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Relevant bibliographies by topics / Tiopurine

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Journal articles

Academic literature on the topic 'Tiopurine'

Author: Grafiati

Published: 1 April 2023

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Journal articles on the topic "Tiopurine"

1

Barun, Franjo, Dražen Zekanović, and Neven Ljubičić. "Azatioprin u liječenju bolesnika s ulceroznim kolitisom." Medica Jadertina 52, no. 2 (2022): 143–53. http://dx.doi.org/10.57140/mj.52.2.8.

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Ulcerozni kolitis kronična je upalna bolest za koju su karakteristične ulceracije sluznice debeloga crijeva i klinički tijek obilježen razdobljima remisije i relapsa bolesti. Klinički se ulcerozni kolitis najčešće očituje učestalim sluzavo-krvavim proljevima. Azatioprin je tiopurin koji imunosupresiju postiže putem svojih aktivnih metabolita. Oni potiču apoptozu T-limfocita, te, inkorporirajući se u replicirajući lanac DNA i blokirajući de novo sintezu purina, smanjuju njihovu proliferaciju. Mjerenjem aktivnosti tiopurin Smetiltransferaze i praćenjem metabolita tiopurina, uspješno se postiže optimizacija terapije. Time se poboljšava klinička djelotvornost liječenja, te sprječava neuspjeh liječenja uzrokovan štetnim nuspojavama azatioprina. Unatoč pretpostavkama da će u budućnosti, zbog razvoja učinkovitijih i sigurnijih lijekova, uloga tiopurina u liječenju bolesnika s ulceroznim kolitisom biti ograničenija, azatioprin i dalje ostaje neizostavan lijek u liječenju bolesnika s ulceroznim kolitisom.

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2

Hartleb, Marek, Ewa Nowakowska-Duława, and Agnieszka Budzyńska. "Leki immunomodulujące – farmakokinetyka, interakcje i objawy niepożądane." Gastroenterologia Praktyczna 9, no. 2 (2017): 36. http://dx.doi.org/10.26625/gp.2017.9.2.32.

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Supresja układu immunologicznego jest podstawą leczenia wielu lokalnych i układowych chorób autoimmunizacyjnych. Przewlekłe stosowanie kortykosteroidów wiąże się z klinicznie istotnymi powikłaniami, co było powodem poszukiwania leków immunosupresyjnych zastępujących kortykosteroidy. Głównym działaniem leków immunomodulujących jest hamowanie proliferacji limfocytów na drodze różnych mechanizmów – alkilujących (cyklofosfamid, chlorambucyl), antymetabolicznych (tiopuryny, metotreksat, mykofenolan mofetylu) lub hamowania kalcyneuryny (cyklosporyna, takrolimus, ewerolimus). Przedstawiono przegląd wiedzy na temat farmakodynamiki, efektów niepożądanych i interakcji lekowych tiopuryn i metotreksatu – konwencjonalnych immunomodulatorów stosowanych w leczeniu nieswoistych zapaleń jelit.

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3

Domènech 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 (2005): 293–94. http://dx.doi.org/10.1157/13078429.

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4

Šmid, Alenka, Janez Jazbec, and Irena Mlinarič-Raščan. "Farmakogenetski označevalci v terapiji akutne limfoblastne levkemije pri otrocih." Slovenian Medical Journal 88, no. 5-6 (2019): 235–48. http://dx.doi.org/10.6016/zdravvestn.2851.

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Posamezniku prilagojeno zdravljenje predstavlja sodoben koncept v medicinski praksi, ki temelji na spoznanju, da se posamezniki različno odzivajo na določeno terapijo. Osrednji element prilagojenega zdravljenja predstavljajo biološki označevalci, med katere uvrščamo tudi genetske. Med najuspešnejše primere uvajanja farmakogenetskih označevalcev v klinično prakso z namenom prilagajati odmerjanje zdravil posamezniku sodi zdravljenje akutne limfoblastne levkemije (ALL). Ta predstavlja približno 80 % vseh oblik levkemije, ki se pojavijo pri otrocih, mlajših od 15 let, kar jo uvršča na prvo mesto po pogostosti raka v otroštvu. V zadnjih desetletjih smo bili priča izjemnemu napredku na področju zdravljenja ALL, kljub temu pa je le-to še vedno neuspešno pri nekaterih bolnikih bodisi zaradi toksičnih stranskih učinkov, bodisi zaradi neučinkovitosti uporabljenih zdravil, kar vodi v ponovitev bolezni. Dodaten problem predstavljajo še dolgoročni toksični učinki kemoterapije, ki se lahko pojavijo tudi več let po zaključenem zdravljenju. Prav iz teh razlogov se je v zadnjih letih veliko študij posvetilo odkrivanju bioloških označevalcev, na podlagi katerih bi lahko zdravljenje prilagodili posamezniku in s tem izboljšali njegovo učinkovitost in varnost. Najbolje proučeni so genetski dejavniki, povezani s toksičnostjo 6-merkaptopurina (6-MP), ki predstavlja temelj vzdrževalnega zdravljenja ALL. Encim tiopurin-S-metiltransferaza (TPMT) igra poglavitno vlogo pri deaktiviranju tiopurinov in v veliki meri vpliva na razlike v odzivu posameznikov na zdravljenje. Znano je, da so za znižane encimske aktivnosti v največji meri odgovorni polimorfizmi v genu za TPMT, vendar je ujemanje med genotipom in encimsko aktivnostjo nepopolno. V zadnjem desetletju so identificirali nove farmakogenetske označevalce, povezane s toksičnostjo 6-MP in drugih zdravil, ki se uporabljajo za zdravljenje otroške ALL, vendar se še ne uporabljajo v klinični praksi.

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5

Gisbert, 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 (2003): 481–84. http://dx.doi.org/10.1016/s0025-7753(03)73996-7.

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6

Jorquera, Andrés, Sandra Solari, Valeska Vollrath, et al. "Genotipo y fenotipo de la enzima tiopurina metiltransferasa en población chilena." Revista médica de Chile 140, no. 7 (2012): 889–95. http://dx.doi.org/10.4067/s0034-98872012000700009.

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7

Coraminas, Héctor, Montserrat Domènech, Dolors González-Juan, et al. "Aplasia medular tras administración de azatioprina: papel del polimorfismo genético de la tiopurina metiltransferasa." Medicina Clínica 115, no. 8 (2000): 299–301. http://dx.doi.org/10.1016/s0025-7753(00)71540-5.

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8

Tárnok, András. "A tiopurinkezelés súlyos mellékhatásainak gyakorisága normális tiopurin-S-metiltranszferáz-genotípusú gyulladásos bélbetegségben szenvedő gyermekekben." Orvosi Hetilap 160, no. 5 (2019): 179–85. http://dx.doi.org/10.1556/650.2019.31277.

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Abstract: Introduction: Genetic polymorphism of thiopurine S-methyltransferase, the key enzyme in metabolism of thiopurines (azathioprine and 6-mercaptopurine) used in the treatment of inflammatory bowel disease, results in different enzyme activities. Decreased enzyme activity causes myelosuppression whereas abnormally high activity results in hepatotoxicity at standard thiopurine doses. Four allele variants (TMPT*2, TMPT*3A, TPMT*3B and TPMT*3C) account for decreased activity in more than 95% of cases. Aim: To evaluate the frequency of severe side effects, such as myelosuppression and hepatotoxicity, at standard or decreased azathioprine doses in children with inflammatory bowel disease who do not exhibit any of the four most common variant alleles. Method: Retrospective analysis of children with inflammatory bowel disease treated with azathioprine at a single tertiary referral center. Results: 51 patients were identified (44: Crohn’s disease, 7: ulcerative colitis; male ratio: 28/51; mean age at diagnosis: 12.4 years). Two patients discontinued azathioprine arbitrarily whereas in one patient it was stopped due to serious pancreatitis and in another one because of severe flu-like symptoms. None of the remaining 47 patients exhibited hepatotoxicity suggesting abnormally high thiopurine S-methyltransferase activity. Four patients (8.5%) had profound myelosuppression on less than 1 mg/kg/day azathioprine requiring discontinuation of the drug, and all of them showed complete bone marrow recovery subsequently. No myelosuppression occurred in the remaining 43 patients on 2.17 ± 0.31 mg/kg/day (mean ± SD) azathioprine treatment. Conclusions: Regular blood tests are necessary on thiopurine therapy despite normal thiopurine S-methyltransferase genotype because of the risk of myelosuppression. The four most common variant alleles were identified in routine genotyping only, therefore most likely rare variant allele(s) or polymorphism of other enzymes involved in thiopurine metabolism account for the aforementioned four cases with profound bone marrow suppression. Thiopurine metabolite monitoring is the key for individualized treatment when optimal dosing can be achieved with the least side effects. Orv Hetil. 2019; 160(5): 179–185.

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9

Gisbert, Javier P., Fernando Gomollón, Carlos Cara, et al. "Actividad de la tiopurina metiltransferasa en la enfermedad inflamatoria intestinal. Un estudio en 7.046 pacientes españoles." Medicina Clínica 125, no. 8 (2005): 281–85. http://dx.doi.org/10.1157/13078420.

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10

Gisbert, 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 (2002): 555–62. http://dx.doi.org/10.1016/s0014-2565(02)71143-0.

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