Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.17.3.2 (xanthine oxidase)
 8,383 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperuricaemia may complicate thalassaemia and may, on occasion, result in obstruction of urine flow on the basis of crystal formation. Prophylactic therapy with xanthine oxidase inhibitors may prevent this complication, but once it has developed, accurate diagnosis and aggressive therapy can reduce morbidity. The present case report illustrates one approach to the management of acute uric acid nephropathy.
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PMID:Acute uric acid nephropathy in thalassaemia. 111 16

Stimulation of uric acid production by the well-known uricosuric drug probenecid was studied using potassium oxonate-treated rats and eviscerated rats subjected to functional hepatectomy. In oxonate-treated rats, probenecid was hyperuricosuric, increasing the glomerular-filtered amounts of uric acid and causing marked hyperuricemia. This could be completely blocked by combination dosing with allopurinol, an inhibitor of xanthine oxidase. In eviscerated rats subjected to functional hepatectomy, probenecid also increased plasma uric acid and urinary uric acid excretion, but when given together with allopurinol, the increase of plasma uric acid was abolished with a remarkable increase of plasma hypoxanthine and xanthine. When probenecid was given by combination dosing with propranolol, a beta adrenoceptor antagonist, the hyperuricemia was also completely blocked. Thus, probenecid is concluded to stimulate uric acid production, probably via some interaction with endogenous catecholamine, resulting in hyperuricemia in rats, although it is a practical hypouricemic drug in humans.
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PMID:Hyperuricemia induced by the uricosuric drug probenecid in rats. 188 91

Uric acid, as the end-product of purine metabolism in humans, presents a clinical problem because of its relative insolubility, particularly in the acid environment of the distal nephron of the kidney. As a result, states of enhanced purine catabolism increase the urate load on the kidney, leading to intrarenal precipitation. Major causes of increased purine metabolism are malignancies with rapid cell turnover, such as leukemias and lymphomas, and the added acceleration of cell lysis that occurs with chemotherapy and radiation. Serum urate levels rise rapidly, and acute renal failure occurs as a consequence of tubular deposition of urate and uric acid. The keys to the diagnosis of acute uric acid nephropathy are the appropriate clinical setting of increased cell lysis, oliguria, marked hyperuricemia, and hyperuricosuria. A urinary uric acid-to-creatinine ratio greater than 1 helps to distinguish acute uric acid nephropathy from other catabolic forms of acute renal failure in which serum urate is elevated. Preventive treatment involves pharmacologic xanthine oxidase inhibition with allopurinol and alkaline diuresis. Occasionally, acute renal failure occurs despite allopurinol because of the tubular precipitation of the precursor metabolites, such as xanthine, which accumulate with xanthine oxidase inhibition. Dialysis therapy may be required both to correct azotemia and to reduce the body burden of urate. Hemodialysis is preferred because it can achieve greater clearance than other dialysis modes.
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PMID:Acute uric acid nephropathy. 219 58

As many as 76 patients suffering from inactive rheumatic fever associated with different stages of heart failure were examined for uricemia, diurnal uricosuria, and xanthine oxidase activity in blood serum. It was established that in rheumatic fever, the activity of xanthine oxidase increased even at the early stages of heart failure. The presence in some of the patient of the enzyme activation combined with hyperuricosuria and normal content of uric acid in blood serum suggests "latent" hyperuricemia. In patients with severe heart decompensation, there was an appreciable activation of xanthine oxidase, which correlated, as a rule, with high hyperuricemia. Activation of xanthine oxidase in patients with rheumatic fever evidences hyperproduction of uric acid. It is advisable that in such cases the uricodepressive treatment may be indicated.
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PMID:[Changes in xanthine oxidase activity in patients with circulatory failure]. 278 95

The antihyperuricemic properties of amflutizole were investigated in studies designed to determine its efficacy and mechanisms of action in individuals with gout and hyperuricemia. In a randomized double blind, multiple dose, crossover study of 29 patients, amflutizole caused a significant dose dependent reduction in serum urate concentrations. Mean serum urate concentrations decreased significantly from 9.6 +/- 1.5 mg/dl to 7.2 +/- 1.3 mg/dl with the 500 mg dosage (p less than 0.01). Detailed studies in 5 patients demonstrated evidence for modest xanthine oxidase inhibition. However, the majority of the antihyperuricemic effect was derived from an enhanced renal clearance of uric acid. Although the drug has significant antihyperuricemic properties, these were inadequate to achieve adequate control of the serum urate concentration in hyperuricemia and gout at the doses utilized.
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PMID:Antihyperuricemic properties of amflutizole in gout. 390 Mar 92

Recent studies have confirmed that gout is an inborn error of metabolism. It has now become evident that the hyperuricemia associated with gout might occur either due to overproduction of uric acid, underexcretion of uric acid or a combination of these processes. Furthermore, patients with excessive purine synthesis may have a specific enzyme defect resulting in altered feedback inhibition of purine synthesis. A neurological disease manifest by mental retardation, choreo-athetosis, aggressive behavior, lip-biting and self-mutilation and associated with decidedly increased purine biosynthesis serves as a prototype of this kind of disorder. Other defects in regulation of purine biosynthesis have been postulated but their existence not yet confirmed. It has been demonstrated that urate crystals which are deposited from hyperuricemic body fluids set up an acute inflammatory reaction by means of a variety of chemical mediators. Thus, acute gouty arthritis is now recognized as an example of "crystal induced" synovitis. The treatment of gout consists of (1) the control of acute gouty attacks, and (2) the maintenance of normal serum uric acid concentrations. This latter may be achieved either with uricosuric drugs or with xanthine oxidase inhibition. With these principles in mind, it is now possible to avoid many of the severe crippling effects of gout and to restore the vast majority of gouty patients to useful and productive lives.
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PMID:Current concepts of hyperuricemia and gout. 577 83

The results of animal experiments and clinical observations concerning the pathological role of hyperuricaemia and the effect of allopurinol treatment in acute metabolic disturbances and critically ill patients is reported. In uricase enzyme blocked rats treated by oxonic acid, urate nephropathy could be elicited by endogenous purine catabolism in shock. Hyperuricaemia aggravated the shock, while allopurinol increased the survival time. In shock resistant rats hyperuricaemia did not develop when shock was elicited. Allopurinol prevented hyperuricaemia and increased the physical performance of swimming rats, while in experimental DIC allopurinol reduced markedly the hyperuricaemia and the kidney damage. In clinical studies a close correlation was observed between the degree of hyperuricaemia and the severity of illness. Serum uric acid values were lowered in cases treated by peritoneal dialysis. In randomized control studies of newborns with IRDS the survival rate was improved by allopurinol treatment. In critically ill patients with various illnesses allopurinol prevented the progression of the pathological process and improved the clinical condition. The effect of allopurinol in acute clinical metabolic disturbances may be due to its protection against the renal damage by hyperuricaemia and against purine loss by inhibition of xanthine oxidase during the hypoxic stress and the enhancement of hypoxanthine salvage by HGPRT. Allopurinol reduced the production of superoxide radicals and thus the effect of injury may also be moderated by xanthine oxidase blockade.
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PMID:Role of hyperuricaemia in critically ill patients especially newborns. 638 36

Xanthine oxidase activity was studied in patients with hyperlipoproteinemia type IV. A significant increase of this enzyme as compared with normals was found. Furthermore, a positive correlation between xanthine oxidase and triglycerides has been observed. This explains the hyperuricemia commonly found in hypertriglyceridemic patients of Type IV.
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PMID:Xanthine oxidase and triglycerides in serum of patients with hyperlipoproteinemia, type IV. 654 57

Urinary tract calculi composed primarily of xanthine are rare in adults and children. However, there is risk of xanthine calculi formation in children with hereditary xanthinuria and children on xanthine oxidase inhibitor therapy for hyperuricemia. We describe the clinical presentation and management of 2 children with the Lesch-Nyhan syndrome (a congenital disorder of purine metabolism) and xanthine calculi. Little information has been available to direct the urologic management of such patients. We have based a plan for management upon our clinical experience with these children, as well as upon in vitro dissolution studies of the calculi. We have had some clinical success using an alternating acid/base dissolution therapy developed in the laboratory.
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PMID:Xanthine calculi in the Lesch-Nyhan syndrome. 686 3

Gout may be a primary or a secondary disorder. In both types of gout, overproduction or underexcretion of uric acid, or a combination of these abnormalities, may be the underlying mechanism. Controversy exists over the need for treatment of asymptomatic hyperuricemia. Treatment of tophi requires use of both uricosurics and allopurinol. A xanthine oxidase inhibitor is the drug of choice for patients with uric acid stones and for those with renal insufficiency.
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PMID:Hyperuricemia and gout: an update. 689 39


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