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)

Molybdenum belongs to a group of essential microelements and occurs in all components of the environment. Major Mo sources for man are foods, especially vegetable, to a lesser extent drinking water. Its metabolism is primarily influenced by interaction with other metals, specifically copper and iron. In the organism it is primarily accumulated in the liver, kidneys, skin and hard tissues. In the blood it binds specifically with alpha-2-macroglobulin, in the erythrocytic membrane with spectrin; it enhances the osmotic resistance of red blood cells. From the organism it is eliminated in the urine, bile and feces. The biochemical importance of molybdenum lies in that it catalyzes the oxidation of xanthine and purine bases and the reduction of nitrates and molecular nitrogen; it is also present in the prosthetic group of flavoprotein enzymes. As shown in both epidemiological and animal studies, molybdenum ions may prevent dental caries. Long-term overexposure to Mo may produce molybdenosis (teart) in cattle. Increased exposures of humans may be primarily encountered in the foundry industry, but the toxic manifestations are invariably nonspecific, similarly as in the case of other heavy metals. Molybdenum-exposed workers may also show elevated uric acid concentrations in their blood, simultaneously with clinical symptoms resembling gout (gout-like syndrome). A similar finding may also occur among individuals living in areas characterized by elevated molybdenum and decreased copper contents in soil. The maximum allowable concentration limits established for soluble and insoluble molybdenum compounds in the workplace air have been accepted in many countries, but their values vary in a wide range. No specific exposure test for molybdenum has been developed as yet.
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PMID:Effects of molybdenum on the organism (a review). 639 29

An outbreak of urolithiasis that doubled the annual mortality rate of chickens in a large flock of table-egg-layers is described. Despite the presence of a large unilateral urolith and/or severe renal atrophy, the layers often maintained active egg production and apparent homeostasis until a small urolith blocked the ureteral flow from the contralateral kidney. This terminal episode appeared to produce acute obstructive renal failure, rapidly developing visceral gout (visceral urate deposition), uremia, and death. The atrophy observed appeared to be acquired and progressive. Histologic features in the kidneys were acute to chronic glomerulonephritis, interstitial nephritis, and pyelonephritis. Epizootiologic and microbiologic studies indicated that a combination of infectious and noninfectious mechanisms may have been involved. Causative roles for calcium-phosphate imbalance, infectious bronchitis (IB), Newcastle disease (ND), and adenovirus or reovirus infections could be neither excluded nor confirmed. Contributory factors may have been spray ND-IB and other vaccinations of 15-week-old ND-IB-susceptible pullets, water deprivation, shipping stress, Mycoplasma synoviae infection, immune complex disease, and mycotoxins.
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PMID:Epizootiology, pathology, and microbiology of an outbreak of urolithiasis in chickens. 672 98

To differentiate between extrarenal and renal causes of hyperuricaemia and gout, clearances of urate and creatinine were monitored for 3 1/2 days in fifty-two individuals (seven with a history of gout) with no gross impairment of renal function (creatinine clearance 52-137 ml/min). Dietary purine intake was kept constant. Monophasic circadian fluctuations of fractional urate excretion (= urate clearance over creatinine clearance) were observed with peak values in the afternoon, about 50% higher than during the night. Circadian fluctuations of urinary flow rate were almost identical. However, enhancement of urinary flow rate due to water diuresis had no effect on urate clearance. Despite wide variation of plasma urate concentrations among different individuals (+/- 30% SD), daily urate excretion varied little (+/- 4% SD) and did not correlate with plasma urate (r = 0.03). Thus extrarenal factors appear not to account for the occurrence of hyperuricaemia in these patients. In contrast, a clearcut negative correlation was apparent between plasma urate concentration and fractional urate clearance (r = 0.72), which could fully account for the variations of plasma urate concentration. To elucidate further the mechanism responsible for antiuricosuria in hyperuricaemic patients, the effects of the uricosuric agents benzbromarone and probenecid were tested. A clearcut correlation was apparent between control fractional urate excretion and uricosuric effect of both benzbromarone and probenecid (r = 0.83 and 0.88, respectively), suggesting that anti-uricosuria was due to defective secretion. In an additional series, the uricosuric effect of probenecid was tested in ten patients with renal insufficiency. In these patients the uricosuric effect was clearly blunted, indicating that urate reabsorption is reduced in renal insufficiency.
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PMID:Renal handling of urate in healthy man in hyperuricaemia and renal insufficiency: circadian fluctuation, effect of water diuresis and of uricosuric agents. 677 56

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

Salt poisoning developed in captive sandhill cranes (Grus canadensis) when sea salt was added to normal drinking water to produce a sodium chloride concentration of 1%. Two of 18 cranes died and 2 were euthanatized when moribund. Muscle weakness, paresis, dyspnea, and depression were observed. Brain and serum sodium, serum uric acid, and plasma osmolality values were abnormally high. Lesions were those of visceral gout, renal tubular necrosis, nephrosis, and skeletal muscle necrosis.
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PMID:Iatrogenic salt poisoning in captive sandhill cranes. 732 5

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

The present review summarizes the current knowledge on the multiple effects of alcohol overconsumption on the kidney function as well as on water, electrolyte and acid-base homeostasis. In contrast to the well known transitory diuretic effects, the overall long-term effect of chronic alcohol overconsumption is water and salt retention with expansion of extracellular volume. Furthermore, depletion of magnesium, phosphate and calcium is also frequently found in alcohol-dependent patients. These electrolyte disturbances may be associated with the alcohol-induced hypoparathyroidism and parathyroid hormone resistance of the skeletal muscle as well as with the decrease of serum osteocalcin. Metabolic acidosis with lower arterial blood pH and plasma bicarbonate concentrations was revealed in alcoholic patients upon admission and a significant correlation between chronic alcohol overconsumption and increased incidence of hyperuricemia and gout attacks was also reported. Alcohol seems to have dual effects on the blood pressure. Increased blood pressure was demonstrated in men above 80 g and in women above 40 g ethanol consumption daily. In contrast, young adults consuming only 10 to 20 g per day had lower blood pressure than the abstinent group indicating a J-curve relationship. This is in line with the lowered risk for coronary heart disease associated with regular consumption of small alcohol amounts. The mechanisms responsible for the association between alcohol overconsumption and postinfectious glomerulonephritis have not been elucidated yet. Finally severe alcohol abuse predisposes to acute renal failure and seems to be associated with the general catabolic effects.
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PMID:Alcohol abuse: potential role in electrolyte disturbances and kidney diseases. 987 14

Molybdenum does not exist naturally in the pure metallic form and of the 5 oxidation states (2-6) the predominant species are Mo(IV) and Mo(VI). Molybdenum rapidly polymerizes to a wide variety of complex polymolybdate compounds in solution. The vast majority of molybdenum is used in metallurgical applications (stainless steel, cast-iron alloys). Ammonium tetrathiomolybdate is an experimental chelating agent for Wilson's disease. For the general population, the diet is the most important source of molybdenum and concentrations in water and air usually are negligible. The average daily dietary intake is about 0.1-0.5 mg m.o. Molybdenum is an essential element with relatively low toxicity. Enzymes containing molybdenum catalyze basic metabolic reactions in the carbon, sulfur, and nitrogen cycles. Elimination of molybdenum occurs via the kidney and usually is complete within several weeks. Molybdenosis (teart) is a form of molybdenum toxicity that produces a disease in ruminants similar to copper-deficiency. Little data are available on the human toxicity of molybdenum. A gout-like syndrome and pneumoconiosis have been associated with excessive concentrations of molybdenum, but the inadequate design of the studies prevents an adequate determination of the etiology of these effects.
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PMID:Molybdenum. 1038 58

Calcification of tophi is a well-known secondary phenomenon in gout. Because there are no data available on the nature of the calcium component, light and scanning electron microscopic as well as X-ray microanalysis studies were performed on calcified tophi. In unstained histological slides, urate crystals were detected as negative birefringent needles; after incubation of the slides in distilled water, the urate crystals had disappeared, only positive birefringent calcium pyrophosphate dihydrate (CPPD) crystals of different size remained. An identical result was obtained by scanning electron microscopy. By X-ray microanalysis, peaks for calcium and phosphorus were measured, indicating the presence of CPPD. The occurrence of CPPD crystals in urate tophi as well as in foreign body granulomata indicates that the occurrence of CPPD is not restricted to articular tissues. The biochemical mechanism leading to the appearance of these crystals remains unknown, but it may be assumed that an increase of connective tissue destruction may be responsible for this calcification process.
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PMID:[Mixed tophi. Calcium pyrophosphate dihydrate crystals in gout tophi]. 1101 85


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