ELIDA PAULA BENQUIQUE OJOPI
Projetos de Pesquisa
Unidades Organizacionais
LIM/27 - Laboratório de Neurociências, Hospital das Clínicas, Faculdade de Medicina
2 resultados
Resultados de Busca
Agora exibindo 1 - 2 de 2
- Association of the UGT1A1-53(TA)(n) polymorphism with L-thyroxine doses required for thyrotropin suppression in patients with differentiated thyroid cancer(2011) VARGENS, Daniela D.; NEVES, Ronaldo R. S.; BULZICO, Daniel A.; OJOPI, Elida B.; MEIRELLES, Ricardo M. R.; PESSOA, Cencita N.; PRADO, Carolina M.; GONCALVES, Pedro A.; LEAL, Vera L. G.; SUAREZ-KURTZ, GuilhermeThere is a considerable interindividual variation in L-thyroxine [ 3,5,3',5'-tetraiodo-l-thyronine (T-4)] dose required for thyrotropin (thyroid-stimulating hormone) suppression in patients with differentiated thyroid cancer. To investigate whether uridine diphosphate-glucuronosyl transferase 1A1 (UGT1A1)-mediated T-4 glucuronidation in liver affects T-4 dose, we genotyped 101 patients for the common UGT1A1-53(TA)(n) polymorphism and compared T-4 doses among patients having zero (5/6 and 6/6 genotypes), one (6/7 genotype), or two (7/7 and 7/8 genotypes) copies of the low-expression (TA) 7 and (TA) 8 alleles. A significant trend for decreasing T-4 dose with increasing number of copies of (TA)(7) and (TA)(8) (P = 0.037) and significant difference in T-4 dose across the UGT1A1-53(TA)(n) genotypes (P = 0.048) were observed, despite considerable overlap of T-4 doses among different genotypes. These results are consistent with reduced T-4 glucuronidation in patients with low-expression (TA) 7 and (TA) 8 alleles and provide the first evidence for association between UGT1A1-53(TA)(n) and T-4-dose requirement for thyroid-stimulating hormone suppression in a natural clinical setting. Pharmacogenetics and Genomics 21: 341-343 (C) 2011 Wolters Kluwer Health | Lippincott Williams & Wilkins. Pharmacogenetics and Genomics 2011, 21: 341-343
conferenceObject Refractoriness in Schizophrenia is not Associated with Cyp2d6 and Cyp2c19 Genotypes(2012) BILT, Martinus T. van de; PRADO, Carolina M.; OJOPI, Elida P. B.; ZANETTI, Marcus V.; LOCH, Alexandre A.; SOUSA, Rafael A. T.; MACHADO-VIEIRA, Rodrigo; GATTAZ, Wagner F.Background: All genes that encode the CYP450 enzymes are highly polymorphic, leading to different metabolic profiles. While for antidepressants it’s possible to make dose adjustments based on the CYP2D6 and CYP2C19 genotypes, there are currently no evidences validating genotype based adjustments for antipsychotics. Therefore, we aimed to investigate the hypothesis that the prevalence of ultra-rapid metabolizers of neuroleptics would be increased among refractory schizophrenia patients. Methods: 89 schizophrenia patients were enrolled and divided in two groups: 59 refractory patients according to IPAP algorithm (International Psychopharmacology Algorithm Project) and 30 non-refractory patients. Polymorphisms in CYP2D6 and CYP2C19 genes were evaluated by allelic discrimination using the TaqMan® system. The following alleles were investigated: CYP2D6*1, *2, *3, *4, *5, *6, *9, *10, *15, *17, *29, *35, *39, *40, *41 beyond copy number variations and alleles CYP2C19*1, *2, *3 and *17. The phenotypes were classified in extensive metabolizers (EMs), poor metabolizers (PMs), intermediary metabolizers (IMs) and ultra-rapid metabolizers (UMs). Results: The distribution of the CYP2D6 and CYP2C19 phenotypes were as follows: CYP2D6: - Non-refractory: 13.3%PM + IM, 86.6%EM and 0.0% UM - Refractory: 13.5%PM + IM, 86.4%EM and 0.0%UM CYP2C19: - Non-refractory: 16.6%PM + IM, 53.3%EM and 30.0% UM - Refractory: 27.1%PM + IM, 40.6%EM and 32.2%UM Statistical analysis showed no significant difference between the distribution of the CYP2D6 phenotypes (p=0.244) and CYP2C19 predicted phenotypes (p = 0.755) among the two groups. Conclusions: Our findings do not reinforce the inclusion of genotyping of these genes as a tool in the clinical decision making in refractory schizophrenia.