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

Diuretics can result in various undesired biochemical changes, such as impotence, skin rashes, nausea, dizziness and lethargy as well as subjective side effects. The side effects are mostly predictable, their effects depending on both the circulatory blood volume and on the transport of water and solute in the renal tubules. Two of the commonest side effects are mild hypovolaemia, when any diuretic is used, and mild hypokalaemia when the non-potassium-sparing diuretics, such as thiazides and frusemide are used. Its occurrence is dose dependent and can be corrected by potassium supplements, but potassium-retaining diuretics, which also correct the often associated fall in serum magnesium, are preferable. Many reports link hypokalaemia with cardiac arrhythmias, but some dispute this association in the absence of the concomitant use of digoxin. Hyponatraemia rarely occurs, but can be life threatening. Calcium excretion is markedly reduced, but unlike other electrolyte disturbances from diuretics, this may be valuable: some suggest diuretics have an anti-osteoporotic action. Diuretics increase glucose and insulin resistance and should be used sparingly in diabetics. They rarely cause a non-ketotic hyperosmolar coma. Urate is raised, but clinical gout is not common. Cholesterol elevation has been reported in some studies, but long-term studies indicate that lipid changes are minor. Other rare side effects are not predictable from their pharmacological actions and these include the occurrence of skin rashes, thrombocytopenia, pancreatitis and interstitial nephritis; and ototoxicity from frusemide.
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PMID:Adverse reactions to diuretics. 148 14

Since 1962 our group has performed four studies on uric acid values in blood donors in southern Germany (Bavaria). Uric acid levels in men have increased over the years, from 4.86 mg/dl in 1962 to 6.00 mg/dl in 1971, 5.60 mg/dl in 1984, and 5.90 mg/dl in 1989. Levels in women have increased slightly, from 4.05 mg/dl in 1962 to 4.35 mg/dl in 1971, 4.10 mg/dl in 1984, and 4.16 mg/dl in 1989. Women aged 51 to 60 years had significantly higher uric acid levels than those in the fourth decade. In women treated with oral contraceptives uric acid levels were significantly lower than in other women of the same age. Hypouricemia (uric acid levels less than or equal to 2.0 mg/dl) was observed in three women, none of whom had a history of medication. Hyperuricemia exists when uric acid levels are greater than or equal to 6.5 mg/dl. In 1989 2.6% of the female blood donors and 28.6% of the males were hyperuricemic, with an increased risk of gout, nephrolithiasis, and nephropathy.
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PMID:Uric acid levels in southern Germany in 1989. A comparison with studies from 1962, 1971, and 1984. 229 Mar 9

Urate crystal size change and the modification of coated proteins by oxygen radicals released by stimulated polymorphonuclear cells (PMN) could represent a likely "switch-off" mechanism of the spontaneous resolution of acute gout attack. The absorption spectra and the uric acid, allantoin and urea concentrations were determined before and after in vitro exposition of monosodium urate (MSU) crystals to superoxide anion (O2) photochemically generated. The results showed a complete dissolution of MSU crystals after incubation under O2-, with decrease of uric acid and increase of allantoin and urea concentrations. Our results were confirmed by polarizing, electron microscopy and calorimetric techniques. The results obtained seem to confirm that the spontaneous resolution of acute gout attack could be attributed to the dissolving effect on urate crystals and the modification of coated proteins by O2- released by phagocytizing PMN.
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PMID:The "switch-off" mechanism of spontaneous resolution of acute gout attack. 283 99

Gout is a clinical syndrome with a limited range of manifestations arising as a result of the deposition of crystals of monosodium urate, the final product of purine metabolism in humans. Hyperuricemia is a common chemical aberration that is most often mild and remains asymptomatic. Thus, hyperuricemia should be distinguished from gout, even though urate supersaturation is necessary for the expression of gout. Uric acid overproduction and diminished renal uric acid excretion are the major mechanisms resulting in hyperuricemia, and an understanding of the basis of hyperuricemia in individual gout patients is an important step in determining appropriate treatment and in identifying underlying disorders, offending drugs and toxins, and inherited enzyme defects, all of which can result in hyperuricemia and gout. A scheme is presented for the evaluation of patients with new-onset gout, along with a discussion of the relationships between gout/hyperuricemia and a variety of metabolic disorders that are unusually prevalent in gouty populations.
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PMID:Clinical aspects of monosodium urate monohydrate crystal deposition disease (gout). 305 Nov 56

Uric acid concentrations reportedly are increased in patients being treated with warfarin. We measured uric acid in 40 patients before and during warfarin administration. The mean pre- and post-warfarin uric acid concentrations for our patients were 0.39 mmol/L and 0.40 mmol/L, respectively, not a significant difference. Further observations of hyperuricemic patients started on warfarin are needed to prove that their risk of gout is not increased.
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PMID:Lack of effect of warfarin on uric acid concentration. 337 Jul 97

Uric acid concentration in the serum was investigated 3 times a day using the uricase method in 15 gout inpatients on a hypopurine diet with age- and sex-adjusted caloric content. The highest uric acid concentration was noted at 7 a. m., the lowest concentration value at 11 p. m. The highest renal clearance values were noted from 7 a. m. till 3 p. m., the lowest ones from 11 p. m. till 7 a. m. Similar regularities were noted in 15 rheumatoid arthritic patients, however uric acid concentration in the serum was lower and its renal excretion was 1.7 times more effective.
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PMID:[Circadian rhythm of uric acid levels of the serum in gout]. 358 98

Visceral gout is reported for the first time in a rough legged hawk (Buteo lagopus). Urate crystals were present on the pericardium, thoracic and abdominal air sacs, and the ventral surface of the liver. The liver and spleen also had urate crystals throughout the parenchyma. There was no indication of articular or renal involvement. The immediate cause of death in this hawk was not identified, but appeared to result from multiple factors, including the visceral gout.
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PMID:Visceral gout in a rough legged hawk (Buteo lagopus). 362 18

The relationships between serum uric acid, serum glucose and diabetes have been examined in a survey of 7735 middle-aged men drawn at random from general practices in 24 British towns. There was a positive relationship between serum glucose and serum uric acid concentrations up to about 8.0 mmol/l; at higher levels of glucose, serum uric acid decreased. Uric acid levels were significantly reduced in insulin-dependent diabetics and in those on oral hypoglycaemics and also in 'non-diabetics' with casual glucose levels greater than 10 mmol/l. Both uric acid and glucose concentrations were positively related to body mass index; only uric acid was positively related to alcohol intake. Men on antihypertensive treatment had raised levels of uric acid (significant) and glucose (non-significant). The positive relationship between serum uric acid and serum glucose could not be explained by associations with body mass index, alcohol intake, age, social class, gout or treatment for hypertension. It probably reflects the biochemical interaction between serum glucose and purine metabolism, with increased excretion of uric acid during hyperglycaemia and glycosuria.
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PMID:Serum uric acid, serum glucose and diabetes: relationships in a population study. 362 42

Gout is a disease linked to altered uric acid metabolism with increased uric acid concentration in the blood, the deposition of sodium urate crystals in certain tissues and abscesses. Uric acid derives from ex novo purinogenesis and the catabolism of cellular and alimentary nucleic acids. It is eliminated by uricolysis mainly in the intestines and renal excretion. The restriction of dietary protein purines, fats and calories reduces uricemia and explains the relationship between gout and diet. In Europe 5-18% of adult males suffer from uricemia with gout occurring in 0.5-1%. The incidence among females is much lower. The clinical picture presents an acute phase with a gouty abscess linked to the swollen joints caused by sodium urate crystals and a chronic phase characterised by gouty tophi and chronic gouty arthropathy. Treatment of the acute phase in which ample use is made of colchicine must be followed by medical and dietary treatment of the chronic condition.
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PMID:[Arthropathies and nutrition: gout]. 372 25

Several previous studies have demonstrated an increased prevalence of gout in New Zealand Maoris. The aetiology of the hyperuricaemia and its effect on morbidity, apart from gout, are unknown. A survey of 115 Maori men of working age revealed a history of gout in 10 (8%) and asymptomatic hyperuricaemia in 26 (23%). The relationship of hyperuricaemia with obesity was confirmed. Alcohol did not make an obvious contribution to the prevalence of hyperuricaemia. Hypertension was more common and creatinine clearance lower amongst those with gout, but not significantly so. The frequency of hypertension and mean creatinine clearance were similar to that seen in asymptomatic hyperuricaemia and normouricaemia. Urate clearance was lower in the gouty and hyperuricaemic subjects. The normouricaemic Maoris had a reduced fractional urate clearance compared with normal men elsewhere. They also excreted a relatively small proportion of hydrogen as ammonium. Both these features are characteristic of gout, and suggest that the Maoris' susceptibility to hyperuricaemia has a renal mechanism. Obesity is common amongst the Maoris and accentuates their natural tendency to hyperuricaemia.
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PMID:Hyperuricaemia, gout and kidney function in New Zealand Maori men. 648 33


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