Bibliografías temáticas / "Allopurinolo"

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Literatura académica sobre el tema ""Allopurinolo""

Autor: Grafiati
Publicado: 11 de marzo de 2023

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Artículos de revistas sobre el tema ""Allopurinolo""

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Russmann y Lauterburg. "Lebensbedrohliche Nebenwirkungen der Gichtbehandlung". Therapeutische Umschau 61, n.º 9 (1 de septiembre de 2004): 575–77. http://dx.doi.org/10.1024/0040-5930.61.9.575.

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Die Behandlung der Gicht mit Allopurinol kann schwere unerwünschte Wirkungen zur Folge haben. Neben dem häufigen Hautausschlag unter Allopurinol kann ein selteneres Hypersensitivitäts-Syndrom mit Fieber, Hautexanthem (bis zum Lyell-Syndrom), Hepatopathie, Eosinophilie, Niereninsuffizienz und Vaskulitis lebensbedrohlich sein. Die Inzidenz dieser schweren Nebenwirkung kann wahrscheinlich mit einer der Nierenfunktion angepassten Reduktion der Dosis von Allopurinol gesenkt werden. Da Azathioprin und Mercaptopurin über die Xanthinoxidase, die durch Allopurinol gehemmt wird, metabolisiert werden, kann es bei gleichzeitiger Verabreichung zu lebensbedrohlichen Neutropenien kommen, wenn die Dosis des Allopurinols nicht um zirka 75% reduziert wird. Das urikosurisch wirkende Benzbromaron wurde kürzlich wegen schwerer Leberschädigungen vom Markt genommen.
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A. Wohaieb, Saleh. "Effects of Allopurinol on Ketone Body Metabolism and Tissue Lipid Peroxidation in Alloxan Diabetes in Rats". Iraqi Journal of Pharmaceutical Sciences ( P-ISSN: 1683 - 3597 , E-ISSN : 2521 - 3512) 15, n.º 1 (31 de marzo de 2017): 37–42. http://dx.doi.org/10.31351/vol15iss1pp37-42.

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The aim of the present study is to investigate whether or not xanthine oxidase (XO)–derived reactive oxygen species (ROS) may play a role in the pathogenesis of alloxan (ALX)–induced diabetes in rats using the specific XO inhibitor and hydroxyl radical scavenger, allopurinol The involvement of oxidative stress in ALX – diabetes was assessed by the measurement of plasma and various tissues lipid peroxides levels ( using thiobarbituric acid ( TBA ) reactive substances ). Furthermore, the ability of allopurinol to influence these and other biochemical parameters, including plasma and urine ketones levels were also investigated in diabetic rats. Rats were divided into four groups: control, untreated diabetic, allopurinol – treated diabetic, and insulin – treated diabetics. At the end of the one week experimental period, blood and tissue samples were obtained from anesthesized animals for the measurement of the above – mentioned parameters. Although the single intraperitoneal (i.p.) injection of allopurinol (25 mg/kg body wt.) 1h before or 1h after ALX injection (100 mg/kg body wt., i.p.) failed to prevent the induction of diabetes, it did lower ketonuria and the incidence of early ketosis–associated mortality in diabetic animals in comparison with non–allopurinol–treated diabetic rats. Subsequent administration of allopurinol (25 mg/kg body wt., i.p.) every 48 hr for 1wk (i.e., 3 additional doses) also decreased plasma ketone bodies levels as well as plasma and tissue (heart, liver, kidney, pancreas) lipid peroxides levels in comparison with non–allopurinol–treated diabetic rats. Daily insulin injection (9–12 U/kg body wt., S.C.) for 1wk period normalized all of the above–mentioned abnormalities. The present results suggest that XO–derived ROS play a minor role (if any) in the diabetogenic effect of ALX. On the other hand, although the mechanism (s) underlying the protective effects of allopurinol on the diabetic state is presently unknown, these effects may reflect a possible association between impaired ketone body metabolism and lipid peroxidation: and suggest an effect of allopurinol on ketone body metabolism.
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Kaoutar, Achehboune, Baybay Hanane, Douhi Zakia, Elloudi Sara y Zahra Mernissi Fatima. "Allopurinol: Attention to the Prescription!" Journal of Clinical Cases & Reports 3, S2 (30 de noviembre de 2020): 3–6. http://dx.doi.org/10.46619/joccr.2020.2.s2-1002.

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Allopurinol is a commun hypo-uricemic drug. However, it is main drug reported to be inducing toxidermy. Our goal is to encourage limiting the prescription of this drug and to reserve it for justified cases after some observations. A Retrospective study was conducted in the Dermatology department between 2012 and 2019. We collected all toxidermy cases following Allopurinol. During the study period,39 cases of severe Allopurinol toxidermia, including 22 women and 17 men, a sex ratio of 0.77. The average age was 65 years old. Most of the patients were "poly-medicated". The average time between medication and clinical symptoms was 28.25 days. Clinical manifestations were: macula-papular rash in 12 cases (30%), erythroderma in 14 cases (35%), purpura in 7 cases (17%) and mucosal involvement in 20 cases. Fever in 29 cases, a state of shock in 5 cases. 10 patients required a transfer in intensive care. On the balance sheet; eosinophilia was found in 23 cases, 18 cases of hepatic cytolysis, CPK mb was elevated in 17 cases, acute renal failure in 24 cases. The biopsy was performed in all cases confirming the toxidermy. The Drug reaction eosinophilia and systemic symptoms (DRESS) retained in 29 cases, Stevens-Johnson syndrome (SJS) in 2 cases, Lyell in 4 cases. The management involved stopping the incriminated drug (Allopurinol) and the introduction of an antihistamine and an emollient were prescribed in all patients. Topical steroid in 21 patients. Oral corticosteroid therapy in 14 patients. A bolus of corticosteroid was administered in 4 patients. The evolution was good for 30 patients (77%). However, we recorded 9 deaths in a context of septic shock and multi-visceral failure. In our series, Allopurinol was the cause of severe toxidermia including Lyell syndrome, StevensJohnson and DRESS syndrome. The severity of these diseases should encourage preserving it for the justified cases, and knowing how to adapt the dosage to the renal function, to introduce the treatment in a progressive way and to stop the treatment in case of less signs of toxidermy. The control of the use of this molecule would reduce the cases of this disease.
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Cortes, Jorge, Joseph O. Moore, Richard T. Maziarz, Meir Wetzler, Michael Craig, Jeffrey Matous, Selina Luger et al. "Control of Plasma Uric Acid in Adults at Risk for Tumor Lysis Syndrome: Efficacy and Safety of Rasburicase Alone and Rasburicase Followed by Allopurinol Compared With Allopurinol Alone—Results of a Multicenter Phase III Study". Journal of Clinical Oncology 28, n.º 27 (20 de septiembre de 2010): 4207–13. http://dx.doi.org/10.1200/jco.2009.26.8896.

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Purpose Rasburicase is effective in controlling plasma uric acid in pediatric patients with hematologic malignancies. This study in adults evaluated safety of and compared efficacy of rasburicase alone with rasburicase followed by oral allopurinol and with allopurinol alone in controlling plasma uric acid. Patients and Methods Adults with hematologic malignancies at risk for hyperuricemia and tumor lysis syndrome (TLS) were randomly assigned to rasburicase (0.20 mg/kg/d intravenously days 1-5), rasburicase plus allopurinol (rasburicase 0.20 mg/kg/d days 1 to 3 followed by oral allopurinol 300 mg/d days 3 to 5), or allopurinol (300 mg/d orally days 1 to 5). Primary efficacy variable was plasma uric acid response rate defined as percentage of patients achieving or maintaining plasma uric acid ≤ 7.5 mg/dL during days 3 to 7. Results Ninety-two patients received rasburicase, 92 rasburicase plus allopurinol, and 91 allopurinol. Plasma uric acid response rate was 87% with rasburicase, 78% with rasburicase plus allopurinol, and 66% with allopurinol. It was significantly greater for rasburicase than for allopurinol (P = .001) in the overall study population, in patients at high risk for TLS (89% v 68%; P = .012), and in those with baseline hyperuricemia (90% v 53%; P = .015). Time to plasma uric acid control in hyperuricemic patients was 4 hours for rasburicase, 4 hours for rasburicase plus allopurinol, and 27 hours for allopurinol. Conclusion In adults with hyperuricemia or at high risk for TLS, rasburicase provided control of plasma uric acid more rapidly than allopurinol. Rasburicase was well tolerated as a single agent and in sequential combination with allopurinol.
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Singh, Jasvinder A. y John D. Cleveland. "Hypersensitivity reactions with allopurinol and febuxostat: a study using the Medicare claims data". Annals of the Rheumatic Diseases 79, n.º 4 (5 de febrero de 2020): 529–35. http://dx.doi.org/10.1136/annrheumdis-2019-216917.

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ObjectiveTo assess the risk of hypersensitivity reactions (HSRs) with allopurinol and febuxostat in a population-based study.MethodsWe used the 5% Medicare beneficiary sample (≥65 years) from 2006 to 2012 to identify people with a newly filled prescription for allopurinol, febuxostat or colchicine. We used multivariable-adjusted Cox regression analyses to compare the hazard ratio (HR) of incident HSRs with allopurinol or febuxostat use versus colchicine use; separate analyses were done in people exposed to allopurinol. Propensity-matched analyses (5:1) compared hazards with allopurinol versus febuxostat.ResultsCrude incidence rates of HSRs were as follows: allopurinol, 23.7; febuxostat, 30.7; and colchicine, 25.6 per 1000 person-years. Compared with colchicine, allopurinol, febuxostat and febuxostat+colchicine were associated with significantly higher HRs of HSRs, 1.32 (95% CI: 1.10 to 1.60) and 1.54 (95% CI: 1.12 to 2.12) and 2.17 (95% CI: 1.18 to 3.99), respectively. In propensity-matched analyses, febuxostat did not significantly differ from allopurinol; HR for HSRs was 1.25 (95% CI: 0.93 to 1.67). Compared with allopurinol start dose <200 mg/day, allopurinol start dose ≥300 mg/day, diabetes and female sex were associated with significantly higher hazard of HSRs, 1.27 (95% CI: 1.12 to 1.44), 1.21 (95% CI: 1.00 to 1.45) and 1.32 (95% CI: 1.17 to 1.48), respectively. The majority (69%) of HSRs occurred in the outpatient setting.ConclusionsCompared with colchicine, allopurinol and febuxostat similarly increased the risk of HSRs. Allopurinol and febuxostat did not differ from each other. In allopurinol users, starting dose, female sex and diabetes increased this risk, findings that need further study.
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&NA;. "Allopurinol". Reactions Weekly &NA;, n.º 1380 (diciembre de 2011): 6. http://dx.doi.org/10.2165/00128415-201113800-00019.

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&NA;. "Allopurinol". Reactions Weekly &NA;, n.º 1384 (enero de 2012): 6–7. http://dx.doi.org/10.2165/00128415-201213840-00022.

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&NA;. "Allopurinol". Reactions Weekly &NA;, n.º 1384 (enero de 2012): 7. http://dx.doi.org/10.2165/00128415-201213840-00027.

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&NA;. "Allopurinol". Reactions Weekly &NA;, n.º 1395 (marzo de 2012): 6. http://dx.doi.org/10.2165/00128415-201213950-00016.

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&NA;. "Allopurinol". Reactions Weekly &NA;, n.º 723 (octubre de 1998): 6–7. http://dx.doi.org/10.2165/00128415-199807230-00019.

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Tesis sobre el tema ""Allopurinolo""

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MAILHOS, FABIEN. "Intolerance severe a l'allopurinol : etude sur deux cas". Toulouse 3, 1990. http://www.theses.fr/1990TOU31240.

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Thanassoulis, George. "Gout and allopurinol use in heart failure". Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103495.

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Heart failure (HF) and gout are common medical conditions that lead to significant morbidity and mortality in Canada and the US. We conducted a population-based nested case-control study to investigate the associations between gout, allopurinol use and HF outcomes using administrative data from the province of Quebec. Our analysis demonstrates that a history of gout is associated with increased HF readmission and death in HF patients (adjusted RR 1.63; 95% confidence interval (CI) 1.48-1.80). We also show that chronic allopurinol use, a common medication for gout, is associated with reductions in adverse outcomes in HF patients with a history of gout (adjusted RR 0.69, 95% CI 0.60-0.79). Due to the observational nature of our study, residual confounding due to unknown or unmeasured confounding could still bias our findings. Herein, we present a novel method to estimate and control for such confounding by estimating the confounding risk ratio during the null induction time. Use of this method is illustrated using an example from the literature and we discuss the assumptions, limitations and statistical considerations of our method.
L'insuffisance cardiaque (IC) et la goutte sont des conditions médicales fréquentes qui sont des causes importantes de morbidité et de mortalité au Canada et aux États-Unis. Nous avons entrepris une étude populationelle « case-control » avec des données administratives de la province du Québec pour investiguer l'association entre la goutte ou l'allopurinol avec le prognostic de l'IC. Notre analyse démontre qu'un antécedent de goutte est associé à une hausse du taux de réadmissions à l'hôpital pour l'IC et une augmentation de la mortalité parmi les patients avec IC (RR ajusté 1.63; 95% CI 1.48-1.80). Cependant, nous demontrons que la prise d'allopurinol est associée à une réduction de la réadmission à l'hôpital pour IC et une diminution de la mortalité (RR ajusté 0.69, 95% CI 0.60-0.79). Comme notre étude est observationelle, les facteurs confondants qui ne sont pas disponibles ou qui sont inconnus peuvent biaiser nos résultats. Nous présentons une nouvelle méthode qui permet l'estimation et le contrôle de ces facteurs confondants basée sur l'estimation du « confounding rate ratio ». Nous présentons un example utilisant cette nouvelle méthode, et nous discutons les suppositions, les limitations et les considérations statistiques de cette méthode.
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Shearer, Fiona. "The acute effects of allopurinol in angina". Thesis, University of Dundee, 2018. https://discovery.dundee.ac.uk/en/studentTheses/0614d464-ccb4-4e74-a98a-135700215ee7.

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Angina is pain or constricting discomfort that typically occurs at the front of the chest and may radiate to neck, shoulders, jaw or arms and is precipitated by physical exertion or emotional stress which increases myocardial demand. Allopurinol has been shown to prolong the time to ST depression on ETT, which is a marker of ischaemia. This may be via a number of mechanisms including effect on oxidative stress and endothelial stability. This three arm cross over, double blind study was designed to establish the time of onset of effect of allopurinol and the optimal dose. The primary outcome was time to ST depression. Secondary outcomes were total exercise time and effect on troponin, oxidised LDL, CRP and BNP levels. There were 26 participants with a mean age of 70.1 and 77% male. 5 participants did not complete the study. Due to challenges of recruitment this study was underpowered but it did appear at 24 hours post study drug administration there was an impact on both time to ST depression and total exercise time in the active arms of the trial. Furthermore it was shown total exercise time improved irrespective of whether the participant was in an active or placebo arm. This may suggest the protocol was contaminated by the training effect of repeated high intensity exercise.
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Boussellier, Michael Diquelou Armelle. "Intérêt de l'utilisation de l'allopurinol dans l'insuffisance cardiaque chez le chien étude bibliographique /". [S.l.] : [s.n.], 2008. http://oatao.univ-toulouse.fr/1212/1/picco_1212.pdf.

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Rutherford, Elaine. "The effect of allopurinol on left ventricular mass in haemodialysis patients". Thesis, University of Dundee, 2019. https://discovery.dundee.ac.uk/en/studentTheses/22ac9573-7fde-482a-91bf-c253cdd95252.

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Szwejkowski, Benjamin. "Allopurinol regresses left ventricular hypertrophy in patients with type 2 diabetes". Thesis, University of Dundee, 2014. https://discovery.dundee.ac.uk/en/studentTheses/530c354b-f49b-4c84-af2f-59418aa11db6.

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Left Ventricular Hypertrophy (LVH) is common in Type 2 Diabetes (T2DM) and despite optimal treatment of blood pressure can still persist. We know LVH is a cardiovascular (CV) risk factor in its own right and contributes to high CV event rates in patients with T2DM. Apart from hypertension, other factors contribute to the development of LVH in patients with T2DM, in particular oxidative stress (OS) has been implicated in LVH development. Allopurinol is a potent anti-oxidant, acting by blocking the enzyme Xanthine Oxidase, and has been previously shown to reduce vascular OS. Therefore the main aim of this thesis was to investigate whether allopurinol regresses LVH in patients with T2DM. The trial design was a randomised, double blind, placebo controlled study in 66 patients with T2DM with echocardiographic evidence of LVH. Allopurinol 600mg/day or placebo was given for nine months over the study period. The primary outcome was reduction in left ventricular mass (LVM) as calculated by cardiac magnetic resonance imaging (CMR) at baseline and at nine months follow-up. The secondary end-points were change in flow mediated dilatation (FMD) and augmentation index (AIx). Allopurinol significantly reduced absolute LVM (-2.65 ± 5.91g and placebo group +1.21 ± 5.10g (p=0.012)) and LVM indexed to body surface area (-1.32 ± 2.84g/m2 and placebo group +0.65 ± 3.07g/m2 (p=0.017)). When analysis was made of high and low baseline LVM then the effects of allopurinol were exaggerated in the high LVM mass group. No significant change was seen in either FMD or AIx. This thesis shows that allopurinol regresses LVM in patients with T2DM and LVH and controlled blood pressure. Regressing LVH has been shown previously to improve CV mortality and morbidity. Therefore allopurinol may become a useful therapy to reduce CV events in T2DM patients with LVH.
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Liu, Shiu Cheong Patrick. "Effects of xanthine oxidase inhibitors in pulmonary hypertension associated with chronic lung disease". Thesis, University of Dundee, 2019. https://discovery.dundee.ac.uk/en/studentTheses/ee8678d8-e7c7-498c-b501-ff5522f32ae5.

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Chronic lung diseases are often complicated with pulmonary hypertension (PH). This can lead to disability and poor prognosis. Oxidative stress has been implicated in the development of PH and right ventricular hypertrophy (RVH).A possible new way to treat lung disease related pulmonary hypertension is allopurinol (a xanthine oxidase inhibitor) which decreases both uric acid and oxidative stress. We hypothesised that allopurinol could regress RVH in patients with pulmonary hypertension associated with chronic lung disease (PH-CLD).In a double-blind, randomised controlled clinical trial, 72 patients with PH-CLD (93% diagnosed with chronic obstructive pulmonary disease and 17% with interstitial lung disease) were randomised to receive either allopurinol 300 mg twice daily or placebo for twelve months. The primary outcome was the mean change in right ventricular mass (RVM) as assessed by cardiac magnetic resonance imaging (CMRI) at twelve months. The secondary outcomes were the change in other cardiac parameters measured by CMRI, St George's Respiratory Questionnaire, Short Form 36, spirometry and six-minute walk test (6MWT).The mean age was 71 years, the mean FEV1 was 60% with mean resting SaO2 of 96%. After 12 months, there was no significant change in RVM. There were also no significant changes in other cardiac parameters measured on CMRI, quality of life questionnaires, spirometry and 6MWT. Post-hoc subgroup analysis showed that allopurinol reduced RVM (allopurinol -6.16 g vs placebo 0.75 g, p = 0.02) in COPD patients with more severe airflow limitation. Patients with higher NT-proBNP (> 489 pg/ml) had a greater improvement in left ventricular ejection fraction with allopurinol 5.12 vs placebo -1.62, p = 0.02.In summary, allopurinol had no overall impact but reduced RV mass in COPD patients with more severe airflow limitation. Further studies are warranted to assess the longer term impact of allopurinol in more severe COPD.
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Ko, Robert K. M. "Molecular aspects of myocardial ischemia/reperfusion injury and the protective effects of allopurinol". Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/30699.

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A growing body of evidence has now accumulated supporting the involvement of oxygen-derived free radicals in the development of myocardial ischemia/reperfusion (I/R) injury. We have, therefore, undertaken the present study to examine (1) I/R-related alterations in myocardial antioxidant capacity in pentobarbital anesthetized open-chest rabbits subjected to left circumflex coronary artery ligation followed by reperfusion; (2) the protective effects of pretreatrnent with allopurinol or the 21-aminosteroid U74006F; (3) alternative mechanisms to xanthine oxidase inhibition for allopurinol protection against I/R injury; and (4) the effect of allopurinol treatment on the antioxidant capacity of erythrocytes in pigs used in a heart-lung transplantation study. In the rabbit myocardium, a marked impairment in myocardial antioxidant capacity developed in association with the onset of irreversible injury, as reflected in the enhancement in glutathione (GSH) depletion and formation of thiobarbituric acid-reactive substances (TBARS) following in vitro incubation of tissue homogenate with tert-butylhydroperoxide (TBHP). During the course of post-ischemic reperfusion, the protracted time-course of alterations in antioxidant capacity dissociated them from the early burst of radical formation known to occur at the onset of post-ischemic reperfusion of the myocardium. When the time-dependent changes in functional indices of antioxidant status (TBHP-induced GSH depletion and formation of TBARS) were analysed in relation to activities of antioxidant enzymes, evidence suggestive of functionally relevant impairments in Cu,Zn-superoxide dismutase (Cu,Zn-SOD) and glutathione reductase (GRD) activities was found. These results and our demonstration of significant decreases in the activity of GSH-dependent antioxidant enzymes under acidotic conditions suggest that a transient impairment in the functioning of antioxidant enzymes may be involved in triggering irreversible myocardial I/R injury. Repetitive brief episodes of I/R produced a progressive decrease in myocardial ATP levels, which was not associated with any detectable changes in myocardial antioxidant capacity. Ischemic preconditioning produced by brief episodes of I/R did not affect the severity of subsequently induced I/R injury. These results suggest that brief episodes of myocardial ischemia do not produce oxidative tissue damage and the ischemia-induced depletion in myocardial ATP level is at least partially dissociable from the I/R-related impairment in tissue antioxidant capacity. Isolated Langendorff-perfused rabbit hearts subjected to I/R did not show any changes in antioxidant capacity. However, when intact hearts were subjected to ischemia in vivo and a subsequent reperfusion in vitro, an impairment in myocardial antioxidant capacity became apparent. These results suggest that blood elements, possibly activated neutrophils, may be a crucial factor involved in the development of I/R-induced oxidant injury. Chronic allopurinol pretreatment (1 mg/ml in drinking water or approximately 75 mg/kg/day) for 7 days prior to ischemia provided significant protection against I/R-induced alterations in myocardial antioxidant capacity, but not the decrease in tissue ATP levels. This chronic allopurinol regimen was found to enhance myocardial GRD activity in nonischemic tissue. In addition, both allopurinol and oxypurinol inhibited the transition metal ion-catalysed ascorbate oxidation and lipid peroxidation in vitro, likely as a consequence of their metal chelating properties. Similarly, myoglobin-TBHP-catalysed oxidation of uric acid and lipid peroxidation were also suppressed by allopurinol. All these suggest that allopurinol may favorably alter myocardial antioxidant capacity directly by virtue of its transition metal chelating properties and its antioxidant actions in myoglobin-mediated oxidative processes. The acute administration of 21-aminosteroid U74006F (3 mg/kg, i.v) under conditions comparable to those known to protect against trauma-induced damage in the central nervous system failed to reduce manifestations of oxidative injury in rabbit hearts subjected to ischemia and reperfusion. Although reactive oxy-radicals have been implicated in both types of tissue damage, the observed difference in susceptibility to protection by this steroidal antioxidant suggests that the molecular mechanisms involved are not identical. In the heart-lung transplantation study, erythrocytes from allopurinol-treated pigs (given repeatedly at an oral dose of 50 mg/kg) showed a time/dose-dependent increase in antioxidant capacity as reflected in the decrease in malondialdehyde production following in vitro oxidative challenge. The extent of red cell protection in both donor and recipient animals correlated significantly with the functional viability of the transplanted lung tissue, as assessed by tissue water content. These results suggest that the measurement of erythrocyte antioxidant capacity may provide an useful assessment of generalized alterations in tissue antioxidant status produced by pharmacological interventions.
Medicine, Faculty of
Anesthesiology, Pharmacology and Therapeutics, Department of
Graduate
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Robertson, Alan. "Allopurinol as a possible oxygen sparing agent during exercise in peripheral arterial disease". Thesis, University of Dundee, 2014. https://discovery.dundee.ac.uk/en/studentTheses/6d3e342c-d2fb-4cec-b678-082d1fb2e067.

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Patients with peripheral arterial disease (PAD) can only walk so far before they get leg pain (intermittent claudication) and have to stop. They are also at risk in the future of needing amputation of one of their limbs. Allopurinol is a new possible treatment for this condition as it has been shown in coronary arterial disease to prolong exercise before angina pain occurs. This is thought to be because allopurinol can both prevent oxygen wastage in tissues and prevent the formation of harmful oxidative stress. We hypothesised that allopurinol could prolong the time to leg pain in participants with PAD. In a double-blind, randomised controlled clinical trial 50 participants with PAD were randomised to receive either allopurinol 300mg twice daily or placebo for six months. The primary outcome was change in exercise capacity on treadmill testing at six months. Secondary outcomes were six-minute walking distance, Walking Impairment Questionnaire, SF-36 QoL questionnaire, flow-mediated dilatation and oxidised LDL. Outcome measures were repeated mid-study and at end of study. The mean age of participants was 68.4 years (SD 1.2) with 39/50 (78%) male. Only five participants withdrew in the course of the study, two in the active group and three in the placebo group. There was a significant reduction in uric acid levels in those on active treatment of 52.1% (p<0.001), but no significant change in either the pain-free or the maximum distance they were able to walk. Other measures of exercise capacity, blood vessel function and the participants’ own assessment of their health and walking ability also did not change during the course of the study. In summary, although allopurinol has been shown to be of benefit in a number of other diseases, in this study there was no evidence of any improvement following treatment in patients with peripheral arterial disease.
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Rathore, Dinesh Singh. "Effect of allopurinol and hemin on some biological markers of aging in broiler chickens". Morgantown, W. Va. : [West Virginia University Libraries], 1999. http://etd.wvu.edu/templates/showETD.cfm?recnum=784.

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Thesis (M.S.)--West Virginia University, 1999.
Title from document title page. Document formatted into pages; contains xi, 77 p. : ill. Vita. Includes abstract. Includes bibliographical references.
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Más fuentes

Libros sobre el tema ""Allopurinolo""

1

Harissulis, Stefanos y W. Ewald. Therapie mit Allopurinol. Heidelberg: Steinkopff, 1986. http://dx.doi.org/10.1007/978-3-642-72397-1.

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Devlin, John W. A concurrent allopurinol utilization review. London: Victoria Hospital, 1989.

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3

Parker, Philip M. y James N. Parker. Allopurinol: A medical dictionary, bibliography, and annotated research guide to Internet references. San Diego, CA: ICON Health Publications, 2004.

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Harissulis, Stefanos. Therapie mit Allopurinol: Klinische Wirksamkeit verschiedener Allopurinol-Präparate. Steinkopff-Verlag, 1986.

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Harrisulis, S. y W. Ewald. Therapie Mit Allopurinol: Klinische Wirksamkeit Verschiedener Allopurinol-Präparate. Steinkopff, Dietrich, 2013.

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Publications, ICON Health. Allopurinol - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References. ICON Health Publications, 2004.

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Dalbeth, Nicola. Urate-lowering therapy agents. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198748311.003.0009.

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Xanthine oxidase (allopurinol or febuxostat) is considered first-line urate-lowering therapy. Combination therapy with uricosuric agents may be required. The choice of urate-lowering therapy is dictated by co-morbidities, particularly renal and hepatic impairment. Appropriate monitoring for drug adverse effects as well as serum urate to ensure targets are achieved is required.
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Dalbeth, Nicola. Gout. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0141.

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Gout is a common and treatable disorder of purine metabolism. Gout typically presents as recurrent self-limiting episodes of severe inflammatory arthritis affecting the foot. In the presence of persistent hyperuricaemia, tophi, chronic synovitis, and joint damage may develop. Diagnosis of gout is confirmed by identification of monosodium urate (MSU) crystals using polarizing light microscopy. Hyperuricaemia is the central biochemical cause of gout. Genetic variants in certain renal tubular urate transporters including SLC2A9 and ABCG2, and dietary factors including intake of high-purine meats and seafood, beer, and fructose, contribute to development of hyperuricaemia and gout. Gout treatment includes: (1) management of the acute attack using non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids, or low-dose colchicine; (2) prophylaxis against gout attacks when commencing urate-lowering therapy (ULT), with NSAIDs or colchicine; and (3) long-term ULT to achieve a target serum urate of less than 0.36 mmol/litre. Interleukin (IL)-1β‎ is a central mediator of acute gouty inflammation and anti-IL-1β‎ therapies show promise for treatment of acute attacks and prophylaxis. The mainstay of ULT remains allopurinol. However, old ULT agents such as probenecid and benzbromarone and newer agents such as febuxostat and pegloticase are also effective, and should be considered in patients in whom allopurinol is ineffective or poorly tolerated. Management of gout should be considered in the context of medical conditions that frequently coexist with gout, including type 2 diabetes, hypertension, dyslipidaemia, and chronic kidney disease. Patient education is essential to ensure that acute gout attacks are promptly and safely managed, and long-term ULT is maintained.
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Dalbeth, Nicola. Gout. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0141_update_003.

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Gout is a common and treatable disorder of purine metabolism. Gout typically presents as recurrent self-limiting episodes of severe inflammatory arthritis affecting the foot. In the presence of persistent hyperuricaemia, tophi, chronic synovitis, and joint damage may develop. Diagnosis of gout is confirmed by identification of monosodium urate (MSU) crystals using polarizing light microscopy. Hyperuricaemia is the central biochemical cause of gout. Genetic variants in certain renal tubular urate transporters including SLC2A9 and ABCG2, and dietary factors including intake of high-purine meats and seafood, beer, and fructose, contribute to development of hyperuricaemia and gout. Gout treatment includes: (1) management of the acute attack using non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids, or low-dose colchicine; (2) prophylaxis against gout attacks when commencing urate-lowering therapy (ULT), with NSAIDs or colchicine; and (3) long-term ULT to achieve a target serum urate of less than 0.36 mmol/litre. Interleukin (IL)-1β‎ is a central mediator of acute gouty inflammation and anti-IL-1β‎ therapies show promise for treatment of acute attacks and prophylaxis. The mainstay of ULT remains allopurinol. However, old ULT agents such as probenecid and benzbromarone and newer agents such as febuxostat and pegloticase are also effective, and should be considered in patients in whom allopurinol is ineffective or poorly tolerated. Management of gout should be considered in the context of medical conditions that frequently coexist with gout, including type 2 diabetes, hypertension, dyslipidaemia, and chronic kidney disease. Patient education is essential to ensure that acute gout attacks are promptly and safely managed, and long-term ULT is maintained.
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Zboncak, Allison. ALLOPURINOL: Most Potent Medication for the Treatment of Gout or Kidney Stones, and to Decrease Levels of Uric Acid in People Who Are Receiving Cancer Treatment. Independently Published, 2019.

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Capítulos de libros sobre el tema ""Allopurinolo""

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Beyer, Karl-Heinz. "Allopurinol". En Biotransformation der Arzneimittel, 38–39. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74386-3_9.

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Chen, Pei, Shuen-Iu Hung, Shih-Yang Chen y Yuan-Tsong Chen. "Allopurinol". En Pharmacogenomic Testing in Current Clinical Practice, 213–23. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-283-4_13.

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Mehlhorn, Heinz. "Allopurinol". En Encyclopedia of Parasitology, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27769-6_115-2.

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Mehlhorn, Heinz. "Allopurinol". En Encyclopedia of Parasitology, 94. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-43978-4_115.

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de Groot, Anton C. "Allopurinol". En Monographs In Contact Allergy, 72–73. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003158004-20.

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Harissulis, Stefanos y W. Ewald. "Einleitung und Fragestellung". En Therapie mit Allopurinol, 1–46. Heidelberg: Steinkopff, 1986. http://dx.doi.org/10.1007/978-3-642-72397-1_1.

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Harissulis, Stefanos y W. Ewald. "Material und Methode". En Therapie mit Allopurinol, 47–55. Heidelberg: Steinkopff, 1986. http://dx.doi.org/10.1007/978-3-642-72397-1_2.

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Harissulis, Stefanos y W. Ewald. "Ergebnisse". En Therapie mit Allopurinol, 56–102. Heidelberg: Steinkopff, 1986. http://dx.doi.org/10.1007/978-3-642-72397-1_3.

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Harissulis, Stefanos y W. Ewald. "Diskussion". En Therapie mit Allopurinol, 103–9. Heidelberg: Steinkopff, 1986. http://dx.doi.org/10.1007/978-3-642-72397-1_4.

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Harissulis, Stefanos y W. Ewald. "Zusammenfassung". En Therapie mit Allopurinol, 110–11. Heidelberg: Steinkopff, 1986. http://dx.doi.org/10.1007/978-3-642-72397-1_5.

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Actas de conferencias sobre el tema ""Allopurinolo""

1

Giles, Rachel. "Allopurinol disappoints in ALL-HEART". En ESC Congress 2022, editado por Marc Bonaca. Baarn, the Netherlands: Medicom Medical Publishers, 2022. http://dx.doi.org/10.55788/52a39bf1.

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Sukmawan, Yedy Purwandi, Keni Idacahyati y Wina Widiyanti. "Allopurinol Administration: When is More Effective?" En 2nd Bakti Tunas Husada-Health Science International Conference (BTH-HSIC 2019). Paris, France: Atlantis Press, 2020. http://dx.doi.org/10.2991/ahsr.k.200523.077.

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Liu Shiu Cheong, Patrick, Brian Lipworth, Jonathan Weir-Mccall y Allan Struthers. "Allopurinol reduces RV mass in patients with severe COPD". En ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.oa1635.

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Fleischmann, R., P. Winkle, JN Miner, X. Yan, L. Hicks, S. Valdez, J. Hall y M. Hernandez-Illas. "AB0880 Pharmacodynamic effects and safety of verinurad (RDEA3170) in combination with allopurinol versus allopurinol alone in adults with gout: a phase 2a, open-label study". En Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.5429.

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Mrug, Sylvie, Catheryn Orihuela, Elizabeth Rahn, Kenneth Saag y Angelo Gaffo. "AB0867 DEPRESSIVE SYMPTOMS INFLUENCE SUCCESS OF ALLOPURINOL AS URATE LOWERING THERAPY". En Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.1295.

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Sung, YY, YS Lee, HK Kim y DS Kim. "Synergistic anti-hyperuricemic effect of combined medication of Alpinia oxyphylla and Allopurinol". En 67th International Congress and Annual Meeting of the Society for Medicinal Plant and Natural Product Research (GA) in cooperation with the French Society of Pharmacognosy AFERP. © Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-3400092.

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Zlatkovic-Svenda, Mirjana y Marija Radak-Perovic. "AB0895 EFICACY AND SAFETY OF ALLOPURINOL WHILE TITRATING HYPERURICAEMIA IN GOUTY PATIENTS". En Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.3490.

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Asaiphanit, S. y P. Narongroeknawin. "SAT0371 Factors associated with allopurinol adherence and treatment outcome among gout patients". En Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.2252.

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Hepburn, AL, MB Hogarth, SG Ball, SA Kaye y MD Feher. "SAT0100 Fenofibrate reduces serum urate in patients with hyperuricaemia established on allopurinol". En Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.483.

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Puntoni, Matteo, Daniela Branchi, Alessandra Argusti, Silvia Zanardi, Cristiano Crosta, Emanuele Meroni, Francesco Munizzi et al. "Abstract A69: Randomized, presurgical study of allopurinol vs. placebo in subjects with colorectal adenomas". En Abstracts: AACR International Conference on Frontiers in Cancer Prevention Research‐‐ Nov 7-10, 2010; Philadelphia, PA. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1940-6207.prev-10-a69.

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Informes sobre el tema ""Allopurinolo""

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Xie, Hong, Nan Hu, Ting Pan, Jun-Cai Wu, Deng-Chao Wang y Miao Yu. Effectiveness and safety of different doses of febuxostat compared with allopurinol in the treatment of hyperuricemia: A meta-analysis of randomized controlled trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, noviembre de 2022. http://dx.doi.org/10.37766/inplasy2022.11.0017.

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