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Journal articles on the topic '"Allopurinolo"'

Author: Grafiati

Published: 11 March 2023

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1

Russmann and Lauterburg. "Lebensbedrohliche Nebenwirkungen der Gichtbehandlung." Therapeutische Umschau 61, no. 9 (September 1, 2004): 575–77. http://dx.doi.org/10.1024/0040-5930.61.9.575.

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Die Behandlung der Gicht mit Allopurinol kann schwere unerwünschte Wirkungen zur Folge haben. Neben dem häufigen Hautausschlag unter Allopurinol kann ein selteneres Hypersensitivitäts-Syndrom mit Fieber, Hautexanthem (bis zum Lyell-Syndrom), Hepatopathie, Eosinophilie, Niereninsuffizienz und Vaskulitis lebensbedrohlich sein. Die Inzidenz dieser schweren Nebenwirkung kann wahrscheinlich mit einer der Nierenfunktion angepassten Reduktion der Dosis von Allopurinol gesenkt werden. Da Azathioprin und Mercaptopurin über die Xanthinoxidase, die durch Allopurinol gehemmt wird, metabolisiert werden, kann es bei gleichzeitiger Verabreichung zu lebensbedrohlichen Neutropenien kommen, wenn die Dosis des Allopurinols nicht um zirka 75% reduziert wird. Das urikosurisch wirkende Benzbromaron wurde kürzlich wegen schwerer Leberschädigungen vom Markt genommen.

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2

A. Wohaieb, Saleh. "Effects of Allopurinol on Ketone Body Metabolism and Tissue Lipid Peroxidation in Alloxan Diabetes in Rats." Iraqi Journal of Pharmaceutical Sciences ( P-ISSN: 1683 - 3597 , E-ISSN : 2521 - 3512) 15, no. 1 (March 31, 2017): 37–42. http://dx.doi.org/10.31351/vol15iss1pp37-42.

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The aim of the present study is to investigate whether or not xanthine oxidase (XO)â€“derived reactive oxygen species (ROS) may play a role in the pathogenesis of alloxan (ALX)â€“induced diabetes in rats using the specific XO inhibitor and hydroxyl radical scavenger, allopurinol The involvement of oxidative stress in ALX â€“ diabetes was assessed by the measurement of plasma and various tissues lipid peroxides levels ( using thiobarbituric acid ( TBA ) reactive substances ). Furthermore, the ability of allopurinol to influence these and other biochemical parameters, including plasma and urine ketones levels were also investigated in diabetic rats. Rats were divided into four groups: control, untreated diabetic, allopurinol â€“ treated diabetic, and insulin â€“ treated diabetics. At the end of the one week experimental period, blood and tissue samples were obtained from anesthesized animals for the measurement of the above â€“ mentioned parameters. Although the single intraperitoneal (i.p.) injection of allopurinol (25 mg/kg body wt.) 1h before or 1h after ALX injection (100 mg/kg body wt., i.p.) failed to prevent the induction of diabetes, it did lower ketonuria and the incidence of early ketosisâ€“associated mortality in diabetic animals in comparison with nonâ€“allopurinolâ€“treated diabetic rats. Subsequent administration of allopurinol (25 mg/kg body wt., i.p.) every 48 hr for 1wk (i.e., 3 additional doses) also decreased plasma ketone bodies levels as well as plasma and tissue (heart, liver, kidney, pancreas) lipid peroxides levels in comparison with nonâ€“allopurinolâ€“treated diabetic rats. Daily insulin injection (9â€“12 U/kg body wt., S.C.) for 1wk period normalized all of the aboveâ€“mentioned abnormalities. The present results suggest that XOâ€“derived ROS play a minor role (if any) in the diabetogenic effect of ALX. On the other hand, although the mechanism (s) underlying the protective effects of allopurinol on the diabetic state is presently unknown, these effects may reflect a possible association between impaired ketone body metabolism and lipid peroxidation: and suggest an effect of allopurinol on ketone body metabolism.

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3

Kaoutar, Achehboune, Baybay Hanane, Douhi Zakia, Elloudi Sara, and Zahra Mernissi Fatima. "Allopurinol: Attention to the Prescription!" Journal of Clinical Cases & Reports 3, S2 (November 30, 2020): 3–6. http://dx.doi.org/10.46619/joccr.2020.2.s2-1002.

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Allopurinol is a commun hypo-uricemic drug. However, it is main drug reported to be inducing toxidermy. Our goal is to encourage limiting the prescription of this drug and to reserve it for justified cases after some observations. A Retrospective study was conducted in the Dermatology department between 2012 and 2019. We collected all toxidermy cases following Allopurinol. During the study period,39 cases of severe Allopurinol toxidermia, including 22 women and 17 men, a sex ratio of 0.77. The average age was 65 years old. Most of the patients were "poly-medicated". The average time between medication and clinical symptoms was 28.25 days. Clinical manifestations were: macula-papular rash in 12 cases (30%), erythroderma in 14 cases (35%), purpura in 7 cases (17%) and mucosal involvement in 20 cases. Fever in 29 cases, a state of shock in 5 cases. 10 patients required a transfer in intensive care. On the balance sheet; eosinophilia was found in 23 cases, 18 cases of hepatic cytolysis, CPK mb was elevated in 17 cases, acute renal failure in 24 cases. The biopsy was performed in all cases confirming the toxidermy. The Drug reaction eosinophilia and systemic symptoms (DRESS) retained in 29 cases, Stevens-Johnson syndrome (SJS) in 2 cases, Lyell in 4 cases. The management involved stopping the incriminated drug (Allopurinol) and the introduction of an antihistamine and an emollient were prescribed in all patients. Topical steroid in 21 patients. Oral corticosteroid therapy in 14 patients. A bolus of corticosteroid was administered in 4 patients. The evolution was good for 30 patients (77%). However, we recorded 9 deaths in a context of septic shock and multi-visceral failure. In our series, Allopurinol was the cause of severe toxidermia including Lyell syndrome, StevensJohnson and DRESS syndrome. The severity of these diseases should encourage preserving it for the justified cases, and knowing how to adapt the dosage to the renal function, to introduce the treatment in a progressive way and to stop the treatment in case of less signs of toxidermy. The control of the use of this molecule would reduce the cases of this disease.

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4

Cortes, Jorge, Joseph O. Moore, Richard T. Maziarz, Meir Wetzler, Michael Craig, Jeffrey Matous, Selina Luger, et al. "Control of Plasma Uric Acid in Adults at Risk for Tumor Lysis Syndrome: Efficacy and Safety of Rasburicase Alone and Rasburicase Followed by Allopurinol Compared With Allopurinol Alone—Results of a Multicenter Phase III Study." Journal of Clinical Oncology 28, no. 27 (September 20, 2010): 4207–13. http://dx.doi.org/10.1200/jco.2009.26.8896.

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Purpose Rasburicase is effective in controlling plasma uric acid in pediatric patients with hematologic malignancies. This study in adults evaluated safety of and compared efficacy of rasburicase alone with rasburicase followed by oral allopurinol and with allopurinol alone in controlling plasma uric acid. Patients and Methods Adults with hematologic malignancies at risk for hyperuricemia and tumor lysis syndrome (TLS) were randomly assigned to rasburicase (0.20 mg/kg/d intravenously days 1-5), rasburicase plus allopurinol (rasburicase 0.20 mg/kg/d days 1 to 3 followed by oral allopurinol 300 mg/d days 3 to 5), or allopurinol (300 mg/d orally days 1 to 5). Primary efficacy variable was plasma uric acid response rate defined as percentage of patients achieving or maintaining plasma uric acid ≤ 7.5 mg/dL during days 3 to 7. Results Ninety-two patients received rasburicase, 92 rasburicase plus allopurinol, and 91 allopurinol. Plasma uric acid response rate was 87% with rasburicase, 78% with rasburicase plus allopurinol, and 66% with allopurinol. It was significantly greater for rasburicase than for allopurinol (P = .001) in the overall study population, in patients at high risk for TLS (89% v 68%; P = .012), and in those with baseline hyperuricemia (90% v 53%; P = .015). Time to plasma uric acid control in hyperuricemic patients was 4 hours for rasburicase, 4 hours for rasburicase plus allopurinol, and 27 hours for allopurinol. Conclusion In adults with hyperuricemia or at high risk for TLS, rasburicase provided control of plasma uric acid more rapidly than allopurinol. Rasburicase was well tolerated as a single agent and in sequential combination with allopurinol.

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5

Singh, Jasvinder A., and John D. Cleveland. "Hypersensitivity reactions with allopurinol and febuxostat: a study using the Medicare claims data." Annals of the Rheumatic Diseases 79, no. 4 (February 5, 2020): 529–35. http://dx.doi.org/10.1136/annrheumdis-2019-216917.

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

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6

&NA;. "Allopurinol." Reactions Weekly &NA;, no. 1380 (December 2011): 6. http://dx.doi.org/10.2165/00128415-201113800-00019.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 1384 (January 2012): 6–7. http://dx.doi.org/10.2165/00128415-201213840-00022.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 1384 (January 2012): 7. http://dx.doi.org/10.2165/00128415-201213840-00027.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 1395 (March 2012): 6. http://dx.doi.org/10.2165/00128415-201213950-00016.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 723 (October 1998): 6–7. http://dx.doi.org/10.2165/00128415-199807230-00019.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 736 (January 1999): 7. http://dx.doi.org/10.2165/00128415-199907360-00018.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 1171 (September 2007): 5. http://dx.doi.org/10.2165/00128415-200711710-00010.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 1171 (September 2007): 6. http://dx.doi.org/10.2165/00128415-200711710-00013.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 1193 (March 2008): 5. http://dx.doi.org/10.2165/00128415-200811930-00013.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 1126 (November 2006): 6. http://dx.doi.org/10.2165/00128415-200611260-00017.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 1129 (November 2006): 4–5. http://dx.doi.org/10.2165/00128415-200611290-00008.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 1131 (December 2006): 6. http://dx.doi.org/10.2165/00128415-200611310-00010.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 1135 (January 2007): 5. http://dx.doi.org/10.2165/00128415-200711350-00016.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 1144 (March 2007): 7. http://dx.doi.org/10.2165/00128415-200711440-00018.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 1154 (June 2007): 5. http://dx.doi.org/10.2165/00128415-200711540-00014.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 1361 (July 2011): 5–6. http://dx.doi.org/10.2165/00128415-201113610-00014.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 1364 (August 2011): 6. http://dx.doi.org/10.2165/00128415-201113640-00017.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 1370 (September 2011): 6–7. http://dx.doi.org/10.2165/00128415-201113700-00012.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 1370 (September 2011): 7. http://dx.doi.org/10.2165/00128415-201113700-00018.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 1374 (October 2011): 7. http://dx.doi.org/10.2165/00128415-201113740-00009.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 542 (March 1995): 4. http://dx.doi.org/10.2165/00128415-199505420-00008.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 554 (June 1995): 4. http://dx.doi.org/10.2165/00128415-199505540-00010.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 556 (June 1995): 5. http://dx.doi.org/10.2165/00128415-199505560-00016.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 577 (November 1995): 4. http://dx.doi.org/10.2165/00128415-199505770-00010.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 586 (February 1996): 5. http://dx.doi.org/10.2165/00128415-199605860-00013.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 591 (March 1996): 6. http://dx.doi.org/10.2165/00128415-199605910-00009.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 602 (May 1996): 5. http://dx.doi.org/10.2165/00128415-199606020-00009.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 607 (June 1996): 4. http://dx.doi.org/10.2165/00128415-199606070-00007.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 426 (November 1992): 5. http://dx.doi.org/10.2165/00128415-199204260-00009.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 438 (February 1993): 4. http://dx.doi.org/10.2165/00128415-199304380-00008.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 442 (March 1993): 5. http://dx.doi.org/10.2165/00128415-199304420-00009.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 451 (May 1993): 4. http://dx.doi.org/10.2165/00128415-199304510-00008.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 457 (June 1993): 5. http://dx.doi.org/10.2165/00128415-199304570-00015.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 634 (January 1997): 6. http://dx.doi.org/10.2165/00128415-199706340-00017.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 655 (June 1997): 6. http://dx.doi.org/10.2165/00128415-199706550-00014.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 787 (February 2000): 6. http://dx.doi.org/10.2165/00128415-200007870-00014.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 828 (November 2000): 7. http://dx.doi.org/10.2165/00128415-200008280-00009.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 1399 (April 2012): 6. http://dx.doi.org/10.2165/00128415-201213990-00015.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 1403 (May 2012): 7. http://dx.doi.org/10.2165/00128415-201214030-00016.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 1407 (June 2012): 6. http://dx.doi.org/10.2165/00128415-201214070-00017.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 1407 (June 2012): 6. http://dx.doi.org/10.2165/00128415-201214070-00019.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 1409 (July 2012): 8. http://dx.doi.org/10.2165/00128415-201214090-00019.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 1409 (July 2012): 8. http://dx.doi.org/10.2165/00128415-201214090-00021.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 1410 (July 2012): 7. http://dx.doi.org/10.2165/00128415-201214100-00021.

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&NA;. "Allopurinol." Reactions Weekly &NA;, no. 1414 (August 2012): 7. http://dx.doi.org/10.2165/00128415-201214140-00016.

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