(Hepatology 2014;59:1406-1414) ”
“Polymorphisms in the interleukin-28B (IL28B) region are associated with spontaneous and treatment-induced viral clearance in hepatitis C virus (HCV) infection. Nevertheless, it is unknown whether genetic variation at the IL28B locus influences the natural history of chronic HCV infection. Thus, we asked whether an association between IL28B polymorphisms and liver fibrosis progression existed. We studied 247 consecutive Atezolizumab research buy patients with chronic HCV, an accurate
estimate of the date of infection, and a liver biopsy performed before any treatment. No patient had a history of alcohol abuse or coinfection with other viruses. We assessed the role of rs8099917 and rs12979860 polymorphisms and the effect of host and environmental factors on fibrosis progression. Blood transfusion (75%) was the main modality of infection. Median age at infection was 21 years, and median interval between learn more infection and liver biopsy was 25 years. One hundred twenty-nine patients (52%) were infected by HCV-1, 74 (30%) by HCV-2, 34 (14%) by HCV-3, and 10 (4%) by HCV-4. Bridging fibrosis/cirrhosis
(Ishak ≥4) was detected in 24% of patients. Age at infection had a marked effect on fibrosis progression by both a linear model and Cox proportional-hazard regression (P < 2E-16). A 12.1% increase in the hazard of advanced fibrosis was estimated for each additional year at infection, suggesting that this was the major explanatory variable in this cohort. Male gender (P < 0.05), HCV genotype 3 (P < 0.001) and steatosis (P < 0.05) were also associated with faster fibrosis progression. Conversely, the two IL28B polymorphisms had no impact on fibrosis progression. Conclusion: In HCV patients with a known date of infection, IL28B
genotype was not associated with fibrosis progression IKBKE rate or with the risk of developing advanced liver fibrosis. (HEPATOLOGY 2011;) Hepatitis C virus (HCV) infection is a global health care burden, with roughly 1%-2% of the European and U.S. populations being chronic carriers of the virus. Although HCV can lead to extrahepatic manifestations in a minority of patients, the prognosis of the disease is directly linked to the restless accumulation of fibrotic tissue in the liver, which, ultimately, alters the liver architecture and its vascularization, leading to the development of cirrhosis and its sequelae. Among the many factors known to substantially contribute to this process by determining a more rapid progressive course of the disease, emphasis has been put on a variety of environmental components, such as alcohol abuse and viral coinfections, and host risk factors, such as insulin resistance, obesity, and immunity.1, 2 More recently, HCV genotype 3 has been shown to be associated with accelerated fibrosis progression, compared to non-3 genotypes.