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PedAM

Pediatric Disease Annotations & Medicines




Disease gout
Phenotype C0740394|hyperuricemia
Sentences 41
PubMedID- 20955624 Background: increase in the incidence of hyperuricemia associated with gout as well as hypertension, renal diseases and cardiovascular diseases has been a public health concern.
PubMedID- 19909378 Febuxostat, a non-purine xanthine-oxidase inhibitor, is a new agent approved for the treatment of hyperuricemia in patients with gout, which may be used when allopurinol is contraindicated.
PubMedID- 24448692 Topiroxostat (formerly known as fyx-051) is an orally administered non-purine analog, selective xanthine oxidase (xo) inhibitor developed for the management of hyperuricemia, including in patients with gout, in japan.
PubMedID- 23840514 It is mainly used for the treatment of hyperuricemia in patients with gout or tumor lysis syndrome.
PubMedID- 21934587 There appears to be a greater risk of developing gout with hyperuricemia, hypertension, and renal disease.
PubMedID- 21170252 This could result in accumulation of uric acid in blood (hyperuricemia) and tissues leading to visceral gout, which might be responsible for high mortality in birds.
PubMedID- 25128519 This finding supports the concept of distinctive mechanisms to account for hyperuricemia in patients with gout with reduced or normal uric acid excretion.
PubMedID- 23112391 The drugs available for the treatment of hyperuricemia in patients with gout are uricosuric agents (e.g.
PubMedID- 22359229 Furthermore, hyperuricemia in gout is most commonly the result of relative urate underexcretion, as the kidney has enormous capacity for urate reabsorption.
PubMedID- 23802027 The observation of a significantly decreased giant cells in gout patients with hyperuricemia is of interesting, but need further confirmation.
PubMedID- 23137576 The approval of new therapies to treat hyperuricemia in gout has led to a new understanding of gout management and medication safety regarding new and old therapies.
PubMedID- 21387258 Dlts included grade 4 (according to national cancer institute common terminology criteria for adverse events [version 3.0]) hyperuricemia with grade 2 gout and grade 3 lipase associated with grade 2 pancreatitis at dose level 2, and grade 3 rash in 2 patients at dose level 3.
PubMedID- 24055166 Affected individuals have hyperuricemia leading to gout and urolithiasis, accompanied by a characteristic severe neurobehavioural phenotype with compulsive self-mutilation, extrapyramidal motor disturbances and cognitive impairment.
PubMedID- 21264183 The prototypical (xo) inhibitor, allopurinol, has been the cornerstone of the clinical management of gout and conditions associated with hyperuricemia for several decades.
PubMedID- 22436129 Febuxostat is a selective, novel, non-purine analog xo inhibitor [7] for the treatment of chronic hyperuricemia in patients with gout [8].
PubMedID- 20091036 The hyperuricemia in gout might be caused by the increased adiposity associated with insulin resistance.
PubMedID- 24877124 Febuxostat, a chemically engineered nonpurine selective inhibitor of xo, received approval in february 2009 from the food and drug administration for the chronic management of hyperuricemia in patients with gout [81].
PubMedID- 23460805 A sensitivity analysis restricting gout to individuals with hyperuricemia or self-reported gout medication use yielded virtually the same findings (supplemental table s5).
PubMedID- 20215410 In this species, hyperuricemia is associated with gout, nephropathy, and increased cardiovascular disease risk.
PubMedID- 22316106 Febuxostat is a selective, non-purine analog xo inhibitor [19] for the treatment of chronic hyperuricemia in patients with gout [20].
PubMedID- 22606238 However, clinical studies have yielded inconsistent results probably because it is important to target a specific population of patients with hf; for instance, patients with moderate-to severe hf that had elevated serum uric acid levels are most likely to benefit from allopurinol treatment, the cornerstone of the clinical management of gout and conditions associated with hyperuricemia for several decades [59].
PubMedID- 24476385 Of particular relevance to the current study is the observation that fructose-induced hyperuricemia is accentuated in patients with gout and first-degree relatives of patients with gout.
PubMedID- 21353107 Background: use of urate-lowering therapy (ult), such as febuxostat or allopurinol, is recommended for the long-term management of hyperuricemia in patients with gout to reduce the incidence of acute flares.
PubMedID- 21898351 Conclusion: our data support the hypothesis that after appropriate long-term treatment of hyperuricemia in gout with urate crystal dissolution being the therapeutic target, lifelong treatment can be targeted to achieve serum urate levels just below the threshold for saturation to avoid new crystal formation, similar to cleaning a dirty dish: more is required to get it clean than to keep it clean.
PubMedID- 26349049 As a drug used to treat hyperuricemia associated with gout, tumor lysis syndrome, and the lesch-nyhan disease, urate oxidase (uox, also called uricase) is an enzyme of considerable biomedical interest123.
PubMedID- 22384520 hyperuricemia with gout, isolated gout without hyperiuricemia or hyperuricemia without gout are conditions which require ordinarily monitoring.
PubMedID- 25971955 Background: hyperuricemia can lead to gout, and may be a risk factor for cardiovascular events, hypertension, diabetes and renal disease.
PubMedID- 25963969 Until recently, the treatment of hyperuricemia in gout mostly hinged on the appropriate use of a single drug, that is, allopurinol, since the use of uricosurics is uncommon.
PubMedID- 24684266 The fda approval of febuxostat for the treatment of hyperuricemia in gout has been a significant step forward.
PubMedID- 24287461 It is suggested that hyperuricemia increases the risk of not only gout, but also other diseases as well, including hypertension, kidney disease, and metabolic syndrome [8].
PubMedID- 20151160 Mutations in the umod gene encoding uromodulin (tamm-horsfall glycoprotein) result in the autosomal dominant transmission of progressive renal insufficiency and hypo-uricosuric hyperuricemia leading to gout at an early age.
PubMedID- 22870483 During the past few years two novel therapeutic agents have been approved by the us food and drug administration for the treatment of hyperuricemia in patients with gout, one of them being febuxostat, a nonpurine selective inhibitor of xanthine oxidase.
PubMedID- 25889813 It was suggested that accumulation of visceral fat rather than subcutaneous fat is associated with metabolic abnormalities and hyperuricemia in patients with gout; therefore, we hypothesized that visceral fat accumulation was increased in non-obese gout patients.
PubMedID- 26515421 Recent epidemiological studies have indicated that hyperuricemia with or without gout increases the risk of cardiovascular diseases and mortality [1–6].
PubMedID- 23762766 hyperuricemia is associated with severe gout and kidney problems.
PubMedID- 25890021 For example, previous studies showed that in the pathogenesis of hyperuricemia, apoe polymorphisms in patients with gout were reported to be associated with reduced renal excretion of urates [17,18].
PubMedID- 25928556 Because low glomerular filtration rate (gfr) leads to hyperuricemia, ckd is associated with hyperuricemia and gout [4].
PubMedID- 22000646 Despite its potential advantage as an antioxidant, sustained hyperuricemia is associated with gout, renal diseases, hypertension, and cardiovascular diseases.
PubMedID- 23738826 A poor metabolic control may lead to long term complications, namely development of hepatocellular adenomas (hca), renal dysfunction, gout and nephrocalcinosis associated with hyperuricemia, and increased risk of pancreatitis, related to severe hypertrigliceridemia [1,2].
PubMedID- 24732692 The hypothetical cohort of 1,000 patients requiring allopurinol for preventing or treating gouty patients with hyperuricemia, and tophaceous gout was entered into the model.
PubMedID- 23133351 hyperuricemia can lead to diseases like gout where uric acid is deposited into tissues, especially in the joints [40].

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