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

Uric acid in blood has been widely accepted as a reliable indicator of hyperuricemia and gout, and its assay method has been established. In the present study, we developed a simple and non-invasive rapid method for the determination of uric acid in hair. Concentration(nmol/mg hair) of uric acid extracted from 10-20 mg of hair(95% < extractability; 0.1N KOH, 37 degrees C, 2 hr) was determined by an enzymatic method using uricase. The concentration of uric acid(nmol/mg hair, mean +/- SD: 0.489 +/- 0.157, n = 16) in hair from hyperuricemic patients was significantly higher than that(0.258 +/- 0.107, n = 8) from healthy volunteers(p < 0.01). Within-run and between-day precisions(reproducibilities, CVs) for the assay were 9.6-10.3%(n = 10 each) and 11.6-16.3%(n = 7 each), respectively. The concentration(y, nmol/mg hair) of uric acid in hair correlated well with that in blood(x, g/l): y = 8.770x-0.123(r = 0.746, Syx = 0.122, n = 23). Changes in the concentration of uric acid in hair of hyperuricemic patient treated with allopurinol paralleled to those in blood. In conclusion, it was confirmed that the concentration of uric acid in hair reflected that in blood, suggesting that measuring uric acid in hair can be available for the metabolic control in hyperuricemia.
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PMID:[Determination of uric acid in scalp hair for non-invasive estimation of uricemic control in hyperuricemia]. 939 46

Uric acid, the naturally occurring product of purine metabolism, is a strong peroxynitrite scavenger, as demonstrated by the capacity to bind peroxynitrite but not nitric oxide (NO) produced by lipopolysaccharide-stimulated cells of a mouse monocyte line. In this study, we used uric acid to treat experimental allergic encephalomyelitis (EAE) in the PLSJL strain of mice, which develop a chronic form of the disease with remissions and exacerbations. Uric acid administration was found to have strong therapeutic effects in a dose-dependent fashion. A regimen of four daily doses of 500 mg/kg uric acid was required to promote long-term survival regardless of whether treatment was initiated before or after the clinical symptoms of EAE had appeared. The requirement for multiple doses is likely to be caused by the rapid clearance of uric acid in mice which, unlike humans, metabolize uric acid a step further to allantoin. Uric acid treatment also was found to diminish clinical signs of a disease resembling EAE in interferon-gamma receptor knockout mice. A possible association between multiple sclerosis (MS), the disease on which EAE is modeled, and uric acid is supported by the finding that patients with MS have significantly lower levels of serum uric acid than controls. In addition, statistical evaluation of more than 20 million patient records for the incidence of MS and gout (hyperuricemic) revealed that the two diseases are almost mutually exclusive, raising the possibility that hyperuricemia may protect against MS.
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PMID:Uric acid, a natural scavenger of peroxynitrite, in experimental allergic encephalomyelitis and multiple sclerosis. 943 51

Therapy of hyperuricemia and gout has to depend on pathogenesis and stage of the disease. Dietary regimen are in the forefront in treatment of asymptomatic hyperuricemia. Uric acid lowering drugs can only be supported in repeated serum-measures from 9 mg/dl up. The therapy of an acute attack of gout primarily is done with non-steroidal antiinflammatory drugs, in rare cases with colchicine or corticoids. Gouty arthritis in intermission, independent of the extent of hyperuricemia, as well as chronic gout are indications for an uric acid lowering pharmacotherapy, usually for life. A special therapeutic challenge arises out of renal complications and the frequent association with the metabolic syndrome.
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PMID:[Therapy of hyperuricemia and gout]. 944 17

Gout in the elderly differs from classical gout found in middle-aged men in several respects: it has a more equal gender distribution, frequent polyarticular presentation with involvement of the joints of the upper extremities, fewer acute gouty episodes, a more indolent chronic clinical course, and an increased incidence of tophi. Long term diuretic use in patients with hypertension or congestive cardiac failure, renal insufficiency, prophylactic low dose aspirin (acetylsalicylic acid), and alcohol (ethanol) abuse (particularly by men) are factors associated with the development of hyperuricaemia and gout in the elderly. Extreme caution is necessary when prescribing nonsteroidal anti-inflammatory drugs (NSAIDs) for the treatment of acute gouty arthritis in the elderly. NSAIDs with short plasma half-life (such as diclofenac and ketoprofen) are preferred, but these drugs are not recommended in patients with peptic ulcer disease, renal failure, uncontrolled hypertension or cardiac failure. Colchicine is poorly tolerated in the elderly and is best avoided. Intra-articular and systemic corticosteroids are increasingly being used for treating acute gouty flares in aged patients with medical disorders contraindicating NSAID therapy. Urate-lowering drugs are indicated for the treatment of hyperuricaemia and chronic gouty arthritis. Uricosuric drugs are poorly tolerated and the frequent presence of renal impairment in the elderly renders these drugs ineffective. Allopurinol is the urate-lowering drug of choice, but its use in the aged is associated with an increased incidence of both cutaneous and severe hypersensitivity reactions. To minimise this risk, allopurinol dose must be kept low. A starting dose of allopurinal 50 to 100mg on alternate days, to a maximum daily dose of about 100 to 300mg, based upon the patient's creatinine clearance and serum urate level, is recommended. Asymptomatic hyperuricaemia is not an indication for long term urate-lowering therapy; the risks of drug toxicity often outweigh any benefit.
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PMID:Gout in the elderly. Clinical presentation and treatment. 978 27

Uric acid, the naturally occurring product of purine metabolism, is widely used as a diagnostic parameter in different diseases. The concentration of uric acid may vary between broad ranges without causing symptoms, like idiopathic hyperuricemia, which behind metabolic disorders were always suggested. Recently the uric acid has been shown as a strong scavenger of oxidative stress molecules or radicals. Uric acid was successfully used to treat experimental allergic encephalomyelitis, the mouse model of multiple sclerosis (M. S.). It was shown, that patients with multiple sclerosis had significantly lower levels of serum uric acid than the control persons. In addition, statistical evaluation of more than 20 million patient records for the incidence of MS and hyperuricemic gout revealed, that the hyperuricemia may protect against MS.
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PMID:[Uric acid as a scavenger in oxidative stress]. 1007 5

We studied 51 pulmonary tuberculosis patients who were initially treated with pyrazinamide (PZA) at our hospital between April 1996 and December 1997. PZA dosage was less than 1.5 g per day, and the chemotherapy course lasted 2 months. Uric acid levels of higher than 8 mg/dl were observed in 44 patients (86%). Arthralgia was observed in 9 patients. Acute gout was observed in only 1 patient who had hyperuricemia prior to PZA treatment and a predisposition for gout. The other 8 patients with arthralgia had symptoms in the shoulders and knees, but no gouty pain. Arthralgia was not related to serum uric acid level and disappeared after PZA treatment was stopped. We concluded that PZA can be used for up to 2 months without the combined administration of allopurinol or benzbromarone even if hyperuricemia or arthralgia develops.
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PMID:[Hyperuricemia and arthralgia during pyrazinamide treatment]. 1021 39

Accurate determination of serum and urinary uric acid concentrations is essential for the diagnosis and classification of gout according to uric acid metabolism derangement. Urine and/or serum samples are often kept at either 4 degrees C or -20 degrees C until assayed, when a large number of samples are handled simultaneously. Our preliminary study indicated a significant decrease in urinary uric acid concentration after preservation, regardless of the storage temperature. Uric acid crystals were often observed in these cases which showed a marked decrease in urinary uric acid concentration after storage. In the present study, we sought the factor(s) that might cause this decrease in urinary uric acid concentration, as well as measures to overcome the problem. High urinary uric acid concentration and low pH proved to play major roles in the decrease in urinary uric acid concentration after storage. In contrast, dilution of the urine samples before storage resulted in no significant change in urinary uric acid concentration. Based on these results, we recommend diluting urine before storage for determination of uric acid concentration and avoiding underestimation.
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PMID:Effect of urine storage on urinary uric acid concentrations. 1081 51

Gout is an inflammatory response to deposition of monosodium urate crystals in and around joints. It is primarily a disease of adult men. In acute gout, treatment options include non-steroidal anti-inflammatory drugs (NSAIDs), colchicine and corticosteroids, administered either intra-articularly, orally or parenterally. Asymptomatic hyperuricaemia does not require specific treatment, but should prompt screening for atherosclerosis risk factors, and general lifestyle modification to reduce serum urate levels. Gout presents differently in the elderly. Both women and men are affected, attacks are frequently polyarticular and in the upper limbs, and the gout may be associated with diuretic use, hypertension and renal impairment. In patients with peptic ulcer disease, selective COX-2 inhibitors provide another treatment option. In the presence of renal impairment, allopurinol is the treatment of choice for urate lowering therapy, but doses of allopurinol and colchicine must be adjusted. Urate lowering therapy should only be used if recurrent episodes of gout occur despite aggressive attempts to reverse or control the underlying causes. It should not be introduced or discontinued during an acute episode of gout, and gout prophylaxis (NSAIDs or colchicine) should be prescribed during the introduction of urate lowering therapy.
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PMID:Clinical manifestations of gout and their management. 1090 73

Uricase-deficient mice develop uric acid nephropathy, with high mortality rates before weaning. Urate excretion was quantitated and renal function was better defined in this study, to facilitate the use of these mice as a model for evaluating poly(ethylene glycol)-modified recombinant mammalian uricases (PEG-uricase) as a potential therapy for gout and uric acid nephropathy. The uric acid/creatinine ratio in the urine of uricase-deficient mice ranges from 10 to >30; on a weight basis, these mice excrete 20- to 40-fold more urate than do human subjects. These mice consistently develop a severe defect in renal concentrating ability, resulting in an approximately sixfold greater urine volume and a fivefold greater fluid requirement, compared with normal mice. This nephrogenic diabetes insipidus leads to dehydration and death of nursing mice but, with adequate water replacement, high urine flow protects adults from progressive renal damage. Treatment of uricase-deficient mice with PEG-uricase markedly reduced urate levels and, when initiated before weaning, preserved the renal architecture (as evaluated by magnetic resonance micros-copy) and prevented the loss of renal concentrating function. PEG-uricase was far more effective and less immunogenic than unmodified uricase. Retention of uricase in most mammals and its loss in humans and some other primates may reflect the evolution of renal function under different environmental conditions. PEG-uricase could provide an effective therapy for uric acid nephropathy and refractory gout in human patients.
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PMID:Diabetes insipidus in uricase-deficient mice: a model for evaluating therapy with poly(ethylene glycol)-modified uricase. 1131 59

Hyperuricemia has been labeled both a risk factor and marker for cardiovascular pathology in addition to being associated with gout and kidney disease. Uric acid in vitro acts as a potent antioxidant capable of scavenging hydroxy radicals and peroxynitrite and reacting with nitric oxide. Some clinical studies have provided evidence that, in vivo, uric acid is oxidized under conditions associated with high oxidant stress and may spare other antioxidants such as ascorbic acid. The plasma level of uric acid is controlled by the rates of production and excretion or degradation of uric acid. Under most circumstances, it is the renal clearance of uric acid which primarily determines the plasma concentration. Many factors of exogenous and endogenous origin can influence renal tubular absorption and secretion of uric acid. We suggest that renal urate clearance is not haphazard but regulated by an unknown signal that is issued in response to the level of oxidative stress. Since much cardiovascular pathology is now believed to have an inflammatory component and is associated with enhanced production of free radicals, the accompanying hyperuricemia may be viewed as a compensatory response of potential benefit.
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PMID:Renal regulation of plasma total antioxidant capacity. 1139 10


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