Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Copresent rheumatoid arthritis (RA) and gout is seldom reported. This study summarizes the findings of eight cases of copresent RA and gout and compares them with 31 pure RA cases. Additional reported cases were retrieved from the current literature by Medline search. Patients with copresent RA and gout were older (p = 0.014) and predominantly male (p < 0.01). Synovial fluid, positive for urate crystals, was aspirated most frequently from the knee (five out of eight), followed by the first metatarsophalangeal joint (three out of eight). Serum creatinine and urate levels in the copresent group were significantly higher (p < 0.01, both), and serum hemoglobin was lower (p = 0.04) than those with pure RA. Copresent subjects had much lower percentage of positive rheumatoid factor (RF) tests than patients with pure RA (37.5 vs 80.6%). Only one copresent subject had both RF and anti-cyclic citrullinated peptide antibody. Of copresent subjects, 75% had gouty arthritis before diagnosis of RA, which is consistent with earlier reports. Seven copresent subjects had gout attacks under disease-modifying antirheumatic drug use. This study revealed that polyarthritis negative for RF in a previously gouty patient may be RA and vice versa. This combination occurs more frequently in males. Moreover, anti-CCP antibody examination is not helpful for this diagnosis. Therefore, physicians must obtain synovial fluid for analysis in joints with intense swelling, especially in old RA subjects with renal insufficiency or involvement of lower extremities. Conversely, RA must be considered in gouty patients with polyarticular involvement.
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PMID:Rare copresent rheumatoid arthritis and gout: comparison with pure rheumatoid arthritis and a literature review. 1900 47

Hyperuricemia is present in approximately 5% of the population. The vast majority is asymptomatic and at no clinical risk. Allopurinol, an analog of hypoxanthine, has been widely used in clinical practice for more than 30 years for the treatment of hyperuricemia and gout. Two percent of patients develop a mild exanthema when on this drug, which usually resolves after withdrawal of the drug. A syndrome characterized by exfoliative dermatitis, hepatitis, interstitial nephritis, and eosinophilia, termed allopurinol hypersensitivity syndrome, has been described, and its etiology related to the accumulation of one of allopurinol's metabolites, oxypurinol, of which clearance is decreased in the setting of renal insufficiency and the use of thiazide diuretics. The term DRESS (Drug Rash with Eosinophilia and Systemic Symptoms) Syndrome has been recently used to describe an entity presenting with similar features.
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PMID:Allopurinol-induced recurrent DRESS syndrome: pathophysiology and treatment. 1835 Apr 53

Gout is a crystal deposition disease. European and Japanese guidelines of management for gout recommend that serum urate concentration should be maintained below 6.0 mg/dL to promote crystal dissolution leading to prevention of recurrent gouty attack. Although allopurinol is recommended to be an adequate drug for urate lowering therapy in all gouty patients by European guideline, it is desirable that allopurinol is indicated in patients with overproduction type and benzbromarone in patients with underexcretion type, recommended by Japanese guideline. Asymptomatic hyperuricemia dose not equate to gout. As there is no evidence to support treatment of isolated hyperuricemia with urate lowering therapy currently, it is difficult to establish lowering goal of serum urate level in patients with asymptomatic hyperuricemia. Advice regarding lifestyle and treatment of associated comorbidity should be preferred to urate lowering therapy. However, urate lowering therapy may be indicated in high risk patients with hyperuricemia who are suffered from hypertension, diabetes mellitus, ischemic heart disease and renal insufficiency.
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PMID:[Establishment of therapeutic goal and plan of gout and asymptomatic hyperuricemia]. 1840 23

Inhibitors of xanthine oxidoreductase decrease production of uric acid, thus they act as hypouricemic drugs. Allopurinol, a prototypical xanthine oxidoreductase inhibitor, has been widely prescribed for treatment of gout and hyperuricemia. However, severe side effects of allopurinol may occur in patients with renal insufficiency. Recently, novel nonpurine selective inhibitors of xanthine oxidoreductase have been developed as potential alternatives to allopurinol. They have different inhibition mechanisms, utilizing the enzyme structure and the reaction mechanism. Such variation of the inhibition mechanism affects/in vivo/hypouricemic effects of the inhibitors.
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PMID:[Inhibitors of xanthine oxidoreductase]. 1840 26

An inhibitor of xanthine dehydrogenase (XDH), allopurinol, and uricosuric agents, probenecid and benzbromarone, have been used for more than 20 years in the treatment of hyperuricemia and gout. However, they are inconvenient in some situations. With regard to allopurinol, the dosage reduction is recommended in patients with renal insufficiency for preventing from rare adverse effect, bone marrow depression. Benzbromarone also has quite rare adverse effect, fulminant hepatitis. Recently several new therapies have been developed such as new XDH inhibitors urate transporter (URAT) 1 inhibitor, and a modified recombinant uricase. The dosage reduction of the new XDH inhibitors, febuxostat and FYX-051, is not necessary in patients with renal insufficiency because renal excretion is not main excretory pathway. JTT-552 is a first medicine targeting on URAT1. Polyethylene glycol (PEG) conjugation with recombinant uricase sufficiently reduces the immunogenicity to permit repeated dosing and the clinical trials are ongoing for patients with treatment-failure gout and hyperuricemia.
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PMID:[New antihyperuricemic medicine: febuxostat, Puricase, etc]. 1840 28

Febuxostat is a novel non-purine selective inhibitor of xanthine oxidase being developed for the management of hyperuricaemia in patients with gout. To critically review the clinical trial data, safety profile, pharmacology, and role of febuxostat for the treatment of hyperuricemia and gout. A review of the literatures on febuxostat was performed. All available human studies describing the pharmacology of febuxostat were included; including pharmacodynamics, efficacy, and safety of febuxostat. Available studies, patents and abstracts were identified through PubMed (1990-December 2006), Delphion, Cochrane Databases, and the American College of Rheumatology and European League Against Rheumatism Web sites. Key search terms were febuxostat, TMX-67, and TEI-6720. Febuxostat has been used at a dose of 80 to 120 mg for the management of hyperuricemia in gout. The drug is mainly metabolized by the liver and therefore mild-moderate renal impairment does not appear to impede its effect. However, given the limited long-term liver function safety data, failure of a large percentage of patients taking febuxostat to achieve the primary end point of serum urate levels less than 6.0 mg/dL, and higher drop out rate in the Febuxostat group in the clinical trials, the exact role of febuxostat as a urate-lowering therapy remains uncertain. Febuxostat is a promising alternative to allopurinol for the treatment of gout and hyperuricemia. The optimal length of colchicines prophylactic therapy for chronic gout, clinical significance of abnormal liver function tests results during therapy, and safety in patients with moderate or severe hepatic and renal insufficiency warrant further investigation. A post-market surveillance is also needed to address the safety issue of long-term febuxostat treatment.
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PMID:Febuxostat: a novel non-purine selective inhibitor of xanthine oxidase for the treatment of hyperuricemia in gout. 1907 68

Patients treated with cyclosporine after organ transplantation are at particular risk for the development of hyperuricemia and tophaceous gout. The appearance of tophi or clinical gout can occur within a short time of initiation of cyclosporine therapy. Treatment decisions for the often accelerated and severe gouty arthritis must take into consideration numerous drug interactions as well as the degree of allograft dysfunction, or renal insufficiency due to the effects of disease or medication.
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PMID:Gout in the transplant patient. 1907 10

Colchicine myopathy can complicate standard treatment of gout, especially in those patients with underlying renal insufficiency. The symptoms of this disorder are frequently insidious, and the diagnostic tests used in its evaluation are mostly nonspecific. It is important to be aware of this entity, as the discontinuation of colchicine will allow a prompt remission. Definitive diagnosis usually requires histologic examination where a characteristic vacuolar myopathy is typically present. Magnetic resonance imaging can be useful in the localization of optimal biopsy sites, although its use as a diagnostic modality in these patients is speculative.
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PMID:Colchicine neuromyopathy. 1907 54

Treatment of gout and hyperuricemia can be difficult in patients with chronic renal failure. At present, there is no study available comparing the efficacy of the most widely used agent, allopurinol, and the uricosuric benzbromarone for the control of hyperuricemia in patients with renal insufficiency. We describe an open, randomized, actively controlled, comparative trial in patients with clearance of creatinine from 20 to 80 mL/ min/1.73 m(2). Patients were randomized to take benzbromarone (100-200 mg/day) or allopurinol (100-300 mg/day). Outcome variables were the following: reduction of serum urate (Sur), Sur & tl; 6 mg/dL (357 micromol/L), reduction of gouty bouts and reduction of tophi. During 9-24 months of follow-up 36 patients were studied.The reduction of Sur was higher with benzbromarone, and only 1 of 17 patients taking benzbromarone did not achieve Sur < 6 mg/dL versus 7 of 19 taking allopurinol. Patients who did not reach optimal Sur levels with allopurinol were more frequently taking diuretics and showed lower fractional excretion of urate and higher initial Sur levels than patients with proper control of Sur. Seven patients with suboptimal control of serum urate were changed to benzbromarone 100 mg/day, which showed efficacy similar in those who were initially randomized to benzbromarone. A reduction of gouty bouts and size of tophi was observed after proper control of Sur. Allopurinol is effective in controlling hyperuricemia, but patients with higher initial Sur levels or taking concomitant diuretic therapy are less prone to reach therapeutic goals.Benzbromarone is useful for the control of hyperuricemia in patients with renal insufficiency even with concomitant diuretic administration; patients benefited include those who previously had no improvement by taking allopurinol.
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PMID:Treatment of chronic gout in patients with renal function impairment: an open, randomized, actively controlled study. 1907 56

Elevated plasma urate levels are associated with metabolic, cardiovascular, and renal diseases. Urate may also form crystals, which can be deposited in joints causing gout and in kidney tubules inducing nephrolithiasis. In mice, plasma urate levels are controlled by hepatic breakdown, as well as, by incompletely understood renal processes of reabsorption and secretion. Here, we investigated the role of the recently identified urate transporter, Glut9, in the physiological control of urate homeostasis using mice with systemic or liver-specific inactivation of the Glut9 gene. We show that Glut9 is expressed in the basolateral membrane of hepatocytes and in both apical and basolateral membranes of the distal nephron. Mice with systemic knockout of Glut9 display moderate hyperuricemia, massive hyperuricosuria, and an early-onset nephropathy, characterized by obstructive lithiasis, tubulointerstitial inflammation, and progressive inflammatory fibrosis of the cortex, as well as, mild renal insufficiency. In contrast, liver-specific inactivation of the Glut9 gene in adult mice leads to severe hyperuricemia and hyperuricosuria, in the absence of urate nephropathy or any structural abnormality of the kidney. Together, our data show that Glut9 plays a major role in urate homeostasis by its dual role in urate handling in the kidney and uptake in the liver.
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PMID:Glut9 is a major regulator of urate homeostasis and its genetic inactivation induces hyperuricosuria and urate nephropathy. 1970 26


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