title: Alcoholic Liver Disease: High Risk or Low Risk for Developing Hepatocellular Carcinoma?
abstract: In this review we critically assess the literature to evaluate the level of risk posed by alcohol as both a primary etiology of hepatocellular carcinoma (HCC) and as a cofactor in its development. Although there have been conflicting findings, based on the body of evidence to date, it appears that the linkage between compensated alcoholic liver disease-associated cirrhosis and HCC is best characterized as medium-high risk, with the risk increasing with age and with quantity and duration of alcohol consumption and is more pronounced in females. While abstinence is the most effective way to reduce HCC risk, its effect seems largely dependent on the severity of liver damage at the point of cessation. Alcohol clearly interacts with other etiologies and conditions including viral hepatitis B and C, hereditary hemochromatosis, diabetes, and obesity to increase the risk for developing HCC, either synergistically or additively. Continued progress in genetics, especially through mechanistic-based and genome-wide association studies may ultimately identify which single nucleotide polymorphisms are risk factors for the onset of alcoholic liver disease and its progression to HCC and lead to the development of targeted therapeutics which may help providers better manage at-risk patients.
authors.affiliation: Division of Hepatology, St. Joseph's Hospital and Medical Center, Creighton University School of Medicine, 500 West Thomas Road, Suite 900, Phoenix, AZ 85013, USA.
authors.forename: Kartik
authors.initials: K
authors.lastname: Joshi
authors.affiliation: Division of Hepatology, St. Joseph's Hospital and Medical Center, Creighton University School of Medicine, 500 West Thomas Road, Suite 900, Phoenix, AZ 85013, USA; Division of Infectious Disease, St. Joseph's Hospital and Medical Center, Creighton University School of Medicine, 500 West Thomas Road, Suite 900, Phoenix, AZ 85013, USA.
authors.forename: Anita
authors.initials: A
authors.lastname: Kohli
authors.affiliation: Division of Hepatology, St. Joseph's Hospital and Medical Center, Creighton University School of Medicine, 500 West Thomas Road, Suite 900, Phoenix, AZ 85013, USA.
authors.forename: Richard
authors.initials: R
authors.lastname: Manch
authors.affiliation: Division of Hepatology, St. Joseph's Hospital and Medical Center, Creighton University School of Medicine, 500 West Thomas Road, Suite 900, Phoenix, AZ 85013, USA; Division of Hepatology and Gastroenterology, Stanford University Hospitals and Clinics, 300 Pasteur Drive, Palo Alto, CA 94304, USA. Electronic address: rgish@robertgish.com.
authors.forename: Robert
authors.initials: R
authors.lastname: Gish
mesh_terms: D064829:Alcohol Abstinence; D000428:Alcohol Drinking; D006528:Carcinoma, Hepatocellular / Q000209:etiology*; D048909:Diabetes Complications / Q000209:etiology; D005260:Female; D006432:Hemochromatosis / Q000150:complications; D019694:Hepatitis B, Chronic / Q000150:complications; D019698:Hepatitis C, Chronic / Q000150:complications; D006801:Humans; D008104:Liver Cirrhosis, Alcoholic / Q000150:complications; D008108:Liver Diseases, Alcoholic / Q000150:complications*; D008113:Liver Neoplasms / Q000209:etiology*; D008297:Male; D009765:Obesity / Q000150:complications; D020641:Polymorphism, Single Nucleotide; D012307:Risk Factors
keywords: Alcoholic liver disease; Cirrhosis; Diabetes; Hepatitis B; Hepatitis C; Hepatocellular carcinoma risk; Obesity