No association of promoter variations of HMOX1 and UGT1A1 genes with liver injury in chronic hepatitis C
Jazyk angličtina Země Mexiko Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
21911884
PII: S1665-2681(19)31511-X
Knihovny.cz E-zdroje
- MeSH
- biopsie MeSH
- chronická hepatitida C enzymologie genetika patologie MeSH
- fenotyp MeSH
- frekvence genu MeSH
- genetická predispozice k nemoci MeSH
- genetická variace * MeSH
- glukuronosyltransferasa genetika MeSH
- hemoxygenasa-1 genetika MeSH
- Hepacivirus genetika MeSH
- jaterní cirhóza enzymologie genetika patologie virologie MeSH
- játra enzymologie patologie virologie MeSH
- lidé MeSH
- mikrosatelitní repetice MeSH
- promotorové oblasti (genetika) * MeSH
- RNA virová krev MeSH
- studie případů a kontrol MeSH
- virová nálož MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Geografické názvy
- Česká republika MeSH
- Názvy látek
- glukuronosyltransferasa MeSH
- hemoxygenasa-1 MeSH
- HMOX1 protein, human MeSH Prohlížeč
- RNA virová MeSH
- UGT1A1 enzyme MeSH Prohlížeč
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). MATERIAL AND 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). CONCLUSION: 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.
Clinically silent LINE 1 insertion in the PNPLA3 gene may impede genotyping of the p.I148M variant
ClinicalTrials.gov
NCT00842205