UGT1A1*28 relationship with abnormal total bilirubin levels in chronic hepatitis C patients Outcomes from a case-control study

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art_SOUZA_UGT1A128_relationship_with_abnormal_total_bilirubin_levels_in_2017.PDF (236.54 KB)
Citações na Scopus
15
Tipo de produção
article
Data de publicação
2017
Editora
LIPPINCOTT WILLIAMS & WILKINS
DOI
Indexadores
Scopus
Web of Science
PubMed
Título da Revista
ISSN da Revista
Título do Volume
Autores
SOUZA, Marcelo Moreira Tavares de
FERREIRA, Aline Siqueira
DASILVAFERREIRA, Camila
PASCHOALE, Helena Scavone
Autor de Grupo de pesquisa
Editores
Coordenadores
Organizadores
Citação
MEDICINE, v.96, n.11, article ID e6306, 5p, 2017
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Gilbert syndrome (GS) is a frequent benign clinical condition, marked by intermittent unconjugated hyperbilirubinemia, mostly due to the polymorphism uridine diphosphate-glucuronosyltransferase 1A1* 28 (UGT1A1* 28). Hyperbilirubinemia has been reported in a GS patient undergoing hepatitis C treatment, and other UGT isoforms polymorphisms have been linked to worse outcomes in viral hepatitis. Yet, little is known to GS contributions' to the liver disease scenario. Our aim was to assess UGT1A1 genotypes' frequency in chronic hepatitis C (CHC) patients and correlate with total bilirubin (TB). This is a case-control study in a large tertiary medical center. Cases were CHC patients confirmed by hepatitis C virus (HCV)-polymerase chain reaction. Exclusion criteria were hepatitis B virus or human immunodeficiency virus (HIV) coinfection. Control were healthy blood donors. UGT1A1 promoter region gene genotyping was performed, and bilirubin serum levels were available for HCV patients. Genotypes and alleles frequencies were similar in case (n= 585; P= 0.101) and control groups (n= 313; P= 0.795). Total bilirubin increase was noticed according to thymine-adenine repeats in genotypes (P < 0.001), and the TB greater than 1mg/dL group had more UGT1A1* 28 subjects than in the group with TB values < 1mg/dL (18.3 vs 5.3; P < 0.001). Bilirubin levels are linked to the studied polymorphisms, and this is the first time that these findings are reported in a chronic liver disease sample. Among patients with increased TB levels, the frequency of UGT1A1* 28 is higher than those with normal TB. Personalized care should be considered to GS, regarding either abnormal bilirubin levels or drug metabolism.
Palavras-chave
chronic, Gilbert syndrome, hepatitis C, hyperbilirubinemia
URI
https://observatorio.fm.usp.br/handle/OPI/20038
Referências
  1. Abumiya M, 2014, DRUG METAB PHARMACOK, V29, P449, DOI 10.2133/dmpk.DMPK-14-RG-031
  2. Ando Y, 1998, ANN ONCOL, V9, P845, DOI 10.1023/A:1008438109725
  3. Astolfi RH, 2011, MED HYPOTHESES, V77, P162, DOI 10.1016/j.mehy.2011.03.047
  4. Bajro MH, 2012, CANCER GENET-NY, V205, P163, DOI 10.1016/j.cancergen.2012.01.015
  5. Beutler E, 1998, P NATL ACAD SCI USA, V95, P8170, DOI 10.1073/pnas.95.14.8170
  6. Bins S, 2016, PHARMACOGENOMICS, V17, P1483, DOI 10.2217/pgs-2016-0063
  7. BOCK KW, 1991, CRIT REV BIOCHEM MOL, V26, P129, DOI 10.3109/10409239109081125
  8. Bosma PJ, 2003, J HEPATOL, V38, P107, DOI 10.1016/S0168-8278(02)00359-8
  9. BOSMA PJ, 1995, NEW ENGL J MED, V333, P1171, DOI 10.1056/NEJM199511023331802
  10. Costa E, 2006, BLOOD CELL MOL DIS, V36, P91, DOI 10.1016/j.bcmd.2005.09.002
  11. Culley CL, 2013, ANN PHARMACOTHER, V47, P561, DOI 10.1345/aph.1R550
  12. Deterding K, 2009, ANN HEPATOL, V8, P246
  13. Fertrin KY, 2002, AM J MED GENET, V108, P117, DOI 10.1002/ajmg.10209
  14. Fujita K, 2011, CANCER CHEMOTH PHARM, V67, P237, DOI 10.1007/s00280-010-1445-3
  15. Gammal RS, 2016, CLIN PHARMACOL THER, V99, P363, DOI 10.1002/cpt.269
  16. Girard H, 2005, HEPATOLOGY, V42, P448, DOI 10.1002/hep.20770
  17. Goey AKL, 2016, J CLIN PHARMACOL, V56, P461, DOI 10.1002/jcph.625
  18. Guillemette C, 2000, CANCER RES, V60, P950
  19. Innocenti F, 2004, J CLIN ONCOL, V22, P1382, DOI 10.1200/JCO.2004.07.173
  20. Iolascon A, 1999, HAEMATOLOGICA, V84, P106
  21. Lankisch TO, 2005, MOL PHARMACOL, V67, P1732, DOI 10.1124/mol.104.007146
  22. Lin JP, 2006, CIRCULATION, V114, P1476, DOI 10.1161/CIRCULATIONAHA.106.633206
  23. Lin JP, 2009, ATHEROSCLEROSIS, V206, P228, DOI 10.1016/j.atherosclerosis.2009.02.039
  24. Liu CY, 2008, CANCER, V112, P1932, DOI 10.1002/cncr.23370
  25. Lok AS, 2012, GASTROENTEROLOGY, V143, P619, DOI 10.1053/j.gastro.2012.05.037
  26. Lubomirov R, 2011, J INFECT DIS, V203, P246, DOI 10.1093/infdis/jiq043
  27. MACKLON AF, 1979, CLIN PHARMACOKINET, V4, P223, DOI 10.2165/00003088-197904030-00004
  28. MARTIN JF, 1976, GASTROENTEROLOGY, V70, P385
  29. Monaghan G, 1996, LANCET, V347, P578, DOI 10.1016/S0140-6736(96)91273-8
  30. Piratvisuth T, 2013, PLOS ONE, V8, DOI 10.1371/journal.pone.0054279
  31. Premawardhena A, 2003, BLOOD CELL MOL DIS, V31, P98, DOI 10.1016/S1079-9796(03)00071-8
  32. Souza MMT, 2009, CLIN GASTROENTEROLOG
  33. Tseng CS, 2005, AM J GASTROENTEROL, V100, P1758, DOI 10.1111/j.1572-0241.2005.41857.x
  34. Tsezou A, 2000, HAEMATOLOGICA, V85, P319
  35. Vardhanabhuti S, 2015, OPEN FORUM INFECT DI, V2, DOI 10.1093/ofid/ofv085
  36. von Elm E, 2007, LANCET, V370, P1453, DOI 10.1016/S0140-6736(07)61602-X
  37. Xiao XG, 2015, ONCOTARGETS THER, V8, P3575, DOI 10.2147/OTT.S95149
  38. Xu CL, 2016, CANCER CHEMOTH PHARM, V78, P119, DOI 10.1007/s00280-016-3057-z
  39. [Anonymous], 2009, GENET MED, V15, P15

Coleções
Artigos e Materiais de Revistas Científicas - FM/MGT
Artigos e Materiais de Revistas Científicas - HC/ICESP
Artigos e Materiais de Revistas Científicas - HC/ICHC
Artigos e Materiais de Revistas Científicas - HC/InRad
Artigos e Materiais de Revistas Científicas - LIM/07
Artigos e Materiais de Revistas Científicas - ODS/03