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)

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

Forty-nine patients with gout, many with hypertension and/or renal calculi, were given hydrochlorothiazide, furosemide, or ticrynafen. Diuresis and increased clearances of sodium (Na), potassium (K), chloride (Cl), and calcium (Ca) occurred after a single dose of hydrochlorothiazide, 100 mg, or furosemide, 40 mg, orally. There was very slight change in urate and phosphorus clearances. With prolonged use of hydrochloride or furosemide, diuresis and increased electrolyte excretion disappeared. Urate and Ca excretion fell with hydrochlorothiazide. With long-term use of furosemide, urate excretion was suppressed, but Ca excretion was sustained. Ticrynafen produced diuresis and increased clearances of Na, K, and Cl. Calcium excretion was increased after a single dose and minimally decreased after long-term use. Most striking was the severe and rather sustained uricosuria. Though ticrynafen is an effective uricosuric, natriuretic, and antihypertensive agent, its hepatotoxicity and nephrotoxicity mitigate against its clinical use.
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PMID:Effects of diuretics on urate and calcium excretion. 723 11

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

We demonstrated the simultaneous occurrence of psoriatic arthropathy and the 2 major types of crystalline arthritis--pseudogout and gout. The crystals found within aspirated synovial fluid and exudative leukocytes were unequivocally identified using the compensating polarizing microscope as calcium pyrophosphate dihydrate in one case and sodium monourate in the other. The surface topography of the intracellular sodium monourate crystals were also displayed.
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PMID:Psoriatic arthropathy and crystal-induced synovitis. 737 24

Factors influencing the nucleation of monosodium urate (NaHU) were studied with supersaturated solutions of sodium urate at physiologic conditions of temperature, pH, and ionic strength. Spontaneous nucleation of NaHU did not occur at urate concentrations of 5 mM (84 mg%) in the presence of 140 mM Na ion. Addition of synovial fluids from gout patients greatly enhanced nucleation, whereas fluids from degenerative joint disease patients moderately enhanced nucleation, and fluids from rheumatoid arthritis patients had only a slight effect. Hyaluronic acid and purines minimally enhanced urate crystallization, whereas other connective tissue components had no effect.
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PMID:Studies on the nucleation of monosodium urate at 37 degrees c. 737 87

The difference between gout and rheumatoid arthritis was reproduced experimentally in the rat by combining adjuvant arthritis with an oxonate uric acid raising diet and injections of crystals of sodium urate. The factorial experiment using 3 factors confirms the inhibition or arthritis by a uric acid raising diet and shows that the injections of crystals, which preceed the injection of Freund's adjuvant, increase the arthritic lesions in normo-uricemic rats and reduces them slightly in hyperuricemic rats. This effect of the injection of crystals increases gradually with time.
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PMID:[Effect of a high serum uric acid diet and injections of urate crystals on adjuvant arthritis in the rat]. 745 97

Gout is a disease caused by deposits of sodium urate crystals in tissues. This disease, already known of Hippocrates, is now due to new causes, notably iatrogenic, and has new clinical forms. The typical initial attack usually occurs in men in their fifties and affects the big toe; in the absence of treatment it evolves towards chronic tophaceous gout. When gout occurs in subjects younger than 30 years, these must be investigated for enzyme deficit which is usually partial. The incidence of gout in women is ever increasing, being encouraged by treatments with diuretic drugs. Gout is often atypical, affecting predominantly the hands and with rapid development of tophus. In transplanted patients other drugs, such as cyclosporin, may induce an early, polyarticular and tophaceous gout. Alcohol is a facilitating factor of hyperuricaemia. Disturbances of metabolism, such as hyperlipidaemia, obesity or arterial hypertension, are often associated with hyperuricaemia. With an early and well-conducted treatment the passage to chronicity and the occurrence of complications can be avoided.
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PMID:[What remains of gout in 1993?]. 817 71

Patterns of rheumatic diseases and antirheumatic drug usage in different regions of India were analysed. The data was collected from a post-marketing surveillance of diclofenac sodium (Voveran) in 11931 patients. The common conditions were-rheumatoid arthritis (RA) 28.1%, osteoarthrosis (OA) 24.8%, soft-tissue rheumatism 12.4%, cervical spondylosis 6%, ankylosing spondylitis (AS) 3.5%, gout 2%. East zone had a significantly lower proportion of osteoarthritis (20.9%). The age distribution and sex ratios of RA, OA and AS were in line with literature reports. The severity of illness was moderate in 62% and duration was more than 6 months in 50.2%. Data on NSAID usage showed a preponderance of combinations and ibuprofen. There were no significant differences in NSAID usage across diseases or regions.
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PMID:Patterns of rheumatic diseases and antirheumatic drug usage in 11931 Indian patients. 786 May 74

To investigate whether or not DL-sodium lactate inhibits the renal excretion of purine bases and oxypurinol, we administered physiological saline containing 0.2 mol DL-sodium lactate to 7 normal subjects intravenously. DL-sodium lactate infusion decreased the urinary excretion and the fractional clearance of uric acid, xanthine and oxypurinol, but the fractional clearance of hypoxanthine was not affected. These results suggested that the implications of DL-sodium lactate-induced hyperuricemia must be considered in patients with gout on its long term and high dose administration, and that the implications of DL-sodium lactate-induced prolongation of half-life of oxypurinol must be considered in hyperuricemic patients treated with allopurinol. However, since the high dose and long term administration of DL-sodium lactate is clinically rare, the effect of DL-sodium lactate infusion on the urinary excretion of uric acid, xanthine and oxypurinol may not be clinically important.
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PMID:Effect of DL-sodium lactate infusion on excretion of purine bases and oxypurinol. 831 59

The changes in adenine nucleotide concentration induced by acetate were investigated in rat liver in situ and in isolated rat hepatocytes. Adenosine monophosphate (AMP) concentration increased approximately threefold within 15 minutes after intraperitoneal injection of sodium acetate. A small but significant decrease in adenosine triphosphate (ATP) concentration also occurred. Consequently, the ATP/AMP ratio decreased from approximately 14 (the value found in control or sodium chloride-injected rats) to approximately 3 (the value found in sodium acetate-injected rats). Adenosine diphosphate (ADP) concentration increased slightly, but this was statistically nonsignificant. Total adenine nucleotide concentrations after acetate injection remained essentially the same as those in control rats. Adenylate energy charge decreased after acetate administration. No significant changes in nicotinamide adenine dinucleotide (NAD) or nicotinamide adenine dinucleotide phosphate (NADP) concentrations were found after sodium acetate injection. Similar patterns of changes in adenine nucleotide concentrations were found in isolated rat hepatocytes incubated in the presence of acetate. These data indicate that acetate, which appears in human blood either during hemodialysis with acetate-containing solution or after ethanol consumption, may alter energy equilibrium of adenine nucleotides in the liver. This is due to the conversion of ATP to AMP in the course of acetate to acetyl-coenzyme A (CoA) activation. It is therefore possible that accelerated ATP turnover in the liver may contribute both to the "intolerance to acetate" in patients subjected to dialysis with the sodium acetate-containing solution and to the pathogenesis of gout associated with excessive ethanol consumption.
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PMID:Acetate-induced changes of adenine nucleotide levels in rat liver. 849 21


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