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World J Clin Oncol. Dec 10, 2017; 8(6): 429-436
Published online Dec 10, 2017. doi: 10.5306/wjco.v8.i6.429
Epidemic of non-alcoholic fatty liver disease and hepatocellular carcinoma
Adnan Said, Aiman Ghufran
Adnan Said, Division of Gastroenterology and Hepatology, Department of Medicine, William S. Middleton VAMC, University of Wisconsin School of Medicine and Public Health, Madison, WI 53705, United States
Aiman Ghufran, Gastroenterology and Hepatology, Medical College of Wisconsin, Milwaukee, WI 53226, United States
Author contributions: Said A and Ghufran A contributed equally to this work; Said A designed the research, performed literature search and wrote the paper; Ghufran A performed literature search and wrote the paper.
Conflict-of-interest statement: Neither of the authors has any conflict of interest related to the manuscript submitted for publication.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Adnan Said, MD, MS, Associate Professor, Division of Gastroenterology and Hepatology, Department of Medicine, William S. Middleton VAMC, University of Wisconsin School of Medicine and Public Health, 4223 MFCB, 1685 Highland Avenue, Madison, WI 53705, United States. axs@medicine.wisc.edu
Telephone: +1-608-2634034 Fax: +1-608-2655677
Received: May 20, 2017
Peer-review started: May 23, 2017
First decision: June 14, 2017
Revised: September 6, 2017
Accepted: October 30, 2017
Article in press: October 30, 2017
Published online: December 10, 2017
Processing time: 198 Days and 7.4 Hours
Abstract

Non-alcoholic fatty liver disease (NAFLD) associated hepatocellular carcinoma (HCC) incidence is increasing worldwide, paralleling the obesity epidemic. Although most cases are associated with cirrhosis, HCC can occur without cirrhosis in NAFLD. Diabetes and obesity are associated risk factors for HCC in patients. Given the sheer magnitude of the underlying risk factors (diabetes, obesity, non-cirrhotic NAFLD) screening for HCC in the non-cirrhotic population is not recommended. Optimal screening strategies in NAFLD cirrhosis are not completely elucidated with Ultrasound having significant limitations in detection of liver lesions in the presence of obesity and steatosis. Consequently NAFLD-HCC is more often diagnosed at a later stage with larger tumors and reduced opportunities for curative treatments as opposed to HCC in other causes of cirrhosis. When HCC is found at a curative stage treatments including liver transplantation, resection and loco-regional therapies are associated with good results similar to that seen in HCV-HCC. Future strategies under study include the use of chemopreventive and antioxidant agents to reduce development of cirrhosis and non-alcoholic steatohepatitis (NASH). Strategies to reverse NASH via weight loss, control of associated conditions like diabetes are key strategies in reducing the increasing incidence of NASH-HCC. Novel therapeutic agents for NASH are in trials and if successful in achieving reversal of NASH will be an important strategy in reducing NAFLD-HCC.

Keywords: Non-alcoholic fatty liver disease; Hepatocellular carcinoma; Screening; Epidemiology; Pathophysiology; Diagnosis; Liver transplant; Resection; Locoregional therapy; Treatment

Core tip: Non-alcoholic fatty liver disease (NAFLD) related hepatocellular carcinoma (HCC) is rapidly increasing worldwide. HCC in NAFLD is often detected at a more advanced stage than in hepatitis C virus (HCV). Challenges include earlier recognition of cirrhosis in NAFLD to allow earlier screening for liver cancer. NAFLD also has a higher proportion of HCC occurring in the absence of cirrhosis. Given the sheer number of patients with non-cirrhotic NAFLD, screening for HCC in this population is not practical. Instead prevention and treatment of non-alcoholic steatohepatitis to prevent cirrhosis should be an important strategy. When NAFLD-HCC is found at a curative stage, results with liver transplant, resection and loco-regional therapy are similar to that seen in HCV-HCC.