Chapters authored
Comparative Study of IFN-Based Versus IFN-Free Regimens and Their Efficacy in Treatment of Chronic Hepatitis C Infections
The hepatitis C viral (HCV) infection is a global health burden, WHO estimates 130–150 million people chronically infected with hepatitis C virus worldwide. Additional 3–4 million people become newly infected annually and more than 350,000 people die each year of HCV-related liver diseases. HCV infection exhibits higher genetic diversity with regional variations in genotypic prevalence resulting big challenges on disease management. Introduction of DAAs revolutionised the new era of all oral therapy in treatment of chronic hepatitis C infection and is the regimens of choice in present days. However, IFN-based combination therapy with sofosbuvir has promising efficacy in genotypes 3, 4, 5 or 6 infections compared to genotypes 1 and 2 infections. So, these regimens could be an option in DAAs regimen failure cases. The poor availability of data on recent DAAs (IFN-free) regimens questioned on regular use and cost effectiveness is the another challenge with DAAs regimens. So phase III trials (sofosbuvir and velpatasvir) of recent DAAs with pangenotypic actions and better tolerability in HCV infected patients are the future advances in treatment of chronic hepatitis C. After all those recent combination therapies with better SVR, the combination of pegylated interferon with ribavirin is the only option available where unavailability of other regimens still exists.
Part of the book: Advances in Treatment of Hepatitis C and B
Hepatic Lipid Homeostasis in NAFLD
Non-alcoholic fatty liver disease (NAFLD) is currently the most common liver disease, affecting 25% of world population. Hepatic steatosis has 60–90% prevalence among obese patients. It is also associated with multitude of detrimental effects and increased mortality. This narrative chapter investigates hepatic lipid homeostasis in NAFLD, focusing on the four molecular pathways of hepatic steatosis to lipid homeostasis in the liver. Hepatic steatosis is a consequence of lipid acquisition pathways exceeding lipid disposal pathways. In NAFLD, hepatic uptake of fatty acids and de novo lipogenesis surpass fatty acid oxidation and lipid export. The imbalance of the hepatic lipid may promote cellular damage by inducing oxidative stress in peroxisomes and cytochromes, especially with compromised mitochondrial function. Lipid export may even decrease with disease progression, sustaining the accumulation of lipids. NAFLD has a complex molecular mechanism regulating hepatic lipid homeostasis. Thus, as well as inter-individual differences, any intervention targeting one or more pathway is likely to have consequences on multiple cellular signaling pathways. We should be taken into careful consideration when developing future treatment options for NAFLD.
Part of the book: Non-alcoholic Fatty Liver Disease