Published online Oct 7, 2016. doi: 10.3748/wjg.v22.i37.8294
Peer-review started: May 4, 2016
First decision: July 13, 2016
Revised: August 3, 2016
Accepted: August 23, 2016
Article in press: August 23, 2016
Published online: October 7, 2016
Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in the United States and represents an increasingly important etiology of hepatocellular carcinoma (HCC) with annual cumulative incidence rates ranging from 2% to 12% in cohorts of NAFLD cirrhosis. While the risk of progression of NAFLD to HCC remains higher among patients with fibrosis or cirrhosis, an increasing amount of literature describes NAFLD-HCC as a disease that can occur in the absence of cirrhosis. Efforts to characterize the pathogenesis of NAFLD-HCC have suggested mechanisms that strongly associate with states of hyperinsulinemia and chronic inflammation, cellular mechanisms including adaptive immune responses and hepatic progenitor cell populations, and genetic polymorphisms including mutations of PNPLA3. Current literature describes NAFLD-HCC mostly as a disease of late presentation with lower rates of receipt of curative therapy and worse prognosis. However, a growing body of evidence has reported comparable and potentially more favorable disease-free and overall survival rates among patients with NAFLD-HCC after receipt of curative treatment. This review summarizes current evidence of epidemiology, pathophysiology, disease presentation, demand and receipt of curative therapy, post-treatment outcomes, and overall survival of NAFLD-associated HCC.
Core tip: This review summarizes the epidemiology, pathogenesis, disease presentation, demand and receipt of curative treatment, and post-treatment outcomes of hepatocellular carcinoma (HCC) in nonalcoholic fatty liver disease (NAFLD). The review highlights the developing understanding of NAFLD-HCC pathogenesis, which has broadened to include genetic polymorphisms, adaptive immune responses, and cellular regenerative pathways using hepatic progenitor cell populations. While NAFLD-HCC has been described to have poorer prognosis as compared with other HCC etiologies, this review features summarized evidence that disease-free and survival rates among patients with NAFLD-HCC are comparable and potentially favorable after receipt of curative treatment.