“Histologically, NASH shares characteristics with alcoholic liver disease, primarily proinflammatory fat accumulation in parenchymal cells, [and] key players in NASH progression to HCC are suggested to include genetic modifications, proinflammatory high-fat and/or high-fructose diets, and oxidative and endoplasmic cellular stresses,” they wrote. “In HCV progression to HCC, the presence of the HCV core protein may induce HCC without the prerequisite load of genetic errors normally required for cancer development, skipping or accelerating some of the classic steps of cancer induction.”
The authors did note that their model represented a base scenario that assumed the environmental and genetic factors driving NASH would continue along the path of current trends.
“Therefore, the possibility exists that our models underestimate the response of the medical community in addressing the rising nonalcoholic fatty liver disease/NASH epidemic.”
No funding sources or conflicts of interest were declared.
SOURCE: Ahmed O et al. J Clin Exp Hepatology. 2018 Feb 24. doi: 10.1016/j.jceh.2018.02.006.