Thèses sur le sujet « "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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Kwong, Ka-man, et 鄺嘉敏. « Loop-mediated isothermal amplification for the detection of HLA B*58:01 associated allopurinol hypersensitivity ». Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B4669982X.
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Pucheu, Chantal. « Etude de la goutte : traitement par l'allopurinol : données pharmacologiques et toxicologiques ». Bordeaux 2, 1992. http://www.theses.fr/1992BOR2P003.
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Jesus, Laura Caparica Ferreira de. « Xanthinuria secondary to allopurinolt therapy in dogs with canine leishmaniosis : current perspectives of the Iberian Veterinary Community ». Master's thesis, Universidade de Lisboa, Faculdade de Medicina Veterinária, 2021. http://hdl.handle.net/10400.5/21665.
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Dissertação de Mestrado Integrado em Medicina VeterináriaA xantinúria é o maior efeito adverso urinário em cães com leishmaniose tratados com alopurinol. Apesar das medidas preventivas e de maneio serem essenciais aquando desta terapêutica, a informação atualizada acerca do maneio da xantinúria é escassa. Este estudo visou investigar a abordagem médica da comunidade médico veterinária ibérica (IVC) na prevenção e maneio da xantinúria secundária ao tratamento com alopurinol na leishmaniose canina (CanLeish). Foi realizado um estudo transversal que teve como base o desenvolvimento de um questionário online e anónimo o qual foi difundido nas redes sociais da IVC. Este questionário detalhou as características gerais dos inquiridos; os regimes de prescrição do alopurinol; a interrupção do alopurinol e os seus efeitos adversos; a deteção, complicações e diagnóstico da xantinúria, assim como as medidas preventivas e reativas da xantinúria. Foram obtidas 230 respostas (131 de Portugal e 99 de Espanha). A maioria dos inquiridos segue as recomendações internacionais quando usa o alopurinol no tratamento da CanLeish. Um total de 54.6% destes afirmou já ter interrompido a terapêutica antes da sua duração ideal devido ao aparecimento de efeitos adversos além da xantinúria. Cerca de 71.6% dos inquiridos já detetou xantinúria, sendo o aparecimento de sinais clínicos urinários, a complicação mais comum. O método de diagnóstico mais usado para xantinúria é a urianálise. Considerando a prevenção da xantinúria, 75.1% dos clínicos informam os donos sobre a possibilidade de surgirem efeitos adversos associados ao alopurinol, mas apenas 28.4% consideram fazer a transição para uma dieta com baixo teor em purinas. A realização de urianálise e controlos imagiológicos é considerada por 71.2% e 31% dos inquiridos, respetivamente, para monitorizar o tratamento com alopurinol. Após ser detetada xantinúria, a abordagem terapêutica dos inquiridos consiste na interrupção do alopurinol, na diminuição da sua dose, no aumento da frequência de administração ou na sua substituição. Cerca de 72.1% tomam outras medidas, destacando-se a transição para uma dieta com baixo teor de purinas. A frequência estimada de xantinúria na prática clínica diária foi considerada inferior a 25% por 91.7% dos veterinários. Estes resultados revelam que a IVC está consciente da xantinúria como uma complicação comum do tratamento com alopurinol na CanLeish. Apesar das medidas preventivas serem por vezes negligenciadas, os Médicos Veterinários Ibéricos aparentam conhecer as diversas opções que podem ser usadas no maneio da xantinúria.
ABSTRACT - Xanthinuria secondary to allopurinolt therapy in dogs with canine leishmaniosis : current perspectives of the Iberian Veterinary Community - Xanthinuria is the major urinary adverse effect in dogs with leishmaniosis under allopurinol therapy. Although preventive and management measures are essential for its treatment, updated information about xanthinuria management in clinical practice is lacking. This study aimed to investigate the current medical approach of the Iberian Veterinary Community (IVC) on prevention and management of xanthinuria secondary to allopurinol therapy in canine leishmaniosis (CanLeish). A cross-sectional study was conducted based on an online anonymous survey which was diffused via Iberian social network veterinary groups. This questionnaire detailed: general characteristics of the respondents; allopurinol prescription regimens; allopurinol withdrawal and adverse effects; xanthinuria detection, complications, and diagnosis; xanthinuria preventive and reactive measures. A total of 230 answers were obtained from the IVC (131 from Portugal and 99 from Spain). Most clinicians follow international recommendations when using allopurinol in CanLeish therapies. A total of 54.6% of clinicians stated that they had stopped the therapy before its ideal duration due to the appearance of adverse effects other than xanthinuria. About 71.6% of clinicians have detected xanthinuria, being the appearance of urinary clinical signs, the most common complication detected. Urinalysis was the preferred diagnostic method to detect xanthinuria. Considering its prevention, 75.1% of clinicians inform owners about possible adverse effects of allopurinol therapies, although only 28.4% consider an appropriate dietary change to a low purine diet. Urinalysis and imaging controls are used by 71.2% and 31% of clinicians, respectively, to monitor allopurinol therapies. When facing xanthinuria, measures concerning allopurinol therapy are considered, such as discontinuing it, reducing its dosage, increasing its administration frequency, or replacing it. Also, 72.1% of clinicians take other measures, with emphasis on the transition to a low-purine diet. Finally, the estimated frequency of xanthinuria in their daily practice was considered less than 25%, by 91.7% of veterinary surgeons. These findings show that the IVC is aware that xanthinuria is a common complication in CanLeish allopurinol therapies. Although preventive measures are often neglected, clinicians seem to be conscious about the different options that can be used to manage xanthinuria.
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Mazali, Fernanda Cristina 1978. « Nefrotoxicidade experimental por ciclosporina : efeito protetor da normalização dos niveis de acido urico ». [s.n.], 2006. http://repositorio.unicamp.br/jspui/handle/REPOSIP/311154.
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Orientador: Marilda MazzaliDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
Made available in DSpace on 2018-08-08T15:27:17Z (GMT). No. of bitstreams: 1 Mazali_FernandaCristina_M.pdf: 3384913 bytes, checksum: 0d3a47a884265f3d5949b9aff82161a6 (MD5) Previous issue date: 2006
Resumo: Objetivo: Hiperuricemia é uma complicação freqüente da terapêutica com ciclosporina (CsA). Estudos anteriores demonstraram que a hiperuricemia exacerba a lesão intersticial e vascular no modelo experimental de nefrotoxicidade por CsA (CsA ntx). O presente estudo tem como hipótese que a normalização da uricemia preveniria o desenvolvimento da nefropatia crônica por CsA. Metodologia: A nefropatia crônica por CsA foi induzida em ratos machos, Sprague Dawley, através da injeção subcutânea diária de CsA (15mg/kg/dia), por um período de 7 semanas, em associação com dieta hipossódica (CSA). O efeito do controle da hiperuricemia foi determinado através do tratamento concomitante com um inibidor de xantina oxidase (alopurinol, 15mg/Kg/dia ? CSA/ALP) ou com um agente uricosúrico (benzbromarona, 15mg/Kg/dia, CSA/BENZ), em bebedouro. O grupo-controle incluiu ratos tratados com veículo (VEH, injeções SC diárias de óleo de oliva). Ao sacrifício foram realizadas análises funcionais e histológicas. Resultados: Os animais do grupo CSA desenvolveram hiperuricemia leve (ácido úrico 4.36 vs 2.49 mg/dl, CSA vs VEH, p<0.05), com hialinose arteriolar, atrofia tubular, fibrose intersticial em faixa, aumento de proliferação celular e redução da expressão de VEGF. O tratamento com alopurinol ou benzbromarona reduziu a lesão renal, assim como os níveis de ácido úrico e creatinina sérica (ácido úrico 2.03 CSA/ALP e 2.93 mg/dl, CSA/BENZ, p<0.05 vs VEH e CSA). Ambos os tratamentos reduziram a fibrose intersticial, a proliferação celular, infiltrado de macrófagos, expressão de osteopontina e hialinose arteriolar, em associação com restauro da expressão de VEGF, com proteção comparável entre as duas drogas. Conclusão: A hiperuricemia exacerba a nefropatia pela CsA em ratos. Tratamento concomitante com alopurinol ou benzbromarone reduz a severidade da lesão. Como ambas as drogas promovem proteção semelhante, concluímos que o efeito protetor é associado ao controle da hiperuricemia, mais importante que o efeito antioxidante do alopurinol
Abstract: Aim: Hyperuricemia frequently complicates cyclosporine (CSA) therapy. Previous studies have shown that hyperuricemia increases the interstitial and vascular lesions in the cyclosporine model. We therefore tested the hypothesis that normalization of uric acid could prevent the development of cyclosporine toxicity. Material and Methods: CSA nephropathy was induced by the administration of CSA (15 mg/kg/day) for 7 weeks to rats on a low salt diet (CSA group). The effect of preventing hyperuricemia on CSA nephropathy was determined by concomitant treatment with the xanthine oxidase inhibitor, allopurinol (CSA-ALP), or with the uricosuric, benzbromarone (CSA-BENZ), in the drinking water. Control groups included rats treated with vehicle (VEH). Histological and functional studies were determined at sacrifice. Results:. CSA treated rats developed mild hyperuricemia with arteriolar hyalinosis, tubular atrophy, striped interstitial fibrosis, increased cell proliferation and decreased VEGF expression. Treatment with either allopurinol (CSA-ALP) or benzbromarone (CSA-BENZ) reduced renal injury. Both treatments reduced interstitial fibrosis, cell proliferation, macrophage infiltration, osteopontin expression and arteriolar hyalinosis in association with restoration of VEGF expression. Both drugs provided comparable protection. Conclusions: An increase in uric acid exacerbates CSA nephropathy in the rat. Concomitant treatment with allopurinol or benzbromarone reduced the severity of renal disease. As both drugs promoted similar protection, we can conclude that the protective effect is associated with lowering uric acid levels, more than the antioxidant effect of allopurinol
Mestrado
Ciencias Basicas
Mestre em Clinica Medica
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Larrègle, Xavier. « Syndrome d'hypersensibilité à l'allopurinol associé à une hypophosphorémie et à des ostéonécroses multiples : à propos d'un cas ». Bordeaux 2, 1995. http://www.theses.fr/1995BOR2M185.
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Galarraga, Bernat. « Effect of anti-rheumatic therapy, folic acid supplementation and allopurinol on surrogate markers of cardiovascular disease in Rheumatoid arthritis ». Thesis, University of Dundee, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.505630.
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Igwe, Elias Nnanna. « Pathophysiological consequences of ischaemia reperfusion injury in peripheral artery occlusive disease : randomised double-blind placebo controlled trial of allopurinol ». Thesis, Imperial College London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.542963.
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Hartmann, Kai [Verfasser]. « Der Einfluss der Xanthinoxidasehemmer Allopurinol und Oxypurinol auf Gewichtsverlauf, Körperzusammensetzung und spontane Aktivität in einem Rattenmodell der Tumorkachexie / Kai Hartmann ». Berlin : Freie Universität Berlin, 2010. http://d-nb.info/1024365654/34.
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Picard-Ami, Luis A. (Luis Alberto). « The role of the xanthine oxidase enszymatic system and allopurinol in the ischemia reperfusion injury of experimental skin and myocutaneous flaps / ». Thesis, McGill University, 1991. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=59978.
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Complications resulting in flap failure and tissue necrosis constitute a serious and frequent problem to the plastic surgeon. Oxygen derived free radicals have been implicated in a variety of pathological processes including the ischemia reperfusion injury (IRI) occurring in skin flaps. Previous work with experimental rat skin flaps has suggested that the xanthine oxidase (XO) enzymatic system may be the major source for these toxic radicals. Before the clinician and the patient can benefit from these experimental findings an animal model which closer resembles the clinical setting needs to be tested. In the laboratory I examined the role of XO and its potent inhibitor allopurinol in the IRI of skin and myocutaneous flaps. I have found negligible levels of XO enzyme in pig and human skin when compared to the rat. I have also found that no beneficial effect on survival could be observed by treating the flaps with several different dose regimens of allopurinol. Based on my results I conclude that it is unlikely that xanthine oxidase is of major importance in the IRI of skin flaps.
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Plummer, Bradley N. « The Role of Oxidative Stress on Calcium-Mediated Arrhythmia Substrates Following Myocardial Infarction ». Case Western Reserve University School of Graduate Studies / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=case1370388993.
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Boucher, François. « Physiopathologie de l'ischémie myocardique et de la reperfusion chez le rat : implication des radicaux libres de l'oxygène ». Grenoble 1, 1992. http://www.theses.fr/1992GRE10019.
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Un processus d'ischemie myocardique se developpe quand un desequilibre apparait entre les besoins tissulaires et les apports en sang arteriel coronaire. Ce desequilibre entraine une cascade d'evenements biochimiques qui peuvent aboutir a terme a la necrose tissulaire. Cependant, les facteurs responsables de la mort cellulaire ne sont pas encore connus avec precision et il apparait que la production exacerbee de radicaux libres derives de l'oxygene pourrait etre largement impliquee dans l'initiation du processus necrotique. Le present travail propose une etude, par la technique du spin trapping, de la production de ces especes radicalaires, sur des modeles de coeurs isoles de rats, soumis a differentes situations experimentales d'ischemie et de reperfusion. La deuxieme partie de ce rapport est consacree a deux tentatives de protection pharmacologiques du myocarde ischemique, par un inhibiteur de la xanthine oxydase: l'allopurinol, et par un antioxydant: l'indapamide
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Araujo, Carolina Fumico Massuda. « Planejamento de ensaio clínico randomizado para avaliação da eficácia do uso de alopurinol no acidente vascular encefálico agudo ». Botucatu, 2019. http://hdl.handle.net/11449/181354.
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Orientador: Edison Iglesias de Oliveira VidalResumo: O acidente vascular cerebral (AVC) é uma das mais importantes afecções clínicas atualmente. A Organização Mundial de Saúde (OMS) define o AVC como sendo um comprometimento neurológico focal ou global que subitamente ocorre com sintomas persistindo para além de 24 horas, ou levando à morte, com provável origem vascular. O AVC agudo é responsável por uma carga substancial de morbidade e mortalidade no mundo representando a segunda causa global de anos de vida perdidos por incapacidade e respondendo por cerca de 10% de todas as mortes. No Brasil e nos Estados Unidos, o risco estimado de AVC ao longo da vida foi de 19,1% e 23,7%, respectivamente. A doença pode gerar sequelas e incapacidades resultando em grande impacto econômico e social. O alopurinol é uma droga inibidora da xantina oxidase (XO), a enzima que catalisa a conversão da hipoxantina em xantina e da xantina em ácido úrico a partir da degradação de purinas. Trata-se de medicamento antigo, seguro, disponível amplamente e com custo baixo utilizado principalmente para a prevenção de crises de gota. Além de seus efeitos sobre a redução dos níveis séricos de ácido úrico, sabe-se que o alopurinol também possui efeitos promissores em condições cardiovasculares. Esses efeitos têm o potencial de contribuírem para o tratamento de pacientes com AVC isquêmico agudo. Atualmente, o alopurinol não faz parte do tratamento padrão de pacientes com esse quadro no SUS ou internacionalmente, porém constitui um medicamento promissor a ser m... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: Stroke is one of the most important clinical conditions currently. The World Health Organization (WHO) defines stroke as a focal or global neurological impairment that suddenly occurs with symptoms persisting beyond 24 hours or leading to death with probable vascular origin. Acute stroke accounts for a substantial burden of morbidity and mortality in the world accounting for the second overall cause of Disability-Adjusted Life Year and accounting for about 10% of all deaths. In Brazil and the United States, the estimated lifetime risk of stroke was 19.1% and 23.7%, respectively. The disease can generate sequelae and incapacities resulting in great economic and social impact. Allopurinol is a xanthine oxidase (XO) inhibitor, the enzyme that catalyzes the conversion of hypoxanthine to xanthine and xanthine to uric acid from purine degradation. It is an old, safe, widely available and low cost drug used primarily for the prevention of gout attacks. In addition to its effects on the reduction of serum uric acid levels, it is known that allopurinol also has promising effects under cardiovascular conditions. These effects have the potential to contribute to the treatment of patients with acute stroke. Currently, allopurinol is not part of the standard treatment of patients with this condition in Brazilian Public Health System or internationally, but it is a promising drug to be better studied. It is known that the conduct of clinical trials with old medicines to discover new applic... (Complete abstract click electronic access below)
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Tollendal, Ana Luisa Silveira Vieira. « Avaliação dos níveis séricos de ácido úrico como fator de risco para o declínio da taxa de filtração glomerular em pacientes com doença renal crônica ». Universidade Federal de Juiz de Fora (UFJF), 2018. https://repositorio.ufjf.br/jspui/handle/ufjf/6722.
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Introdução: A doença renal crônica (DRC) se tornou uma preocupante questão de saúde pública em todo o mundo devido às suas crescentes incidência e prevalência e ao impacto em morbimortalidade por ela desencadeado. O tratamento da DRC se baseia na intervenção em seus fatores de risco. Entretanto, os fatores atualmente conhecidos e sua abordagem não têm sido suficientes para conter a doença. Por esse motivo, torna-se imprescindível a busca por outros fatores associados à sua patogênese. Nesse sentido, a hiperuricemia tem sido apontada, nas últimas décadas, como uma condição associada à DRC, porém sem que ainda tenha sido estabelecida uma associação causal entre ambas. Objetivos: 1. Avaliar as evidências sobre o impacto da hiperuricemia na incidência e progressão da DRC, através de revisão sistemática da literatura; 2. Avaliar o impacto dos níveis séricos de ácido úrico (AU) sobre o declínio da taxa de filtração glomerular (TFG) em uma população de pacientes com DRC. Métodos: Primeiramente, realizou-se revisão sistemática da literatura com busca por artigos publicados no período entre Janeiro de 2005 e Dezembro de 2016, utilizando-se a combinação de palavraschave “chronic renal insufficiency AND hyperuricemia AND uric acid” nos bancos de dados Lilacs e Pubmed. Os resumos dos artigos foram avaliados por dois pesquisadores, de acordo com os critérios de inclusão e exclusão estabelecidos. Na segunda fase do estudo, 788 pacientes incidentes no ambulatório de DRC do Centro Hiperdia Minas/Juiz de Fora tiveram seus registros eletrônicos analisados e o impacto dos níveis de AU na progressão da DRC foi avaliado. Resultados: Relativamente à revisão sistemática, foram encontrados 150 estudos envolvendo seres humanos, dos quais 22 foram elegíveis, 13 estudos avaliaram incidência e 11 avaliaram progressão da DRC (aumento de creatinina, variação da taxa de filtração glomerular, início de terapia renal substitutiva); dois avaliaram ambos os desfechos. Todos os treze artigos que avaliaram associação entre hiperuricemia e incidência de DRC mostraram associação positiva entre ambas. Uma metanálise avaliou impacto da hiperuricemia em 190.718 indivíduos e encontrou relação causal independente para incidência de DRC. Em relação à progressão da DRC, os estudos longitudinais apresentaram resultados conflitantes e três estudos randomizados controlados foram identificados, comparando um grupo tratado com alopurinol e um grupo controle, todos com melhora dos desfechos renais no grupo tratado. Os resultados da análise do banco de dados do Centro HIPERDIA mostraram que pacientes admitidos com hiperuricemia, ou seja, AU maior do que 6,8mg/dL, apresentaram risco quase duas vezes maior (IRR=1,91 95% IC: 1,21-3,00, p=0,005) de progressão rápida da DRC (TFG>5mL/min/ano). Além disso, para cada 1 mg/dL de aumento nos níveis basais de AU houve risco anual 48% maior de progressão rápida (IRR=1,48 95% IC:1,16-1,88, p=0,001). Conclusão: A revisão sistemática sugeriu que hiperuricemia se associa de forma independente com incidência de DRC, porém seu papel na progressão da doença ainda é controverso. Entre os pacientes com DRC do Centro Hiperdia Minas/Juiz de Fora, os níveis séricos aumentados de AU associaramse a maior risco de progressão rápida da doença renal crônica.
Introduction: Chronic kidney disease (CKD) has become a worrisome public health problem worldwide due to its increasing incidence and prevalence as well as its impact on morbidity and mortality. Treatment of CKD is based on risk factor intervention. However, currently known factors and their approach are insufficient to stop the disease. For this reason, it is imperative to search for other factors associated with its pathogenesis. Hyperuricemia has been identified as a condition associated with CKD, but causal association between them has not yet been proved. Objectives: 1. To evaluate the impact of hyperuricemia on the incidence and progression of CKD through a systematic review of the literature; 2. To evaluate the impact of serum uric acid levels on the decline of the glomerular filtration rate (GFR) in a population of chronic renal patients. Methods: Initially a systematic review of the literature was carried out between January 2005 and December 2016. The combination of keywords "chronic renal insufficiency AND hyperuricemia AND uric acid" was used to search in the Lilacs and Pubmed databases. The articles’ abstracts were evaluated by two researchers according to established inclusion and exclusion criteria. Secondly, the electronic records of 788 patients of the CKD outpatient clinic of the Hiperdia Minas/Juiz de Fora Center were analyzed and the impact of uric acid levels on the progression of CKD was evaluated. Results: A total of 150 studies involving humans were found. Twenty two were eligible; 13 studies evaluated incidence and 11 evaluated progression of CKD (increase in creatinine, variation of glomerular filtration rate, initiation of renal replacement therapy); two of the articles evaluated both outcomes. All thirteen articles that assessed the association between hyperuricemia and incidence of CKD showed a positive association between both. A further meta-analysis of 190,718 individuals evaluated the impact of hyperuricemia on the incidence of CKD and found an independent causal relationship. Regarding the progression of CKD, longitudinal studies presented conflicting results; three randomized controlled trials compared a group treated with allopurinol and a control group, all with improvement of the renal outcomes within the treated group. The Hiperdia Center database analysis results showed that patients admitted with hyperuricemia, that is, uric acid higher than 6.8mg/dL, presented almost twice the risk (IRR = 1.91 95% CI: 1, 21-3.00, p = 0.005) of rapid progression of CKD (TFG> 5mL/min/year). In addition, for each 1 mg/dL increase in the uric acid levels baseline, there was an additional 48% annual risk of progression (IRR = 1.48 95% CI: 1.16-1.88, p = 0.001). Conclusion: The systematic review suggested that hyperuricemia is independently related to the incidence of CKD, however, its role in disease progression is still controversial. Among patients with CKD, increased serum uric acid levels were associated with an increased progression of chronic kidney disease.
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Valente, Luiz Eduardo. « Associação do tratamento com alopurinol e desfechos definitivos em portadores de doença renal crônica com hiperuricemia assintomática ». Botucatu, 2019. http://hdl.handle.net/11449/183070.
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Orientador: Luis Cuadrado MartinResumo: Fundamentação: É crescente o número de trabalhos revelando a associação de hiperuricemia assintomática com hipertensão, síndrome metabólica, doenças cardiovasculares e doença renal crônica. Alguns estudos revelam que o tratamento da hiperuricemia assintomática reduz o número de desfechos renais e cardiovasculares. Tal premissa, no entanto, ainda não foi avaliada em uma subpopulação brasileira. Objetivos: Avaliar a associação entre tratamento com alopurinol e ocorrência de desfechos definitivos em portadores de doença renal crônica com hiperuricemia assintomática. Materiais e métodos: Foram avaliados, de forma retrospectiva, pacientes hiperuricêmicos e portadores de doença renal crônica não dialítica, em tratamento no HC-FMB – UNESP, os quais iniciaram acompanhamento no ambulatório de Insuficiência Renal Crônica ou de Nefrologia Geral do HC-UNESP desde janeiro 2002 a dezembro 2017. Com o intuito de avaliar a associação do uso do alopurinol sobre desfechos definitivos (entrada em terapia renal substitutiva, duplicação da creatinina ou morte). Resultados: Foram avaliados 109 pacientes sendo 53 do sexo feminino, cuja média de idade foi de 68 ± 11 anos. Destes, 95 eram brancos, 13 afrodescendentes e um asiático. Vinte e seis pacientes apresentaram o desfecho estudado no período; entre todos os 36 pacientes que iniciaram o uso de alopurinol no primeiro ano seguimento, ocorreram oito desfechos (22%). A proteinúria em 24 h associou-se aos desfechos avaliados Hazzard Ratio de 1,301 (I... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: Rationale: There is increasing number of studies revealing an association of hyperuricemia with hypertension, metabolic syndrome, cardiovascular diseases and chronic kidney disease. Some studies have shown that treatment of asymptomatic hyperuricemia reduces the number of renal and cardiovascular outcomes. This premise, however, has not yet been evaluated in a Brazilian subpopulation. Objectives: To evaluate the association between treatment with allopurinol and the occurrence of definitive outcomes in patients with chronic kidney disease with asymptomatic hyperuricemia. Materials and methods: Hyperuricemic patients with chronic non-dialytic kidney disease under treatment at HC-FMB - UNESP who began follow-up at the Chronic Kidney Insufficiency or General Nephrology outpatient clinic at HC-UNESP, were retrospectively evaluated, from January 2002 to December 2017. In order to evaluate the association of the use of allopurinol on definitive outcomes (renal replacement therapy, creatinine doubling or death). Results: A total of 109 patients were evaluated, of which 53 were females, whose mean age was 68 ± 11 years. Of these, 95 were white, 13 Afro-descendants and one Asian. Twenty-six patients presented the outcome studied in the period; among all 36 patients who started using allopurinol in the first year of follow-up, eight outcomes (22%) occurred. Proteinuria at 24 h was associated with the Hazzard Ratio of 1.301 (95% CI: 1.122 -1.508), p: 0.011. In univariate analysis, phosp... (Complete abstract click electronic access below)
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Beltrão, Fabyan Esberard de Lima. « Alopurinol na prevenção da esteato-hepatite não alcoólica e hiperglicemia induzida por dieta rica em frutose em ratos wistar ». Universidade Federal da Paraíba, 2012. http://tede.biblioteca.ufpb.br:8080/handle/tede/4271.
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Previous issue date: 2012-03-27Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - CAPES
Nonalcoholic fatty liver disease (NAFLD) in the last two decades has been recognized as the most common chronic liver disease in Western countries, paralleling the epidemic of obesity and consumption of high-fructose diet. Researchers suggest that NAFLD may be the hepatic manifestation of metabolic syndrome. Although NAFLD and hyperuricemia are strongly related to metabolic syndrome, few scientists in the literature associated with both diseases. Allopurinol, a potent inhibitor of xanthine oxidase, with anti-inflammatory and antioxidant effects has been shown to prevent the metabolic syndrome induced by fructose. Thus, the main objective of the study is to evaluate the effects of allopurinol in the treatment of nonalcoholic steatohepatitis (NASH) and hyperglycemia in rats fed high-fructose water. Wistar rats were fed along with 20% fructose in drinking water with or without allopurinol (30mg/kg/day) for 14 weeks. A control group received a normal diet. Serum total cholesterol level (P<0,001) and glucose (P<0,05) in fructose group and of triglycerides (P<0,01) and creatinine (P<0,01) in allopurinol group were significantly increased compared to normal control. Significant correlations were found glucose with uric acid (r = 0.51, p <0.001) and creatinine with triglycerides (r = 0.354, p <0.05). Liver histopathology from fructose group showed mild to moderate, steatosis, necroinflammation and fibrosis. Allopurinol treatment decreases macrovesicular steatosis (27%, P<0,01), necroinflammation (72%, P<0,001) and fibrosis (26%, P<0,05) in hepatocytes. Therapy with allopurinol significantly prevented hyperglycemia and increased HDL cholesterol levels in rats and was effective in preventing necroinflammation and fructose-induced hepatic fibrosis. This is the first study to prove the action of a xanthine oxidase inhibitor as a treatment for NASH.
Nas últimas duas décadas a doença hepática gordurosa não alcoólica (DHGNA) tem sido reconhecida como a doença hepática crônica mais comum nos países ocidentais, em paralelo com a epidemia de obesidade e consumo de dieta com alto teor de frutose. Pesquisadores sugerem que DHGNA possa ser a manifestação hepática da síndrome metabólica. Apesar da EHNA e hiperuricemia estarem fortemente relacionadas com a síndrome metabólica, poucos cientistas na literatura consultada associaram as duas patologias. Alopurinol, um potente inibidor da xantina-oxidase, com efeito anti-inflamatório e antioxidante tem sido utilizado para prevenir a síndrome metabólica induzida por frutose. Assim, o objetivo principal do presente estudo é avaliar os efeitos do alopurinol na prevenção da esteatose hepática não alcoólica (EHNA) e hiperglicemia em ratos alimentados com água rica em frutose. Ratos Wistar foram alimentados com 20% de frutose na água de beber, com ou sem alopurinol (30mg/kg/dia) durante 14 semanas. Um grupo controle recebeu uma dieta normal. Níveis de colesterol total (P <0,001) e glicose (P <0,05) no grupo de frutose e de triglicérides (P <0,01) e creatinina (P <0,01) no grupo alopurinol foram significativamente mais elevados, em comparação com o controle normal. As correlações significativas encontradas foram ácido úrico com glicose (r = 0,51, p<0,001) e creatinina com triglicerídeos (r = 0,354, p<0,05). A análise histopatológica hepática do grupo frutose mostrou esteatose, necroinflamação e fibrose de leve a moderada. O tratamento com alopurinol diminuiu esteatose macrovesicular (27%, P <0,01), necroinflamação (72%, P <0,001) e fibrose (26%, P <0,05) em hepatócitos. A terapia com alopurinol evitou significativamente a hiperglicemia e aumentou os níveis de HDL colesterol nos ratos e foi eficaz na prevenção da necroinflamação e fibrose hepática induzida por frutose. Corresponde assim ao primeiro estudo a provar a ação de um inibidor da xantina oxidase como um tratamento para EHNA.
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Silva, Jose Carlos Faes da. « Estudo da congestão venosa após amputação subtotal de membro de ratos : efeito protetor do alopurinol, vitamina c, tirofiban ou heparina na isquemia secundária ». Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/5/5132/tde-05062014-154201/.
Texte intégralRésumé :
A trombose venosa é a principal complicação da microcirurgia vascular e a intervenção precoce é necessária para o salvamento dos retalhos, com índices de sucesso de apenas 50% das revisões cirúrgicas; trombose da microcirculação, produção de radicais livres de oxigênio (RLO) e edema são os elementos principais da lesão de isquemia/reperfusão (I/R), e o planejamento das terapias protetoras tem como objetivo amenizar estas alterações. Os fármacos antioxidantes, antiagregantes plaquetários e anticoagulantes são utilizados no controle da lesão de I/R em diferentes órgãos. Neste estudo, em modelo de amputação subtotal de membro posterior de rato submetido a isquemia global primária, foi testado o efeito protetor dos fármacos alopurinol, heparina, tirofiban ou vitamina C durante a isquemia secundaria pós congestão venosa. Foram operados 100 ratos, que apos isquemia global de 90 minutos, foram divididos em cinco grupos de 20 animais recebendo uma das respectivas drogas na veia femoral contra-lateral: 1ml de solução fisiológica 0,9% no grupo controle (GC), 1ml de alopurinol 45mg/kg no grupo experimental 1 (G1), 1ml de heparina 200UI/kg no grupo experimental 2 (G2), 1ml de tirofiban 50 ug /ml no grupo experimental 3 (G3) e 1 ml de vitamina C 100mg/kg no grupo experimental 4 (G4); o clampe foi então retirado do feixe vascular e se iniciou a reperfusão de 60 minutos; a colocação do clampe vascular apenas na veia femoral direita iniciou a congestão venosa (isquemia secundária) do membro por 90 minutos seguido de outra reperfusão de 60 minutos; O músculo gastrocnêmio foi dissecado e retirado para analise histológica e os animais sacrificados por injeção letal. Foram estudados a porcentagem de viabilidade celular muscular, o edema e o extravasamento de hemácias. A porcentagem de lesão celular do músculo do grupo controle foi 54,6% (±10,6), do G1 31,5% (±13,6), do G2 24,7% (±11,7), do G3 24,6% (±8,6) e do G4 21,3% (±8,6). Os grupos foram comparados por modelo de comparação múltiplas one way-ANOVA e post-hoc Tukey com significância de p < 0,05. A porcentagem de lesão celular foi menor para os grupos G1, G2, G3 e G4 quando comparados ao GC (p < 0,001), e quando comparados os grupos experimentais entre si, apenas o G4 (vitamina C) foi menor estatisticamente que G1(alopurinol) (p < 0,029). A utilização individual dos fármacos alopurinol, heparina ,tirofiban e vitamina C mostraram efeito protetor na congestão venosa secundaria a isquemia global primária, e a vitamina C foi mais efetiva nesta ação que o alopurinol quando comparados os antioxidantes entre si. Quando avaliado o edema, apenas os antioxidantes tiveram índices menores estatisticamente que o GC, enquanto que todos os fármacos diminuíram o extravasamento de hemácias comparados com o grupo controle (p < 0,001)Venous thrombosis is the main complication of vascular microsurgery an early intervention is mandatory to rescue the flap, with a success rate of only 50% of surgical revisions; microcirculation thrombosis, oxygen free radicals production and edema are the main elements of ischemia/reperfusion (I/R) injury, and protective therapies aim to mitigate these changes. Antioxidants, antiplatelets and anticoagulants are used in different organs to control this injury. In this study, in a partial hind limb amputation model submitted to global ischemia, it was tested the protective effect of Allopurinol, Heparin, Tirofiban or Vitamin C during secondary ischemia after venous congestion. A hundred rats divided in five groups of 20 animals each were operated; after global ischemia of 90 minutes each group was injected into the contra lateral femoral vein one of the following solutions: 1 ml of saline solution NaCl 0,9% - control group (CG); 1ml of Allopurinol 45mg/kg - experimental group 1 (G1); 1ml of Heparin 200 UI/kg - experimental group 2 (G2); 1ml of Tirofiban 50 ug /ml - experimental group 3 (G3); 1ml of Vitamin C 100mg/kg - experimental group 4 (G4). Sixty minutes of limb reperfusion was performed, and a secondary period of limb ischemia started with the clamping of the femoral vein only (limb congestion) which lasted for 90 minutes (secondary ischemia). After that, the vein clamp was removed and a 60 minute reperfusion period was observed; at the end of the second reperfusion period, the right gastrocnemius muscle was removed and fixed in 10% formaldehyde, animals were euthanized with a lethal dose of Pentobarbital. Muscle fibers were scored as uninjured or injured based on the morphology of individual fibers; interstitial edema and bleeding were graded on a four-point scale. The control group had more damaged muscle cells 54.6±10.6% when compared to allopurinol 31.5±13,6%, heparin 24.7±11.7%, tirofiban 24.6±8.6% and Vitamin C 21.3±8.6% all reached statistical significance (p < 0.00 0.029). These comparisons were analysed using ANOVA and post-hoc Tukey. The single use of Allopurinol, Heparin, Tirofiban or Vitamin C showed a protective effect on venous congestion after global ischemia, and Vitamin C was more effective than Allopurinol when compared both antioxidants. When evaluating the edema, only the antioxidants had statistically lower rates than the CG, whilst all drugs reduced the extravasation of red blood cells compared with the control group (p < 0.001)
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Settle, Tabatha L. « The effects of a phytogenic feed additive versus an antibiotic feed additive on oxidative stress in broiler chicks and a possible mechanism determined by electron spin resonance and the effect of allopurinol, uric acid sodium salt administration, and inosine on xanthine oxidoreductase activity and plasma uric acid in broilers ». Morgantown, W. Va. : [West Virginia University Libraries], 2010. http://hdl.handle.net/10450/10956.
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Thesis (M.S.)--West Virginia University, 2010.Title from document title page. Document formatted into pages; contains v, 88 p. : ill. (some col.). Includes abstract. Includes bibliographical references.
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Chen, Pao-Liang, et 陳保良. « The effect of ascorbic acid and allopurinol on ischemic stroke ». Thesis, 2014. http://ndltd.ncl.edu.tw/handle/30584128009093848048.
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碩士慈濟大學
生理暨解剖醫學碩士班
102
Based on the data published by World Health Organization in 2013, stroke is the second leading cause of human death in the world. Development of an effective therapy for acute ischemic attack is an urgent issue in basic and preclinical research. Previous studies have shown that ischemia/reperfusion (I/R) of the brain leads to a rapid increase of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in the affected area. The present investigation tested the therapeutic potential of combined treatment of a potent ROS scavenger ascorbic acid and a xanthine oxidase inhibitor allopurinol after stroke, hypothesizing that simultaneous removal of and inhibition of production of ROS post-I/R would reduce oxidative stress and neuronal cell death. After surgical occlusion and reperfusion of the middle cerebral artery (MCA) of male SD rats, various cerebral regions such as primary somatosensory cortex (S1 cortex), secondary somatosensory cortex (S2 cortex), caudate putamen (CPu), and globus pallidus (GP) were insulted. Conversely, the combined ascorbic acid and allopurinol (500 and 50 mg/kg, i.p.) administered immediately after reperfusion of the MCA markedly reduced ischemic infarct volume. To evaluate the oxidative stress in the affected cerebral structures post-I/R, the expression of 3-nitrotyrosine (3-NT) which is produced through tyrosine nitration by peroxynitrite was detected. After ischemic stroke, the 3-NT surge was observed in most affected cerebral areas, whereas combined ascorbic acid and allopurinol treatment prohibited this pathological alteration. In addition, drug treatment significantly prevented the drastic neuronal cell loss due to ischemic stroke. These data suggest that combined treatment of ascorbic acid and allopurinol to simultaneously scavenge ROS and inhibit its production may provide a clinically applicable intervention for the promotion of neuronal cell survival after ischemia.
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Giachello, Carlos Federico. « Utilidad del tratamiento con allopurinol en pacientes con insuficiencia cardíaca severa ». Tesis, 2007. http://hdl.handle.net/10915/5384.
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Wu, Wei-Yi, et 吳威儀. « Recrystallization of Probenecid, Allopurinol and Sulfasalazine Using Supercritical Anti-solvent Precipitation ». Thesis, 2014. http://ndltd.ncl.edu.tw/handle/2779tj.
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碩士國立臺北科技大學
化學工程研究所
102
In this study, recrystallization and micronization of three active pharmaceutical ingredients (APIs), probenecid, sulfasalazine and allopurinol, are studied using the supercritical anti-solvent (SAS) process. Supercritical carbon dioxide is used as anti-solvent. 17 organic solvents listed in ICH Q3C as Class 2 and Class 3 are used as solvent candidates. At fixed temperature, pressure, solution concentration, nozzle diameter, solution flow rate and carbon dioxide flow rate, effects of different solvents on recrystallization and micronization are investigated firstly. In solvents effect, probenecid and allopurinol do not have obvious micronization result. Thus sulfasalazine is selected to study the effect of operating parameters in SAS process using Tetrahydrofuran as solvent. In the recrystallization of probenecid, under the solvent Acetone, the mean size can be reduced from 40μm~200μm to 5μm ~30μm. In the recrystallization of allopurinol, under the solvent NMP, the mean size can be reduced from 10μm~50μm to 2μm. In addition, the crystal habits are modified from irregular to rod-loke. In the recrystallization of sulfasalazine, under the optimizing conditions, the mean size can be reduced from 6μm to 1μm. In addition, the crystal habits are modified from irregular to spherical. Furthermore, the dissolution rate study of original and SAS-process sulfasalazine is also investigated.
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Liu, Chun-Hung, et 劉俊鴻. « Micronization of Allopurinol and Dapsone by Using Supercritical Anti-solvent Method ». Thesis, 2012. http://ndltd.ncl.edu.tw/handle/64245356178912309817.
Texte intégralRésumé :
碩士國立臺灣大學
化學工程學研究所
100
In order to enhance the dissolution rate and bioavailability in human beings, this study focused on the micronization of poor water soluble pharmaceuticals by using supercritical antisolvent method (SAS). The target pharmaceuticals used in this research are Allopurinol and Dapsone. Allopurinol is an oral drug for gout treatment and Dapsone is an oral durg for leprosy. Both two drugs have poor water solubility and low dissolution rate. Therefore, the purpose of this study is trying to make these two drugs micronized and enhance their dissolution rate. In this study, supercritical carbon dioxide was used as antisolvent. Different experimental results were obtained by different effect parameters, including solvent, operation temperature, pressure, solution flow rate, nozzle diameter and solution concentration. About the micronization of Allopurinol, it could be successfully micronized from 8.9 μm to 0.8 μm at the optimal operating conditions. About the micronization of Dapsone, it could also be successfully micronized from 40.9 μm to 2.2 μm at the optimal operating conditions. From the DSC result we can find another crystalline form after SAS processed. After the micronization process, the processed and unprocessed pharmaceuticals were tested by using a dissolution tester. The results of dissolution rate test, both the processed drugs have higher dissolution rate than the original drugs.
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Voß, Andreas. « Analytik und Metabolismus von Benzbromaron bei Mensch und Ratte ; Analytik und Kinetik von Allopurinol, Oxipurinol und Hydrochlorothiazid beim Menschen / ». 1996. http://www.gbv.de/dms/bs/toc/228120594.pdf.
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Chen, Jung-Yi, et 陳蓉誼. « The efficacy and safety of febuxostat versus allopurinol in gout patients with hyperuricemia ». Thesis, 2016. http://ndltd.ncl.edu.tw/handle/34385269354293900819.
Texte intégralRésumé :
碩士高雄醫學大學
藥學系碩士在職專班
104
Objective：To evaluate the efficacy and safety of the usage Febuxostat and Allopurinol in a medical center in Taiwan.The outcomes of efficacy and safety included the target of uric acid（UA）＜6.0 mg/dl, gout flare up, all related side effects and abnormal liver function between Febuxostat and Allopurinol. Methods：A systematic review and meta-analysis was performed to compare Febuxostat to Allopurinol for the efficacy and safety. A retrospective cohort study was used to evaluate the efficacy and safety of Febuxostat and Allopurinol in a medical center in Taiwan. Results：Six randomized controlled trials were included for systematic review and meta-analysis. Febuxostat was found to achieve the target of UA＜6.0 mg/dl more than Allopurinol（RR=1.57, 95％CI, 1.18, 2.09, p=0.002；I2=93％）.Febuxostat may increase the risk of gout flare, but do not indicate any significant difference（RR=1.14, 95％CI, 0.90, 1.46, p=0.29；I2=83％）. Febuxostat may decrease the risk of all of the side effects compared with Allopurinol（RR=0.94, 95％CI, 0.90, 0.98, p=0.003；I2=2％）.There was no significant difference between Febuxostat and Allopurinol in the abnormal liver function test with pooled risk ratio of 0.99（RR=0.99, 95％CI, 0.77, 1.27, p=0.94；I2=0％）. Outcome of retrospective cohort study, the adjusted hazard ratio of efficacy for the target of UA＜6.0 mg/dl for lowering uric acid when comparing Febuxostat to Allopurinol was 4.420（aHR=4.420, 95％CI=2.470, 7.909, p<0.001）. The incidence of the gout flare comparing Febuxostat versus Allopurinol was 3.259（aHR=3.259, 95％CI=0.822, 12.916, p=0.093）. The incidence of the side effects and abnormal liver function test are similar between Febuxostat and Allopurinol（p=0.461 and p=0.322）. Conclusions：Febuxostat compared with Allopurinol increased the chance to achieve the target of UA＜6.0 mg/dl. Retrospective cohort study find that Febuxostat compared with Allopurinol may increase the risk about all of the side effects, but it is different from previous results. Finally, although there are no singnificant different, Febuxostat compared with Allopurinol may increase the risk of gout flares and abnormal liver function.
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Ke, Jing-Hua, et 柯靜華. « Allopurinol-related severe cutaneous adverse reaction : clinical outcomes, risks, and cost-effectiveness of prevention ». Thesis, 2015. http://ndltd.ncl.edu.tw/handle/f2ymq3.
Texte intégralRésumé :
碩士高雄醫學大學
藥學系臨床藥學碩士班
103
Objective Allopurinol is first-line urate-lowering therapy (ULT) for gout or hyperuricemia. The strong association of allopurinol-related severe cutaneous adverse reactions (SCARs) and HLA-B*58:01 allele has been demonstrated in the previous studies. Thus, there were two objective in our study: (1) to assess the uses and effects of genotyping screening for allopurinol on everyday clinical practice and clinical outcomes; (2) to estimate the direct medical costs of allopurinol-related SCARs and cost-effectiveness of HLA-B*58:01 test in allopurinol new users. Methods (1) A cross-sectional study was conducted for patients newly prescribed with allopurinol between January 2011 and December 2014 from a large medical institution in Taiwan. We analyzed the incidence of allopurinol-related SCARs and changes in the pattern of switching from allopurinol to other ULT before and after introduction of febuxostat. (2) The decision analytical model over a time period of 1 year and used the perspective of third-party payer in Taiwan to evaluate the effectiveness and economic outcomes among gout patients with or without HLA-B*58:01 screening test prior to prescribing allopurinol or ULT-na&;#239;ve patients The results were presented as life-day, quality adjusted life-year (QALY), SCAR event, death attributing to SCAR event within in one year, total medical costs of allopurinol-associated medical expenditures, and the incremental cost-effectiveness ratio (ICER). Results (1) A total of 17,532 patients were included and 2,844 were tested for HLA-B*58:01. As a proportion of all new allopurinol users declined from average 23.87% in the pre-HLA B*58:01 screening test introduction period (2010) to 14.28 % in 2014. A total of 2,518 allopurinol new users ever switched from allopurinol to other ULT. The proportion of switching from allopurinol to benzbromarone and sulfinpyrazone among switchers reduced from 63.56%, 32.98% in 2010 to 36.44% and 11.69% in 2014 respectively. The switching rate significantly increased after May 2013, the time that febuxostat was available. Among allopurinol new users, incidence of SCARs or hypersensitivity events reduced from 0.21% to 0%. (2) In base-case analysis, the incidence of SCAR in screening was the lowest. ICER of screening was incremental NT$ 1,481,977 per life-day and NT$ 234,610 per QALY gained relatively. The ICER was lower in patients with comorbid CKD than base-case cohort. Based on the willingness-to pay (WTP) was NT$ 647,900 per QALY in Taiwan, receiving HLA-B*58:01 screening prior to allopurinol was cost-effective compared to alternatives. The study results were sensitive to the probability of alternatives-related hypersensitivity, utility of gout/hyperuricemia, and negative predicted value of genotyping. Conclusions The incidence of allopurinol-related SCAR declined after introducing HLA-B*58:01 screening accompanies by allopurinol new users gradually decreased. The available of febuxostat significantly change the pattern of ULT. HLA-B*58:01 screening is cost-effective compared to alternative ULT. However, the priority of genetic screening should be given to allopurinol user with CKD, or the uses of allopurinol need to be restricted in CKD patients.
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Pan, Ren-You, et 潘仁宥. « The T cell receptor repertoire of carbamazepine- and allopurinol-induced severe cutaneous adverse reactions ». Thesis, 2016. http://ndltd.ncl.edu.tw/handle/tjq6jn.
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Wang, Ching-Huan, et 王靖寰. « The Use of Allopurinol and Benzbromarone for Coronary Artery Disease Prophylaxis in Patients with Gout ». Thesis, 2014. http://ndltd.ncl.edu.tw/handle/n2hpg3.
Texte intégralRésumé :
碩士臺北醫學大學
藥學系(碩博士班)
102
Background Coronary artery disease (CAD), caused by narrowing or obstruction of coronary artery, has been recently reported to be associated with gout. However, studies on the preventive effect of urate-lowering agents on CAD are still limited. The present study, therefore, attempted to preliminarily observe the change in risk of CAD in gout patients prescribed with allopurinol and/or benzbromarone, and further to analyze the dose-response relationship of the both drugs. Methods This retrospective cohort study was conducted using the claims data provided by the National Health Insurance Research Database. Both inpatients and outpatients diagnosed with gout between 2001 and 2008 were enrolled in our study. Patients were excluded from this study if they had history of CAD, heart failure, chronic kidney disease, cancer, or gout; or took either allopurinol or benzbromarone prior to diagnosis of gout. Each disease required at least two separate outpatient diagnostic codes or one inpatient diagnostic code, be it defined in an inclusion criterion, an exclusion criterion, or as a covariate. Besides, prescription with a medication was regarded as exposure to the medication in our study, irrespective of the patients’ medication adherence. To ascertain the effects of allopurinol and benzbromarone on lowering the risks of CAD, we excluded those who were prescribed with allopurinol or benzbromarone after December 31, 2008, who were identified as having CAD before or within 180 days of administration of either allopurinol or benzbromarone, and who took either allopurinol or benzbromarone for fewer than 90 days within 180 days of starting either of the medications. A total of 8,227 gout patients remained and were regarded as the experimental groups. Each patient of the experimental groups was exclusively matched with a gout patient who had never been prescribed with either drug by age and gender in the ratio of 1:1. The matched non-allopurinol-or-benzbromarone- exposed patients were categorized as the comparison group (Group C). We further divided the experimental groups into allopurinol-treated (Group A, N = 1,437), benzbromarone-treated (Group B, N = 4,241), and both-treated groups (Group A+B, N = 2,549). The index date was defined as the date newly prescribed with either drug for the experimental groups or newly diagnosed with gout for Group C. Results Patients of the experimental groups, in general, had no statistically significant change in risk of CAD with the covariates adjusted in comparison with those who were not exposed to either drug (Group C). However, the risk of CAD was negatively correlated with the number of doses in Group A and Group A+B. Each experimental group, in fact, had a lower risk of CAD than Group C after receiving over 360 defined daily doses (DDDs), after which Group A presented the lowest risk of CAD. Conclusion Our findings indicated that a considerable number of doses of allopurinol and benzbromarone are required for CAD prophylaxis, and hence the two drugs might be recommended for gout patients only as an adjuvant medication against the onset of CAD.
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Chen, Jung-Kuei. « The study of T cell repertoire in patients with Allopurinol-induced severe cutaneous adverse reactions (SCAR) ». 2008. http://www.cetd.com.tw/ec/thesisdetail.aspx?etdun=U0001-2707200821245000.
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Chang, Wan-shan, et 張菀珊. « Effect of Gout and Allopurinol Use on Cardiovascular Disease Outcomes:A Population-Based Cohort Study in Taiwan ». Thesis, 2013. http://ndltd.ncl.edu.tw/handle/55706511133769293698.
Texte intégralRésumé :
碩士國立中央大學
資訊工程學系在職專班
101
Gout is a type of metabolic diseases, the disease is often associated with hyperuricemia, acute and chronic arthritis, kidney disease go far. In recent years, studies have shown that patients with gout also cardiovascular disease and death in high risk groups. Allopurinol is frequently used in clinical practice to lower blood uric acid concentrations of the drug, and its mechanism of inhibition of xanthine oxidase and reduce the formation of uric acid. This study intends to use the Taiwan National Health Insurance Research Database information which more than 40-year-old patient with gout use allopurinol whether treatment reducing the incidence of cardiovascular disease. The results show that, if allopurinol compared with non-allopurinol users, the allopurinol users were significant increased risk of cardiovascular events (HR =1.33, 95% CI 1.26–1.41). Compared with low-dose (<100 mg & 100 mg) users, high-dose (≥300 mg) users had significant reductions in the risk of cardiovascular events (HR =0.67, 95% CI 0.48–0.92), which all patients on allopurinol treatment. The results did not show an effect of use allopurinol as a class on reductions cardiovascular disease hospitalization rate in patients with gout. Higher doses of allopurinol risks of cardiovascular events were lower than lower doses in all patients on allopurinol treatment.
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Chou, Chwn-Yu, et 周政郁. « A novel strategy for determination of allopurinol based on competitive behavior of oxygen-consumption by dual-enzyme biosensor ». Thesis, 2014. http://ndltd.ncl.edu.tw/handle/b2pf6f.
Texte intégralRésumé :
碩士淡江大學
化學學系碩士班
102
Two parallel enzymatic oxygen-consumed reaction including oxidation of hypoxanthine by xanthine oxidase (EC 1.17.3.2) and oxidation of catechol by tyrosinase (EC 1.14.18.1) were utilized to constructed novel allopurinol biosensor. In this project, the concentration increase of allopurinol (inhibitor) would inhibit the activity of enzymatic oxygen-consumption by xanthine oxidase. Subsequently, tyrosinase could divvy more oxygen to produce catechol quinone, and it could be observed that more current response was recorded from electrochemical reduction of catechol quinone at 0.0V (vs. Ag/AgCl). In contrast to the determination of traditional inhibition type which the signal was inverse proportional to the concentration of inhibitor, the signal is proportional to the concentration of allopurinol. Moreover, in this biosensor, the monolayer of enzyme modifier and 0.0V detection potential were adapted to obtains fast response (t90%-10% = 2.9 second) and efficiently avoids common interference of substances that co-exist in serum. This allopurinol biosensor possesses linear range 5μM－100μM (R=0.998) that satisfy with therapeutic range (5-15mg/L), sensitivity is 8.79 nA/μM, detection limit is 1.4μM, the relative standard deviation (RSD) is 4.2%. Allopurinol was used to primary treatment of hyperuricemia and its complication. However, it potentially causes serious hypersensitivity such as Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TENS) on several patients after allopurinol treating. Therefore, the determination of allopurinol is important and necessary for clinical monitoring and quality assurance of pharmacy.
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Huang, Yun-Zun, et 黃煜尊. « Constructing Predictive Model of Febuxostat and Allopurinol therapeutic effect in patients with Cardiovascular disease、Renal and Liver dysfunction ». Thesis, 2016. http://ndltd.ncl.edu.tw/handle/mh43cx.
Texte intégralRésumé :
碩士國立雲林科技大學
工業工程與管理系
104
According to statistics, Taiwanese hyperuricemia prevalence of male 22%, female 9.77%. Hyperuricemia have gradually become a common symptom of metabolic diseases in Taiwan. However, urate lowering drugs mainly divided into three categories: Uricostatic agents、Uricosuric agents、Uricolytic agents. Belong to Uricostatic agents, more commonly used drugs contain: Allpourinol and Febuxostat. Allpourinol prone to side effects and serious adverse drug reactions, such as Stevenson's - Johnson syndrome, etc. Febuxostat belong to the Uricostatic agents, side effects are abnormal liver function, diarrhea, nausea, etc. Febuxostat officially listed in 2011, but it relaxed the standard health insurance payments until 2014. Domestic use of the drug is not universal. However, most of the research literature belong abroad, such as: Canada, Britain, Australia and other countries. Lack of monitoring studies after local domestic listing. Therefore, this study will collect data from a Yunlin County Regional Teaching Hospital, medical retrospective study (St. Joseph's Hospital). The use of data mining, decision tree and back-propagation neural, while the construction of Allpourinol Febuxostat patients with cardiovascular, Liver and kidney dysfunction affect treatment outcome to construct a prediction model. The results show that patients with Cardiovascular taking Febuxostat and patients with kidney dysfunction taking Allopruinol using a decision model has the highest accuracy. On the other hand, taking Febuxostat in patients with Liver and kidney dysfunction, taking Allopurinol in patients with Cardiovascular and Liver dysfunction using a neural network model has the highest accuracy.
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PAI, YA-CHUN, et 白雅君. « The Influence Study of Allopurinol and Febuxostat in Thyroid Patient’s Treatment by Taiwanese National Health Insurance Research Database ». Thesis, 2019. http://ndltd.ncl.edu.tw/handle/x7855q.
Texte intégralRésumé :
碩士大仁科技大學
藥學系碩士班
107
Background: Several studies have shown that thyroid dysfunction is associated with hyperuricemia or gout. Recently studies also shown that several gout medications might affect the patient’s thyroid function, however, the results were very contradiction. In this study, whether patient under gout treatment could affect the patient’s thyroid function were investigated by analyzed thyroid medication dosage adjustment. Methods: The medical records of one million subjects between April 1, 2012 and December 31, 2013 were provided by the Taiwan National Health Insurance Research Database were used. Thyroid dysfunctional patients under xanthine oxidase inhibitor, including allopurinol and febuxostat, treatments were collected. Results: Total 508 cases which fitted experimental design criteria were collected. Among them, 480 (94.5%) cases were treated with allopurinol and 395 (77.8%) patients the allopurinol daily dose was less than 300 mg. Total 28 cases were treated with febuxostat and 19 of them had been prior to allopurinol treatment. Conclusions: The data showed that the hypothyroidism patients with gout are over three times than hyperthyroidism with gout and most patients are over 65 years old. The treatment regimen of levothyroxine was unchanged for 153 cases while 142 patients have been repeatedly adjusted.
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Chuang, Pei-Fen, et 莊佩芬. « Evaluation of the clinical dose and effectiveness of allopurinol and benzbromarone on hyperuricemia in patients with different renal function ». Thesis, 2008. http://ndltd.ncl.edu.tw/handle/78434176373964277614.
Texte intégralRésumé :
碩士高雄醫學大學
臨床藥學研究所
96
Background: There are some noticeable points for urate-lowering therapy. 1. The potential of allopurinol severe cutaneous adverse reactions led to the development of clinical guidelines that advocate dosing of allopurinol according to renal function. For achieving therapy target, appropriate dose adjustments of allopurinol should base on serum uric acid level. 2. Benzbromarone may have no effects on patients with severe renal dysfunction and treatment with this drug might lead to potential liver toxicity. 3. Poor compliance with urate-lowering therapy and a fixed dose of allopurinol may result in undertreatment and difficult management of disease. Objective: Dose for prescription, espically the adjusted dose in different renal function and the percent of regular laboratory monitoring are all prescription patterns discussed. The effectiveness of fixed daily dose after 3 months treatment and factors associated with 1 year compliance are all evaluated and analyzed in this study. Patients and methods: This study population is from a regional hospital in Kaohsiung who received allopurinol or benzbromarone prescriptions in 2004. Patients who were less than 18 years, with only one time prescription of urate-lowering drug and with prescriptions from dialysis department are excluded. Prescriptions from emergency department and inpatients are also exclusion criteria to enhance the doses for patients with stable situation. The prescription doses from 2004~2007/6 are analyzed. Newly treated patients with baseline serum uric acid and creatinine, with first 6 months of continued use and with gout are inclusion criteria for three different discussion parts including the daily dose in different renal function, the percent of regular laboratory monitoring and the association between factors and compliance. Results: The most commonly used allopurinol daily dose was 100 mg/day in these prescriptions of study population within 2004 to June 2007. Most patients received allopurinol 100 mg/day as initial daily dose, although with different renal function. More than 50% patients with lower allopurinol daily dose when compared with recommended. Patients receiving daily dose less than 100 mg/day were with more severe renal dysfunction. There were 11 patients receiving benzbromarone with renal function < 30 ml/min/1.73m2. Titrating allopurinol dose might not be considered in 60.0% patients with first 6 months of continued use and the awareness of the liver toxicity of benzbromarone might be less than 50%. In this study, the percent of patient achieving normal uric acid were 18.2% and 92.3% in patients with fixed allopurinol and benzbromarone daily dose 100 mg/day after 3 months treatment. Mean duration of continuous drug treatment was less than 3 months in newly treated patients and compliance with treatment for 1 year was 7.6% in gout patients. Increasing age was associated with compliance (odds ratio, 1.04; 95% confidence interval, 1.01-1.07, P-value=0.0091) and patients with more gout attacks within 1 year before the start of drug treatment was associated with compliance (odds ratio, 1.24; 95% confidence interval, 1.08-1.41, P-value=0.0018). Conclusions: Generally, the initial daily doses were lower than recommended, suggesting conservative therapy for fear of allopurinol severe cutaneous adverse reactions. Adjusting daily dose and monitoring uric acid adequately might bring more benefit of therapy because of few patients with fixed allopurinol 100 mg/day achieved normal uric acid after 3 months treatment. Benzbromarone 100 mg/day may well achieve target uric acid. It is noticeable that the awareness of possible liver toxicity in patients with benzbromarone might be less than 50%. Urate-lowering drugs were not being used long term in this study population. Age and the experience of gout attack before start of drug treatment were associated with compliance.
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Heineke, André [Verfasser]. « Allopurinol, ein Xanthin-Oxidase-Inhibitor, reduziert das linksventrikuläre Remodeling und verbessert die myokardiale Funktion nach experimentellem Myokardinfarkt / vorgelegt von André Heineke ». 2007. http://d-nb.info/986824887/34.
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YANG, AI-CHEN, et 楊艾珍. « The Comparison Study between Patients with Gout under Allopurinol Treatment and Renal Disease - Based on the National Health Insurance Research Database ». Thesis, 2014. http://ndltd.ncl.edu.tw/handle/w26vg9.
Texte intégralRésumé :
碩士嘉南藥理大學
藥學系
103
According to a statistical analysis by the Taiwan Society of Nephrology, Taiwan once had the world’s highest incidence of patients dependent on hemodialysis. The incidence of renal failure caused by medication depends on the various kinds of medicines consumed by the patient and their origins. The purpose of this study is to use the Taiwan National Health Insurance Research Database to compare the kidney failure rates of gouty patients taking generic and brand name allopurinol. 39,716 gouty patients were assigned to five experimental sub-groups who took generic, PIC/S GMP generic, BA/BE generic, PIC/S GMP BA/BE generic, and brand name allopurinol; the counterpart group took no allopurinol. Logistic regression analysis is used. Odds ratio estimates and 95% confidence intervals were calculated using SPSS 12.0, with P values < 0.01 considered statistically significant. The number of gouty patients taking allopurinol to treat their hyperuricemia was 5,623(6.4%). A total number of 607(10.8%) cases of renal failure or 65(1.2%) cases of erythema multiforme patients taking allopurinol were identified. Among the control group, cases of renal failure numbered 4,157(5.6%). Even without taking any allopurinol, it is necessary that hyperurecemia patients have their kidney function checked at least two to three times each year.
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Lin, Chia-Hsien, et 林嘉嫻. « Immunological basis for allopurinol-induced severe cutaneous adverse reactions : HLA-B*58:01-restricted activation of drug-specific T cells and molecular interaction ». Thesis, 2014. http://ndltd.ncl.edu.tw/handle/zsjc5u.
Texte intégralRésumé :
博士國立臺灣大學
微生物學研究所
103
Allopurinol is a commonly prescribed drug for symptomatic hyperuricemia and its complication, gout. The major limitation of allopurinol is that it is a frequent cause of severe cutaneous adverse reactions (SCARs), including hypersensitivity syndrome (HSS), Stevens–Johnson syndrome (SJS), and toxic epidermal necrolysis (TEN). Our previous study showed that susceptibility to these life-threatening reactions induced by allopurinol is genetically determined and is strongly associated with HLA-B*58:01. The underlying mechanism remains unclear, however. To investigate the pathogenesis of allopurinol-SCAR, we aimed to study the interactions between the allopurinol or oxypurinol and HLA-B*58:01 molecules. We enrolled 14 patients with allopurinol-induced SCAR and studied the response of their cultured peripheral blood mononuclear cells (PBMCs) to allopurinol or oxypurinol. In vitro-expanded T lymphocytes from the patients were evaluated for cell phenotype, and their interaction with HLA-B*58:01 and the drug analyzed, based on proliferation ability, cytotoxic T lymphocyte (CTL) response, surface plasmon resonance (SPR) and site-directed mutagenesis. T cell lines from 14 allopurinol-SCAR patients in the presence of allopurinol or oxypurinol were generated. These T-cell lines (TCLs) displayed cross-reactivity between allopurinol and oxypurinol, and both CD4+ and CD8+ T cells were present. The expanded T Cells were activated and restricted by antigen-presenting cells expressing HLA-B*58:01 in the presence of drug. The proliferation of T cells was not altered by the pre-fixation of antigen presenting cells (APC), suggesting the involvement of an antigen-processing-independent pathway. Using SPR analysis, HLA-B*58:01 was shown to exhibit specific binding affinity to allopurinol and oxypurinol. Arg97 between the E and C pocket of HLA-B*58:01 is a key residue involved in drug presentation. This study demonstrates an interaction between HLA and allopurinol or oxypurinol, and provides a molecular-level understanding of allopurinol-induced SCARs associated with HLA-B*58:01.
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Evans, Nicole Paula. « A study of the effectiveness of homoeopathically prepared dilutions of abscisic acid, molybdenum and allopurinol in inhibiting or promoting the germination of barley seeds (Hordeum vulgare) ». Thesis, 2008. http://hdl.handle.net/10321/536.
Texte intégralRésumé :
Dissertation submitted in partial compliance with the requirements for a Masters Degree in Technology: Homoeopathy, Durban University of Technology, 2008.Introduction This study investigated the effectiveness of homoeopathic dilutions of abscisic acid (ABA), molybdenum and allopurinol on inhibiting or promoting the germination of barley seeds (Hordeum vulgare cv. Stirling, ex Caledon, Western Cape, South Africa, 1998 harvest). Recent research involving ABA and seed germination has shown mixed results, with Bruni (2001), finding there to be statistically significant biological effects, but Couchman (2001) not. Objective/Aim/Purpose The purpose of this study was to evaluate the effectiveness of homoeopathic dilutions of ABA, molybdenum and allopurinol (two substances which have an effect on ABA metabolism), especially those above the 10-23 level (Avogadro’s dilution limit), on germination, in light of recent findings. Abscisic acid, a plant hormone and molybdenum, a trace element, both play an essential role in inducing dormancy of the seed. Allopurinol, a therapeutic drug, has also been shown to affect ABA metabolism and therefore seed germination. The study used all three substances individually and in combination, in homoeopathic dilutions ranging from 4CH to 200CH potency. Methodology There were 7 treatments with 5 potencies per treatment (4CH, 9CH, 15CH, 30CH and 200CH). Each potency level for each treatment had a control, which meant there were 5 controls per treatment. The seeds (distally cut) were placed in 9cm Petri dishes (20 seeds in each), with 5 repetitions, 100 seeds per dilution level with one control of 20 seeds. There were thus 600 (120 x 5) seeds per treatment and 4200 seeds in total (600 x 7 treatments). Seeds were germinated in the dark at a constant temperature. Counts were done every 24 hours for 3 days and the data recorded. The criterion for germination was radical emergence. Results The data was analysed statistically using Univariate Analysis of Variance (STATISTICA version 6). The results showed statistically significant interaction between treatments and potencies and a One-Way Anova was then used to analyse each treatment to determine the effectiveness of each potency. Statistically significant differences were noted between potencies for each treatment. From the results it was clear that the most effective treatment for stimulating germination was the treatment utilizing homoeopathic dilutions of allopurinol. The most effective treatment for inhibiting germination was the treatment utilizing ABA in homoeopathic dilutions. The 30CH (10-60) showed a statistically significant effect on the stimulation of germination across almost all treatments, whereas the 15CH (10-30) showed a statistically significant effect in inhibiting germination in most treatments. Conclusion It is evident from the results of this study that all the treatments produced distinct biological effects, whether it be stimulating germination or inhibiting germination in homoeopathic dilution.
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Bosoi, Tudorache Cristina. « Pathogenèse de l’oedème cérébral dans l’encéphalopathie hépatique minimale : rôles du stress oxydatif et du lactate ». Thèse, 2014. http://hdl.handle.net/1866/12110.
Texte intégralRésumé :
L’encéphalopathie hépatique (EH) est un syndrome neuropsychiatrique découlant des
complications de l'insuffisance hépatique. Les patients souffrant d'une insuffisance hépatique chronique (IHC) présentent fréquemment une EH minimale (EHM) caractérisée par des dysfonctions cognitives subtiles qui affectent leur qualité de vie. L'insuffisance hépatique entraîne une hyperammoniémie, le facteur central dans la pathogenèse de l'EH. Pourtant, les taux d'ammoniaque sérique ne sont pas
corrélés avec la sévérité de l'EH lors d'une IHC, suggérant que d'autres facteurs y contribuent. L'oedème cérébral est une caractéristique neuropathologique décrite chez les patients souffrant d'une EHM et plusieurs facteurs dont le stress oxydatif, les altérations du métabolisme énergétique et l'augmentation de la glutamine cérébrale pourraient contribuer à la pathogenèse de l'oedème cérébral lors d'une EHM
induite par une IHC. Les mécanismes sous-jacents exacts ainsi que les relations entre ces facteurs et l'ammoniaque ne sont pas connus. Présentement, le seul traitement efficace de l'IHC est la transplantation hépatique, une option thérapeutique très limitée.
Le but de cette thèse est de contribuer à l'avancement des connaissances sur les mécanismes sous-jacents liés au rôle du stress oxydatif, de la glutamine et du lactate dans la pathogenèse de l'oedème cérébral lors d'une EHM induite par une IHC afin d'envisager de nouvelles options thérapeutiques. Les objectifs précis étaient: 1. Établir le rôle de l’ammoniaque et sa relation avec le stress oxydatif dans la
pathogenèse de l'oedème cérébral lors d'une EHM induite par une IHC. 2. Établir le rôle du stress
oxydatif dans la pathogenèse de l'oedème cérébral, sa relation avec l'ammoniaque et l'effet du traitement
avec des antioxydants. 3. Confirmer l'effet synergique entre l'ammoniaque et le stress oxydatif dans la
pathogenèse de l'oedème cérébral. 4. Établir le rôle du lactate et de la glutamine dans la pathogenèse de
l'oedème cérébral et leur relation avec l’ammoniaque. Pour atteindre ces objectifs, 2 modèles animaux
d'EHM obtenus par microchirurgie chez le rat ont été utilisés: 1) la ligature de voie biliaire, un modèle
d'IHC et 2) l'anastomose porto-cave, un modèle d'hyperammoniémie induite par la dérivation
portosystémique.
Nos résultats démontrent que l'ammoniaque et le stress oxydatif indépendamment n'induisent
pas l'oedème cérébral lors d'une EHM. Pourtant, lorsque les 2 facteurs agissent ensemble ils présentent
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un effet synergique qui entraîne le développement de l'oedème cérébral, le stress oxydatif étant une
première insulte, qui est suivie par l'hyperammoniémie comme deuxième insulte. En plus, le stress
oxydatif a été mis en évidence seulement au niveau systémique, et non au niveau central dans notre
modèle d'IHC en association avec l'oedème cérébral, suggérant que le stress oxydatif systémique est une
conséquence de la dysfonction hépatique et que l'hyperammoniémie n’induit pas le stress oxydatif ni
systémique ni central.
Nous avons démontré qu’une augmentation du lactate cérébral est une conséquence directe de
l'hyperammoniémie et joue un rôle important dans la pathogenèse de l'oedème cérébral lors d'une EHM
induite par une IHC, tandis qu’une augmentation de la glutamine au niveau cérébral n'est pas un facteur
clé.
La compréhension de ces mécanismes a entraîné la proposition de 3 nouvelles stratégies
thérapeutiques potentielles pour l'EHM. Elles ciblent la diminution de l'ammoniaque sérique, la
réduction du stress oxydatif et l'inhibition de la synthèse du lactate.Hepatic encephalopathy (HE) is a metabolic neuropsychiatric syndrome which occurs as a complication of liver failure/disease. Patients with chronic liver disease (CLD) present often with minimal HE (MHE) characterized by subtle cognitive dysfunction which impairs their quality of life. Impaired liver function leads to hyperammonemia which is a central factor in the pathogenesis of HE. However, ammonia alone is poorly correlated with the severity of HE during CLD, strongly suggesting other factors may contribute. Brain edema is a neuropathological feature described in MHE patients and several factors such as oxidative stress, energy metabolism alterations and an increase in glutamine may to contribute to the pathogenesis of brain edema during HE related to CLD. However the exact underlying mechanisms and the relationships between these factors and ammonia are poorly understood. To date, the only effective treatment of CLD remains liver transplantation, a limited therapeutic option. The aim of this thesis is to advance the knowledge into the mechanisms underlying the role of oxidative stress, glutamine and lactate in the pathogenesis of brain edema during MHE associated with CLD in order to uncover new therapeutic options. The study objectives were: 1. Define the role of ammonia and its relationship with oxidative stress in the pathogenesis of brain edema in CLD. 2. Define the role of oxidative stress in the pathogenesis of brain edema, its relationship with ammonia as well as the effect of antioxidant treatment. 3. Confirm a synergistic role of ammonia and oxidative stress in the pathogenesis of brain edema. 4. Define the role of lactate and glutamine in the pathogenesis of brain edema and their relationship with ammonia. To achieve these objectives, we used 2 microsurgical rat models: 1) bile-duct ligation, a cirrhosis model and 2) portacaval anastomosis, a hyperammonemia model following portal-systemic shunting. Our findings demonstrate that ammonia and systemic oxidative stress independently do not induce brain edema in MHE related to CLD. However, when both factors are present, they exert a synergistic effect leading to the development of brain edema with oxidative stress presenting as a “first hit”, followed by hyperammonemia as a “second hit”. Moreover, solely systemic and not central oxidative stress was observed in our CLD rat model in relation to brain edema implying that systemic oxidative stress is a consequence of liver dysfunction and that central oxidative stress is not a direct iv effect of hyperammonemia in the setting of CLD. Moreover, we revealed that increased cerebral lactate is a direct consequence of hyperammonemia and also plays an important role in the pathogenesis of brain edema, while increased cerebral glutamine does not. The understanding of these mechanisms led to the proposal of three different strategies as potential HE therapies. These are directed towards lowering ammonia, reducing oxidative stress and inhibiting lactate synthesis.