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Статті в журналах з теми "Tiopurine"
Barun, Franjo, Dražen Zekanović, and Neven Ljubičić. "Azatioprin u liječenju bolesnika s ulceroznim kolitisom." Medica Jadertina 52, no. 2 (August 26, 2022): 143–53. http://dx.doi.org/10.57140/mj.52.2.8.
Повний текст джерелаHartleb, Marek, Ewa Nowakowska-Duława, and Agnieszka Budzyńska. "Leki immunomodulujące – farmakokinetyka, interakcje i objawy niepożądane." Gastroenterologia Praktyczna 9, no. 2 (August 30, 2017): 36. http://dx.doi.org/10.26625/gp.2017.9.2.32.
Повний текст джерелаDomènech Morral, Eugeni, and Miquel Àngel Gassull Duro. "Actividad eritrocitaria de tiopurina metiltransferasa y tratamiento con tiopurinas en la enfermedad inflamatoria intestinal." Medicina Clínica 125, no. 8 (September 2005): 293–94. http://dx.doi.org/10.1157/13078429.
Повний текст джерелаŠmid, Alenka, Janez Jazbec, and Irena Mlinarič-Raščan. "Farmakogenetski označevalci v terapiji akutne limfoblastne levkemije pri otrocih." Slovenian Medical Journal 88, no. 5-6 (July 10, 2019): 235–48. http://dx.doi.org/10.6016/zdravvestn.2851.
Повний текст джерелаGisbert, Javier P., Luis González-Guijarro, Carlos Cara, José María Pajares, and Ricardo Moreno-Otero. "Actividad de la tiopurina metiltransferasa en pacientes con hepatitis autoinmune." Medicina Clínica 121, no. 13 (January 2003): 481–84. http://dx.doi.org/10.1016/s0025-7753(03)73996-7.
Повний текст джерелаJorquera, Andrés, Sandra Solari, Valeska Vollrath, Irene Guerra, José Chianale, Colomba Cofré, Alexis Kalergis, Patricio Ibáñez, Susan Bueno, and Manuel Álvarez-Lobos. "Genotipo y fenotipo de la enzima tiopurina metiltransferasa en población chilena." Revista médica de Chile 140, no. 7 (July 2012): 889–95. http://dx.doi.org/10.4067/s0034-98872012000700009.
Повний текст джерелаCoraminas, Héctor, Montserrat Domènech, Dolors González-Juan, Begoña González-Suárez, César Díaz, Joan Pujol, Guillermo Vázquez, and Montserrat Baiget. "Aplasia medular tras administración de azatioprina: papel del polimorfismo genético de la tiopurina metiltransferasa." Medicina Clínica 115, no. 8 (January 2000): 299–301. http://dx.doi.org/10.1016/s0025-7753(00)71540-5.
Повний текст джерелаTárnok, András. "A tiopurinkezelés súlyos mellékhatásainak gyakorisága normális tiopurin-S-metiltranszferáz-genotípusú gyulladásos bélbetegségben szenvedő gyermekekben." Orvosi Hetilap 160, no. 5 (February 2019): 179–85. http://dx.doi.org/10.1556/650.2019.31277.
Повний текст джерелаGisbert, Javier P., Fernando Gomollón, Carlos Cara, Marta Luna, Yago González-Lama, José María Pajares, José Maté, and Luis G. Guijarro. "Actividad de la tiopurina metiltransferasa en la enfermedad inflamatoria intestinal. Un estudio en 7.046 pacientes españoles." Medicina Clínica 125, no. 8 (September 2005): 281–85. http://dx.doi.org/10.1157/13078420.
Повний текст джерелаGisbert, J. P., F. Gomollón, J. Maté, and J. M. Pajares. "Terapia individualizada con azatioprina o 6-mercaptopurina mediante monitorización de la actividad de la tiopurina metiltransferasa (TPMT)." Revista Clínica Española 202, no. 10 (January 2002): 555–62. http://dx.doi.org/10.1016/s0014-2565(02)71143-0.
Повний текст джерелаДисертації з теми "Tiopurine"
RANIERI, MICAELA. "Terapie biologiche, tiopurine e neoplasie nelle malattie infiammatorie intestinali: studio monocentrico retrospettivo su 1057 pazienti." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2010. http://hdl.handle.net/2108/1205.
Повний текст джерелаBackground. Whether the growing use of immunomodulatory drugs (ISS) and biologic therapies may increase the cancer risk in Inflammatory Bowel Disease (IBD) is undefined. Aims. In a single-center, cohort study we aimed to assess the frequency and histotype of cancer in a population of 1057 patients (pts) under regular follow up. The frequency of cancer was also assessed in relation to previous ISS and/or anti-TNFs use. Materials and methods. In a cross-sectional study, clinical records from all IBD pts. In follow up from 1984-2009 in our tertiary IBD referral center were reviewed. Data recorded: IBD type/ site/duration, surgery, smoking habits, follow up length, ISS and/or anti-TNFs use. Statistical analysis: Wilcoxon test,t test and χ test. Results. The study population included 1057 IBD pts (512 F 545 M): 555 Crohn’s Disease (CD), 502 Ulcerative Colitis (UC). Cancer was diagnosed in 73/1057 IBD (6.9%; 39M 34F): 47/555 CD (8.5%), 26/502 UC (5.2%). Cancer site/histotype: breast 14 (10 CD, 4 UC); colon 7 (3 CD, 4 UC), skin 7 (5 CD, 2 UC), lymphoma 6 (5 CD, 1 UC), anal canal 2 (2 CD), other cancers 37. Among the 73 pts with IBD and cancer, ISS use reported by 20 (27.3%), anti-TNFs by 10 (13.6%), both ISS and anti-TNFs by 7 pts (9.5%). Age at the diagnosis of cancer: IBD 52.4 yrs (range 21-81), UC 52 (range 27-81), CD 62 (range 13-83). The relation between clinical features and cancer was assessed in 1057 IBD pts (52.4 age range 13-83): 555 CD, 502 UC (IBD duration: UC 7 yrs, range 1-86 vs CD 12 yrs, range 1-76; p=< 0.01). Previous treatments: ISS in 275/1057 IBD (26%), 201/555 CD (36.2%), 74/502 UC (14.7%); Anti-TNFs in 179/1057 IBD (16.9%), 146/555 CD (26.3%), 33/502 UC (6.6%); Concomitant ISS and anti-TNFs in 125/1057 IBD (11.8%), 104/555 CD (18.7%), 21/502 UC (4.2%). Cancer was diagnosed in 73/1057 (6.9%; 39M 34F) IBD pts: 47/555 CD (8.5%), 26/502 UC (5.2%; p=ns). Among the 73 pts with IBD and cancer, ISS use reported by 20/73 (27.3%)(age 51 vs 55 yrs in the 53 pts with cancer and no ISS use; p=ns), including 12/20 CD (0.6%), 8/20 UC (0.4%). Among the 73 pts with IBD and cancer, anti-TNFs use reported by 10/73 IBD (0.14%) (age 53 vs 55 yrs in the 63 pts with cancer and no anti-TNFs; p=ns), including 9/ 47 CD (19.1%), 1/26 UC (3.8%). Among the 73 pts with IBD and cancer, both ISS and anti-TNFs use reported by 7/73 (9.5%)(age 51, vs 54 yrs in the50 pts with no concomitant ISS and anti-TNFs; p=ns), including 7/47 CD (14.8%), 0/26 UC (0%). Cancer site/histotype: breast 11 (11 CD); colon 4 (2 CD), skin 4 (3 CD), lymphoma 3 (3 CD), anal canal 1 (CD), other cancers 18. Conclusions. In our cohort of 1057 IBD pts, a high frequency of cancer was observed, with a not significantly higher trend in CD pts treated with ISS, while anti-TNFs appeared not to significantly increase the cancer risk.
Silva, Marcilene Rezende. "Polimorfismo do gene da tiopurina metiltransferase(TPMT) em uma população de crianças e adolescentes com leucemia linfocítica aguda(LLA)." Universidade Federal de Minas Gerais, 2007. http://hdl.handle.net/1843/ECJS-743MKR.
Повний текст джерелаEsberard, Barbara Cathalá. "Polimorfismos do gene da tiopurina metiltransferase (TPMT) em pacientes com doenças inflamatórias intestinais: avaliação da prevalência e correlação com efeitos colaterais." Universidade do Estado do Rio de Janeiro, 2013. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=6947.
Повний текст джерелаAlthough azathioprine is commonly used for treating patients with inflammatory bowel disease (IBD), there is still concern about potential severe side effects. Determining the Thiopurine-Methyl-Transferase (TPMT) genotype is expected to identify patients predisposition in respect of toxicity prior to azathioprine administration. The aim of this study was to analyze the prevalence of TPMT genotypes and association with drug toxicity in IBD patients from south-eastern Brazil, constituted by a heterogeneous population. We analyzed 146 Crohns disease (CD) and 73 ulcerative colitis (UC) patients, for the presence of the major TPMT genetic variants (TPMP*2, *3A, *3C) by means of specific allele and RFLP PCR. Clinical data were systematically recorded and correlated with the genotype results, and analyzed in multivariate models. Among the side effects recorded from patients taking azathioprine, 14 presented pancreatitis and/or elevation of pancreatic enzymes, while 6 had liver toxicity, and 2 had neutropenia. TPMT polymorphisms were detected in 37/219 patients (8 heterozygous for *2, 11 heterozygous for *3A and 18 heterozygous for *3C). No homozygotic polymorphisms were found. A positive correlation was found between the elevation of pancreatic enzymes and either TPMT*2 or TPMT*3C. The prevalence of polymorphisms in this study (16,89%) was greater than described with caucasian population or other Brazilian studies. Despite the prevalence of genotype *3C, it was not the only polymorphism shown as observed in other populations. Two genetic variants of TPMT gene (*2 and *3C) are associated with azathioprine toxicity in IBD patients from a south-eastern Brazilian population. Genetic testing may help in the selection of the most appropriate medication prior to treatment initiation.
Ribeiro, Aline Corrêa. "Desenvolvimento, validação e aplicação de metodologia analítica em CLAE-UV para monitoramento terapêutico de metabólitos da azatioprina em pacientes com doença de Crohn." Universidade Federal de Juiz de Fora (UFJF), 2017. https://repositorio.ufjf.br/jspui/handle/ufjf/6934.
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Devido à importância que o sistema imune desempenha na doença de Crohn (DC), as tiopurinas são os imunomoduladores mais indicados na terapia. Entretanto, as tiopurinas, como a Azatioprina (AZA) e seus metabólitos intraeritrocitários, levam a uma série de reações adversas ou falha terapêutica, podendo ocasionar em não adesão ou abandono da terapia. A conversão da AZA para os nucleotídeos ativos de 6-tioguanina (6-TGN) é necessária para a eficácia clínica, entretanto, outro metabólito, a 6-metilmercaptopurina (6-MMP), é formado através de uma via concorrente pela tiopurina metil transferase e está relacionado à hepatotoxicidade. Devido à ampla variabilidade interindividual da tiopurina metil transferase e a uma faixa terapêutica estreita, torna-se importante a realização do monitoramento terapêutico do metabólito ativo 6-TGN e da 6-MMP. Neste trabalho, um método cromatográfico (CLAE/HPLC-UV) foi desenvolvido e validado para a quantificação dos metabólitos nos eritrócitos, envolvendo um procedimento de tratamento simples baseado na desproteinização por ácido perclórico seguido de hidrólise ácida e aquecimento para a conversão dos metabólitos em suas respectivas bases livres. A cromatografia foi realizada em coluna C18 (250 x 4,6 mm, 5 μm). A fase móvel consistiu em mistura de solução tampão fosfato de potássio (0,02 mol/L, pH = 3), acetonitrila e metanol, eluição por gradiente, num fluxo de 1,0 mL/minuto, com detecção de UV em 291 ηm e 342 ηm. Os tempos de retenção foram de 6,2 min (6-TGN); 23,1 min (6-MMP) e 24,7 min (cafeína: padrão interno). A resposta do detector foi linear na concentração de 0,89-29,91 μmol/L (r=0,999) para 6-TGN e entre 0,90-30,08 μmol/L (r=0,999) para 6-MMP. Os limites de detecção foram de 0,29 μmol/L e 0,30 μmol/L e os limites de quantificação foram de 0,89 μmol/L e 0,90 μmol/L, para 6-TGN e 6-MMP respectivamente. As médias das recuperações de 87,9% para 6-TGN e 91,9% para 6-MMP. Os CV da repetibilidade, de 5,48 e 10,48% (intradia) e 9,23 e 10,48% (interdia), enquanto os EPR da reprodutibilidade de 11,36 e 9,85% (intradia) e 10,48 e 7,32% (interdia) para 6-TGN e 6-MMP, respectivamente. As concentrações de 6-TGN e 6-MMP foram determinadas para todos os pacientes do estudo e os resultados encontrados variaram de 4,51 a 1515,27 ρmol/8 x 10⁸ eritrócitos para a 6-TGN e de 169,98 a 53951,53 ρmol/8 x 10⁸ eritrócitos para a 6-MMP. Observou-se uma correlação entre os pacientes em terapia combinada AZA e alopurinol e a diminuição da dosagem de AZA, consequentemente a diminuição significativa dos níveis de 6-MMP (2030,71 ρmol/8 x 10⁸ eritrócitos) em comparação com o grupo de pacientes sob monoterapia (9098,43 ρmol/8 x 10⁸ eritrócitos). Um outro achado foi a diminuição estatisticamente significativa da transaminase TGO/AST (25,03 + 18,62 U/L) no grupo de pacientes que apresentavam a doença em atividade, com os níveis de 6-TGN a 540,51 ρmol/8 x 10⁸ eritrócitos e de 6-MMP a 7952,32 ρmol/8 x 10⁸ eritrócitos, semelhante a relatos anteriores da literatura. O método proposto de quantificação por CLAE-UV mostrou-se preciso, exato e reprodutível, podendo ser utilizado como uma importante ferramenta na rotina de monitorização terapêutica de pacientes com DC, permitindo a individualização da dose, o acompanhamento dos efeitos adversos relacionados com a terapia farmacológica, o monitoramento da adesão ao tratamento e a avaliação da evolução clínica do paciente.
The conversion of azathioprine (AZA) to active nucleotides of 6-thioguanine (6-TGN) is essential for clinical efficacy in Crohn's disease. However, other metabolite, 6-methylmercaptopurine (6-MMP), which is formed through a competitive pathway for thiopurine methyltransferase (TPMT), is related to hepatotoxicity of this drug. Due to the wide interindividual variability of TPMT and a narrow therapeutic range it is important to accomplish the therapeutic monitoring of active metabolite 6-TGN and 6-MMP, which is an unusual procedure in Brazil. In this study, a HPLC-UV method for simultaneous quantification of these metabolites was developed, validated and applied in 37 Crohn's disease patients. The chromatographic process was performed on C18 column (250 x 4.6 mm, 5 μm i.d.), mobile phase consisted of potassium phosphate buffer (0.02 mol/L, pH = 3), acetonitrile and methanol, flow rate at 1.0 ml/min and UV detection at 291 ηm and 342 ηm. Retention times were 6.2 min (6-TGN); 23.1 min (6-MMP) and 24.7 min (caffeine: internal standard). The detector response was linear at 0.89-29.91 μmol/L (r=0.999) for 6-TGN and 0.90-30.08 μmol/L (r=0.999) for 6-MMP. Limits of detection were 0.29 μmol/L and 0.30 μmol/L, while the quantification limits were 0.89 μmol/L and 0.90 μmol/L, for 6-TGN and 6-MMP respectively. Precision, accuracy and recovery, were according FDA and ANVISA guidelines. The concentrations of 6-TGN and 6-MMP were determined in patients’ blood and the results found ranged from 4.51 to 1515 ρmol/8 x 10⁸ erythrocytes for 6-TGN and from 169.98 to 53.951 ρmol/8 x 10⁸ erythrocytes for 6-MMP. It was observed a reduction of levels of 6-MMP in patients using AZA + allopurinol therapy (2030.7 ρmol/8 x 10⁸ erythrocytes) when compared with patients undergoing monotherapy (9098.43 ρmol/8 x 10⁸ erythrocytes). Another finding was the correlation between the decrease in GOT transaminase in the group of patients who had the active disease with the increase in the 6-TGN levels, similar to previous reports in the literature. These results indicate that the method developed was reliable, accurate and reproducible, and can be used as an important tool in the routine monitoring of patients with Crohn's disease, allowing the individualization of the dose, the monitoring of the adverse effects related to the pharmacological therapy, monitoring the adherence to the treatment and the evaluation of the clinical evolution of these patients.