels. During an isocaloric sucrose diet in two normal men, the serum urate level increased from 5.3 and 4.0 to peak values of 9.5 and 7.4 mg/dL. The percent uric acid to creatinine clearance decreased from 5.6 and 6.6 to 2.9 and 3.3. The uric acid turnover did not increase. In three gouty patients the mean serum urate increased from 8.5 +/- 1.5 to 10.6 +/- 1.4 mg/dL following an isocaloric sucrose diet. The urine uric acid excretion increased from 0.30 and 0.25 to 0.37 and 0.38 mg/mg creatinine in two patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hyperuricemia and hypertriglyceridemia: metabolic basis for the association. 402 6

The antihypertensive effect and metabolic side effects of bendroflumethiazide have been compared with those of propranolol in two randomly selected groups, of 53 previously untreated middle-aged men during 6 years' treatment for mild to moderately severe essential hypertension. The blood pressure-reduction was the same in the two groups. During the follow-up 1 man in the bendroflumethiazide group and 3 in the propranolol group died while 2, 1 on each treatment, became diabetic. None had gout but serum urate increased in both groups. Glucose tolerance improved significantly in both groups during the first year and this improvement was sustained for the follow-up period. Serum potassium did not differ in the two groups during the first 5 years but during the sixth year it decreased in the diuretic group. Total potassium was, however, unchanged in both groups. These results indicate that the frequency of metabolic side effects during diuretic treatment of mild to moderately severe essential hypertension is low and has been grossly exaggerated. Since the antihypertensive effect and side effects were equal with both drugs, and since the diuretics are cheaper, they should be the drug of first choice in this type of hypertension.
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PMID:beta-blockers or diuretics in hypertension? A six year follow-up of blood pressure and metabolic side effects. 611 Sep 54

1. GSD-I is described in a child with partial deficiency of hepatic glucose-6-phosphatase. 2. Growth retardation and hepatosplenomegaly were major clinical features. 3. Hyperlipidaemia, lactic acidaemia, hyperuricaemia and reduced uric acid clearance were major biochemical findings. 4. Although the glucose response to glucagon and galactose was impaired, there was a striking absence of hypoglycaemia which may be attributable to residual catalytic activity of the enzyme. 5. Preliminary studies of the crude liver enzyme showed it to have a normal pH inactivation profile and apparent Km with a reduced Vmax. 6. No evidence of increased PP-ribose-P availability in fresh liver tissue was detected. 7. Continuous glucose feeding resulted in accelerated growth without complete correction of lactic acidosis or hyperuricaemia. 8. GSD-I with partial deficiency of hepatic glucose-6-phosphatase should be considered in patients with gout or hyperuricaemia associated with hypertriglyceridaemia and lactic acidaemia even in the absence of hypoglycaemia.
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PMID:Clinical and enzymological studies in a child with type I glycogen storage disease associated with partial deficiency of hepatic glucose-6-phosphatase. 615 47

The effect of weight loss produced by gastric exclusion on the metabolism of previously morbidly obese persons was examined. A standardized gastric exclusion procedure was performed in 150 morbidly obese patients during a 6 year period. These patients were followed for from 6 to 60 months (mean 27.8 months). The mean excess weight loss was 75 percent and was maintained from 2 to 5 years. A small but significant decrease was noted during the first 3 to 6 postoperative months in the parameters of protein metabolism examined. Although this may reflect mild depletion in protein stores, of greater importance was the demonstration that these parameters spontaneously corrected themselves by 12 months. Mild abnormalities in serum electrolyte concentrations were noted in the postoperative period. They appeared to be related to dehydration, were not clinically significant, and also resolved spontaneously. Clinically significant abnormalities in divalent ions were absent. Significant and sustained reductions in blood pressure, fasting glucose concentration, serum triglyceride values, and uric acid and hepatic enzyme concentrations were demonstrated in the entire population. A small and non-sustained decrease in cholesterol was seen. Hypertension was eliminated in 96 percent of the affected subpopulation, diabetes in 100 percent, gout in 100 percent, hyperlipidemia in 92 percent, and improved hepatic function was found in 95 percent. These changes should reduce the overall morbidity and mortality of the patient population in the future.
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PMID:Prospective metabolic evaluation of 150 consecutive patients who underwent gastric exclusion. 671 48

An appreciation of the physiology of fasting is essential to the understanding of therapeutic dietary interventions and the effect of food deprivation in various diseases. The practice of prolonged fasting for political or religious purposes is increasing, and a physician is likely to encounter such circumstances. Early in fasting weight loss is rapid, averaging 0.9 kg per day during the first week and slowing to 0.3 kg per day by the third week; early rapid weight loss is primarily due to negative sodium balance. Metabolically, early fasting is characterized by a high rate of gluconeogenesis with amino acids as the primary substrates. As fasting continues, progressive ketosis develops due to the mobilization and oxidation of fatty acids. As ketone levels rise they replace glucose as the primary energy source in the central nervous system, thereby decreasing the need for gluconeogenesis and sparing protein catabolism. Several hormonal changes occur during fasting, including a fall in insulin and T(3) levels and a rise in glucagon and reverse T(3) levels. Most studies of fasting have used obese persons and results may not always apply to lean persons. Medical complications seen in fasting include gout and urate nephrolithiasis, postural hypotension and cardiac arrhythmias.
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PMID:Fasting: the history, pathophysiology and complications. 675 55

Thiazide diuretics and loop-diuretics, often used for treatment of hypertension, interfere with various metabolic reactions: An increase of uric acid in plasma is a regular finding, but gout will not be caused, an elevation of plasma lipoproteins has been observed but did not proceed to pathological values, in a number of patients blood glucose has been raised but without producing diabetes mellitus. In general, these metabolic interference are of minor pathological significance. Special treatment for these side-effects are needed in a few cases only. The indicated use of thiazide diuretics should not be disregarded because of their effects on regulatory mechanisms of metabolism.
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PMID:[Metabolic effects of diuretics (author's transl)]. 679 54

Uric acid metabolism was investigated in 69 insulin-treated male diabetic outpatients and in 23 healthy male subjects, because of a reported coincidence between diabetes and gout. All subjects had normal serum creatinine concentrations and none received diuretic treatments. Compared with normal, the diabetics had significantly lower mean serum uric acid concentrations (0.34 +/- 0.08 (SD) mmol/l versus 0.23 +/- 0.06 mmol/l, p less than 0.001). 17% of the diabetic patients had serum concentrations below the normal mean--2 SD. In contrast, the diabetic patients had a 42% increase in renal uric acid excretion rate (p less than 0.01), and an 83% increase in the ratio of uric acid clearance/creatinine clearance (p less than 0.001). These indices of renal uric acid excretion were both positively correlated to fasting blood glucose levels (r=0.57, p less than 0.001, and r=0.50, p less than 0.001, respectively), to the degree of glycosuria (r=0.73, p less than 0.001, and r=0.63, p less than 0.001, respectively), and to the magnitude of water diuresis (r=0.60, p less than 0.001, and r=0.39, p less than 0.01, respectively). The hypouricaemia observed in these insulin-dependent diabetic male subjects may probably be caused by the increased renal excretion of uric acid in the presence of hyperglycaemia. The study gave no evidence of increased serum uric acid concentrations in insulin-dependent diabetics. It is therefore likely that any coincidence between gout and diabetes derives from other coexisting serum uric acid raising factors.
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PMID:Renal hypouricaemia in insulin treated diabetes mellitus. 704 28

Turkey poults were fed diets containing oosporein at concentrations of 0, 500, 1,000, and 1,500 micrograms/g from hatching until three weeks of age. Low feed consumption resulted in poor growth rates at every dietary level of oosporein; however, a dose-related increase in water consumption was observed. The most significant effect of dietary oosporein was severe visceral and articular gout, with death ensuing in 24 and 52% of the poults at the 1,000 and 1,500 micrograms/g levels, respectively. Gout and mortality were absent at 0 and 500 micrograms/g. In addition to tissue urate deposition, necropsies revealed dehydration, swollen pale kidneys, hemorrhagic proventriculitis with mucosal necrosis, gizzard enlargement and lining discoloration, an increase in gall bladder size, and focal hepatic necrosis. The relative weights of the kidney, liver, proventriculus, gizzard, and pancreas were increased in a dose-related fashion; spleen and bursa weights were unaffected. Among plasma constituents, uric acid, urea, and the activities of glutamic-oxalacetic transaminase and lactic dehydrogenase were elevated in response to dietary oosporein; albumin, potassium, phosphorus, and calcium were decreased. The toxin had no effect on plasma total protein, sodium, glucose, cholesterol, triglycerides, alkaline phosphatase, or creatine phosphokinase. These data substantiate the original classification of oosporein as a nephrotoxin and etiologic agent of gout in avian species.
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PMID:Oosporein-toxicosis in the turkey poult. 709 45

We reviewed 11 patients with rheumatoid subcutaneous bursitis involving the olecranon bursa in 10 and an adventitious bursa in 1. All patients had a positive latex fixation test for rheumatoid factors. The mean bursal fluid white blood count (WBC) was 2,924/mm3 compared with a mean joint fluid WBC of 15,608/mm3 in 32 consecutive cases of classical or definite rheumatoid arthritis (p less than 0.001). Bursal fluid glucose and complement concentrations were low. Cholesterol crystals were present in 5 of 6 nodular bursae, and in none of the 5 non-nodular bursae (p less than 0.05). Two patients had acicular cholesterol crystals that had previously led to an erroneous diagnosis of gout.
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PMID:Rheumatoid subcutaneous bursitis. 732 71

In a series of four experiments, diets containing oosporein at graded concentrations from 0 to 600 microgram/g were fed to male broiler chicks from hatching to 3 weeks of age. At dietary toxin levels of 100 microgram/g and below, no detrimental effects were observed. Dietary oosporein concentrations of 200 microgram/g and above elicited dose-related mortality resulting from severe visceral and articular gout. Three-week cumulative mortality percentages were 0, 13, 30, 57, and 95% for the 0, 200, 300, 400, and 600 microgram/g levels, respectively. Upon necropsy, the prominent lesions observed were massive urate deposits in various tissues, swollen and pale kidneys, dehydration, proventricular enlargement with mucosal necrosis, and a green discoloration of the gizzard lining. The effects on the proventriculus and gizzard occurred at doses as low as 200 microgram/g and were the most sensitive indicators of oosporein-toxicosis. In addition to the proventriculus, the relative weights of the kidney and liver were significantly increased in a dose-related fashion. A significant reduction in 3-week body weight at 400 microgram/g apparently resulted from the lower feed consumption concomitantly observed at this level of dietary toxin. Oosporein also caused an increase in water consumption at 400 and 600 microgram/g. Blood analyses indicated no toxin-related effect on plasma glucose, plasma protein, packed red blood cell volume, hemoglobin, and prothrombin times. The plasma concentration of uric acid was significantly elevated at 400 microgram/g. These data and mechanistic considerations suggest that oosporein should be classified as a nephrotoxin in the broiler chicken.
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PMID:Avian gout caused by oosporein, a mycotoxin produced by Caetomium trilaterale. 732 19


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