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

The comparative acute, oral toxicity of ochratoxin A for three day-old avian species is presented. The seven-day LD50 value for White Leghorns was calculated to be 3.4 +/-0.19 mgm./kg., for turkeys to be 5.9 +/- 0.72 mgm./kg., and for Japanese quail to be 16.5 +/- 0.56 mgm./kg., body weight. The dose-response curves are linear and parallel through one standard deviation on either side of the LD50 when log-dose is plotted against probit for survivors. It is suggested that the mechanism of action of ochratoxin A is similar in the three species, though the potency differs. The reduction in weight gain of Leghorn survivors was proportional to dose, and was observed in two separate traials over an overall dosage range from 0.2 mgm./kg. to 5 mgm./kg. The turkeys showed only a slight reduction in weight gain at doses less than 4mgm./kg., a more marked reduction being observed at higher dose levels. The quail did not show reduction of weight gain at dose levels below 10.9 mgm./kg., though the reduction was proportional to dose at higher levels. All birds dying of acute ochratoxicosis revealed a progression of symptoms from listlessness, huddling, occassionally diarrhoea, ataxia, prostration and death. Viscereal gout was observed at necropsy of the Leghorns.
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PMID:Acute oral ochratoxicosis in day-old White Leghorns, turkeys and Japanese Quail. 93 32

Molybdenum toxicity and the interactions between copper, molybdenum and sulphate are reviewed. The main signs of molybdenum poisoning are poor growth and anaemia (rat, chick, rabbit, cattle and sheep), anorexia (rat), diarrhoea and achromotrichia (cattle and sheep), joint and bone deformities (rat, rabbit, cattle), central nervous system degeneration and loss of crimp in wool (sheep). The following topics are discussed: (1) The effect of sulphate and sulphur compounds on molybdenum toxicity. (2) The effect of molybdenum on tissue copper levels. (3) The effect of molybdenum on the distribution of copper in plasma. (4) The effect of molybdenum on uptake and excretion of copper. (5) The possible existence of copper(II) molybdate in vivo. (6) The influence of molybdenum on sulphide production by ruminal micro-organisms. (7) Competition between molybdenum and sulphate in intestinal transport. (8) Interaction of sulphur with copper in vivo. (9) The possible involvement of molybdenum in gout and multiple sclerosis in humans.
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PMID:Molybdenum toxicity: interactions between copper, molybdenum and sulphate. 100 22

1. A commercial 62-week-old layer flock experienced an acute drop in egg production and an increase in shell-less egg production within 2 days of consuming feed erroneously formulated to contain over 30 g/kg instead of 3 g/kg sodium bicarbonate (NaHCO3). Other symptoms included increased water consumption, diarrhoea and increased mortality associated with visceral gout. 2. An experiment was conducted to assess the responses of hens under controlled conditions. Twenty Dekalb XL Single Comb White Leghorn hens (50 weeks old) were placed in individual cages, having ad libitum access to water from trough waterers. Ten hens were fed the TEST (High NaHCO3) feed for one week (Test group), and ten hens remained on normal commercial layer ration (Control group). 3. Hens in the Test group had high water consumption and watery droppings, but egg production and mortality were not affected. Physiological evaluations indicated the Test feed caused metabolic alkalosis. Plasma sodium, urine pH and urinary sodium excretion were increased, and glomerular filtration rates were decreased in the Test group. 4. These physiological effects are consistent with known responses to excess sodium intake in domestic fowl. The reduced egg production and increased mortality caused by the Test feed under commercial conditions may be related to more severe dehydration experienced by hens in multi-bird cages supplied by cup-type watering systems.
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PMID:Excess sodium bicarbonate in the diet and its effect on Leghorn chickens. 132 26

Twenty-one Myrtaceae collections belonging to 10 species, 5 of which are used in Chilean folk medicine, were assayed for inhibitory activity towards the enzyme xanthine oxidase. Most leaf and stem extracts were devoid of activity or showed a weak inhibitory effect. Chilean ethnobotanical data on the species are linked to the astringent properties of Myrtaceae and their use for treating wounds and diarrhea. The results show the advantage of using proper plant selection criteria when searching for new drugs to treat human gout.
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PMID:Xanthine oxidase inhibitory activity of Chilean Myrtaceae. 192 22

Adverse treatment effects were assessed in 840 elderly hypertensive patients randomly assigned to active treatment (a combination of triamterene and hydrochlorothiazide) or placebo; methyldopa was added to the regimen in one third of the treated patients. Symptoms of dry mouth, nasal stuffiness, and diarrhea were reported by significantly more treated patients than placebo control subjects. More patients receiving diuretics plus methyldopa than diuretics alone reported dry mouth and diarrhea. Significantly more treated patients than control subjects showed evidence of a high serum creatinine level, mild hypokalemia, and gout. More treated patients tended to have diabetes. The benefits of treatment outweighed these adverse treatment effects.
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PMID:Adverse treatment effects in the trial of the European Working Party on High Blood Pressure in the Elderly. 200 59

We have performed the first controlled study of colchicine in acute gout, to determine its efficacy and toxicity, and to define the natural history of acute gout. Two-thirds of colchicine-treated patients improved after 48 hours, but only one-third of the patients receiving placebo demonstrated similar improvement. The colchicine-treated patients responded earlier; significant differences from placebo were shown after 18-30 hours. All patients given colchicine developed diarrhea after a median time of 24 hours (mean dose of colchicine 6.7 mg). This side effect occurred before relief of pain in most patients.
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PMID:Does colchicine work? The results of the first controlled study in acute gout. 331 32

A patient with gout and schizophrenia is described who during a schizophrenic paroxysm with paranoid-hypochondriac-hallucinatory syndrome attempted to commit suicide and took 200 tablets milurit (20 g). He developed the picture of acute intoxication with nausea, vomiting, profuse diarrhea, abdominal pain, flushing, temperature, collapse manifestations, hepatomegaly, direct hyperbilirubinemia, elevated transaminase, leukopenia, accelerated ESR. After reanimation and infusion therapy, the patient recovered within 4 days and 2 weeks later all blood indices reached the limits of the norm.
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PMID:[Acute allopurinol (milurit) poisoning]. 402 4

Of 29 524 hospitalised medical patients monitored in a drug surveillance programme 1835 (6.2%) received the xanthine oxidase inhibitor allopurinol. After the exclusion of skin reactions adverse effects were attributed to this drug in 33 (1.8%) patients, the most frequent being haematological abnormalities (11 patients, 0.6%) and diarrhoea and drug fever (5 each, 0.3%). Adverse effects were dose-related. Reactions were unrelated to age, weight, reason for therapy, admission blood urea, or albumin concentrations. Acute exacerbation of gout was troublesome in 3 patients (1 in 600 exposed).
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PMID:Acute adverse reactions attributed to allopurinol in hospitalised patients. 724 70

Although gout and hyperuricaemia are usually thought of as conditions of indulgent male middle age, in addition to the well-known uricosuria of the newborn, there is much of importance for the paediatric nephrologist in this field. Children and infants may present chronically with stones or acutely with renal failure from crystal nephropathy, as a result of inherited deficiencies of the purine salvage enzymes hypoxanthine-guanine phosphoribosyltransferase (HPRT) and adenine phosphoribosyltransferase (APRT) or of the catabolic enzyme xanthine dehydrogenase (XDH). Genetic purine overproduction in phosphoribosylpyrophosphate synthetase superactivity, or secondary to glycogen storage disease, can also present in infancy with renal complications. Children with APRT deficiency may be difficult to distinguish from those with HPRT deficiency because the insoluble product excreted, 2,8-dihydroxyadenine (2,8-DHA), is chemically very similar to uric acid. Moreover, because of the high uric acid clearance prior to puberty, hyperuricosuria rather than hyperuricaemia may provide the only clue to purine overproduction in childhood. Hyperuricaemic renal failure may be seen also in treated childhood leukaemia and lymphoma, and iatrogenic xanthine nephropathy is a potential complication of allopurinol therapy in these conditions. The latter is also an under-recognised complication of treatment in the Lesch-Nyhan syndrome or partial HPRT deficiency. The possibility of renal complications in these three situations is enhanced by infection, the use of uricosuric antibiotics and dehydration consequent upon fever, vomiting or diarrhoea. Disorders of urate transport in the renal tubule may also present in childhood. A kindred with X-linked hereditary nephrolithiasis, renal urate wasting and renal failure has been identified, but in general, the various rare types of net tubular wasting of urate into the urine are recessive and relatively benign, being found incidentally or presenting as colic from crystalluria. However, the opposite condition of a dominantly inherited increase in net urate reabsorption is far from benign, presenting as familial renal failure, with hyperuricaemia either preceding renal dysfunction or disproportionate to it. Paediatricians need to be aware of the lower plasma urate concentrations in children compared with adults when assessing plasma urate concentrations in childhood and infancy, so that early hyperuricosuria is not missed. This is of importance because most of the conditions mentioned above can be treated successfully using carefully controlled doses of allopurinol or means to render urate more soluble in the urine. Xanthine and 2,8-DHA are extremely insoluble at any pH. Whilst 2,8-DHA formation can also be controlled by allopurinol, alkali is contraindicated. A high fluid, low purine intake is the only possible therapy for XDH deficiency.
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PMID:Gout, uric acid and purine metabolism in paediatric nephrology. 843 71

The autopsy report of Ludwig van Beethoven written by Dr Johann Wagner in 1827 reveals that he had renal calculi that had not been diagnosed during his lifetime, together with perirenal fibrosis. The most comprehensive interpretation of this autopsy finding is that the regular calcareous deposits in every one of his renal calices represented calcified necrotic papillae. Severe urinary obstruction or diabetes as possible causes of papillary necrosis were not present. Analgesic abuse because of headaches, back pain, and attacks of rheumatism or gout may be presumed on the basis of Beethoven's uncontrolled way of taking medication. Salicin, a commonly used analgesic substance of that time (dried and powdered willow bark), is able to cause papillary necrosis. Perirenal fibrosis may be due to chronic infection or drug intake. Beethoven's other well-known diseases are deafness caused by otosclerosis of the inner ear, relapsing attacks of diarrhea as the symptoms of irritable bowel syndrome, and liver cirrhosis following viral hepatitis and chronic alcohol consumption. Liver cirrhosis also may cause papillary necrosis. In Beethoven's case, renal papillary necrosis was most probably the consequence of analgesic abuse together with decompensated liver cirrhosis. The autopsy report of Beethoven is the first case of papillary necrosis recorded in the literature.
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PMID:Beethoven's renal disease based on his autopsy: a case of papillary necrosis. 850 20


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