title: No association of promoter variations of HMOX1 and UGT1A1 genes with liver injury in chronic hepatitis C.
abstract: BACKGROUND
  Heme oxygenase-1 (HMOX1) and bilirubin UDP-glucuronosyltransferase (UGT1A1), both enzymes involved in bilirubin homeostasis, play an important role in oxidative stress defense.
  
  
  OBJECTIVE
  To assess the effect of promoter variations of HMOX1 and UGT1A1 genes on the progression of fibrosis in patients chronically infected with the hepatitis C virus (HCV).
  
  
  METHODS
  The study was performed on146 chronic HCV infection patients, plus 146 age- and sex-matched healthy subjects. The (GT)n and (TA)n dinucleotide variations in HMOX1 and UGT1A1 gene promoters, respectively, were determined by fragment analysis in all subjects.
  
  
  RESULTS
  No differences were found in the frequencies of each particular allele of both genes, between HCV patients and a control group (p > 0.05). Furthermore, no association was detected (p > 0.05) between either the HMOX1 or the UGT1A1 promoter variants and the individual histological stages of liver disease in the HCV positive patients. Finally, no differences in the HMOX1 and UGT1A1 genotype prevalence rates were found between pre-cirrhotic and cirrhotic patients (p > 0.05).
  
  
  CONCLUSIONS
  Based on our data, microsatellite variations in the HMOX1 and UGT1A1 genes are not likely to protect from progression of liver disease in patients with chronic hepatitis C.
authors.affiliation: Department of Internal Medicine, 1st. Faculty of Medicine, Charles University in Prague and Central Military Hospital, Prague, Czech Republic.
authors.forename: Petr
authors.initials: P
authors.lastname: Urbánek
authors.forename: Martin
authors.initials: M
authors.lastname: Leníček
authors.forename: Lucie
authors.initials: L
authors.lastname: Muchová
authors.forename: Iva
authors.initials: I
authors.lastname: Subhanová
authors.forename: Ladislav
authors.initials: L
authors.lastname: Dušek
authors.forename: Nikola
authors.initials: N
authors.lastname: Kaspříková
authors.forename: Petr
authors.initials: P
authors.lastname: Hrabal
authors.forename: Radan
authors.initials: R
authors.lastname: Bruha
authors.forename: Libor
authors.initials: L
authors.lastname: Vítek
mesh_terms: D001706:Biopsy; D016022:Case-Control Studies; D018153:Czech Republic; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D014644:Genetic Variation; D014453:Glucuronosyltransferase / Q000235:genetics*; D051547:Heme Oxygenase-1 / Q000235:genetics*; D016174:Hepacivirus / Q000235:genetics; D019698:Hepatitis C, Chronic / Q000201:enzymology / Q000235:genetics* / Q000473:pathology; D006801:Humans; D008099:Liver / Q000201:enzymology* / Q000473:pathology / Q000821:virology; D008103:Liver Cirrhosis / Q000201:enzymology / Q000235:genetics* / Q000473:pathology / Q000821:virology; D018895:Microsatellite Repeats; D010641:Phenotype; D011401:Promoter Regions, Genetic; D012367:RNA, Viral / Q000097:blood; D019562:Viral Load; D000099148:UGT1A1 Enzyme
chemical_list: D014453:Glucuronosyltransferase; D051547:Heme Oxygenase-1; D012367:RNA, Viral; D000099148:UGT1A1 Enzyme; C496541:HMOX1 protein, human