期刊
HEPATOLOGY
卷 51, 期 6, 页码 1904-1911出版社
WILEY
DOI: 10.1002/hep.23592
关键词
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资金
- National Center for Research Resources, National Institutes of Health (NIH) [UL1 RR024128-01]
- NIH Roadmap for Medical Research
- Duke Clinical Research Institute
- National Health and Medical Research Council of Australia
- Gastroenterology Society of Australia
- NIH at Duke University Medical Center [T32-DK007012-31]
- Echosers
- Idera Pharmaceutical
- Intarcia
- Medtronic
- Osiris Therapeutics
- Three Rivers Pharmaceuticals
- ViroChem Pharma
- Abbott Laboratories
- Biolex
- Gilead
- GlaxoSmithKline
- GlobeImmune
- Hoffman-LaRoche
- Human Genome Sciences
- Merck Group
- Novartis
- Pfizer
- Pharmasset
- Vertex
Recently, genetic polymorphisms occurring in the interferon (IFN)-lambda gene region were associated with response to IFN-based treatment of hepatitis C infection. Both infection with the hepatitis C virus and IFN therapy are associated with decreased serum cholesterol and high cholesterol has been associated with increased likelihood to respond to IFN. We sought to determine if the IFN-lambda gene variant was also associated with serum lipid levels in chronic hepatitis C patients. We compared genotypes of the rs12979860 polymorphism, located proximal to the IL28 gene, with serum lipid and apolipoprotein levels in 746 subjects with chronic hepatitis C virus infection, not currently undergoing treatment, using multivariable analysis of variance. Levels of total cholesterol (P = 6.0 x 10(-4)), apolipoprotein B (P = 1.3 x 10(-6)) and low-density lipoprotein (LDL) cholesterol (P = 8.9 x 10(-10)) were significantly higher in subjects carrying the rs12979860 CC responder genotype compared with those with the CT or TT genotype. Levels of triglycerides (P = 0.03), apolipoprotein A-I (P = 0.06), and apolipoprotein E (P = 0.01) were slightly lower in the rs12979860 CC genotype group, whereas levels of high-density lipoprotein cholesterol (P = 0.78) and apolipoprotein C-III (P = 0.74) did not vary by rs12979860 genotype. Conclusion: Our results suggest that low levels of LDL cholesterol in chronic hepatitis C patients may be a marker of host endogenous IFN response to hepatitis C and that subjects with the rs12979860 CC responder genotype may have a lower endogenous IFN response to the virus. (HEPATOLOGY 2010;51:1904-1911)
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