No association of promoter variations of HMOX1 and UGT1A1 genes with liver injury in chronic hepatitis C
Language English Country Mexico Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
21911884
PII: S1665-2681(19)31511-X
Knihovny.cz E-resources
- MeSH
- Biopsy MeSH
- Hepatitis C, Chronic enzymology genetics pathology MeSH
- Phenotype MeSH
- Gene Frequency MeSH
- Genetic Predisposition to Disease MeSH
- Genetic Variation * MeSH
- Glucuronosyltransferase genetics MeSH
- Heme Oxygenase-1 genetics MeSH
- Hepacivirus genetics MeSH
- Liver Cirrhosis enzymology genetics pathology virology MeSH
- Liver enzymology pathology virology MeSH
- Humans MeSH
- Microsatellite Repeats MeSH
- Promoter Regions, Genetic * MeSH
- RNA, Viral blood MeSH
- Case-Control Studies MeSH
- Viral Load MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Geographicals
- Czech Republic MeSH
- Names of Substances
- Glucuronosyltransferase MeSH
- Heme Oxygenase-1 MeSH
- HMOX1 protein, human MeSH Browser
- RNA, Viral MeSH
- UGT1A1 enzyme MeSH Browser
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