Page 19 - Read Online
P. 19

Page 14 of 16                                              Teschke. Hepatoma Res 2019;5:40  I  http://dx.doi.org/10.20517/2394-5079.2019.0017

               acetaldehyde metabolism attacking hepatocellular DNA. Upregulation of ROS production occurs via CYP
               2E1 following prolonged alcohol consumption and represents a major risk factor of AHCC. To prevent
               AHCC, individuals with an alcohol problems must early be identified in order to achieve alcohol abuse,
               because only a long period of abstinence will substantially reduce the risk of AHCC initiation, short term
               abstinence contributes not or little to risk reduction. Concomitant chronic liver diseases are additional
               risks factors in the context of AHCC and deserve effective treatment. Of special risks are infections by
               HBV and HCV and genetic liver disease such as hereditary hemochromatosis with its high Fe content in
               the liver. AHCC represents a late stage of ALD mostly in connection with AC and does not provide early
               clinical warning symptoms.


               DECLARATIONS
               Authors’ contributions
               The author contributed solely to the article.

               Availability of data and materials
               Not applicable.

               Financial support and sponsorship
               None.


               Conflicts of interest
               The author declared that there are no conflicts of interest.

               Ethical approval and consent to participate
               Not applicable.


               Consent for publication
               Not applicable.


               Copyright
               © The Author(s) 2019.



               REFERENCES
               1.   WHO. Cancer. Available from: https://www.who.int/news-room/fact-sheets/detail/cancer. [Last accessed on 6 Nov 2019]
               2.   Crawford JM. Histologic findings in alcoholic liver disease. Clin Liver Dis 2012;16:699-716.
               3.   Rawla P, Sunkara T, Muralidharan P, Raj JP. Update in global trends and aetiology of hepatocellular carcinoma. Contemp Oncol (Pozn)
                   2018;22:141-50.
               4.   Wu D, Cederbaum AI. Alcohol, oxidative stress, and free radical damage. Available from: https://pubs.niaaa.nih.gov/publications/
                   arh27-4/277-284.htm. [Last accessed on 6 Nov 2019]
               5.   Seitz HK, Bataller R, Cortez-Pinto H, Gao B, Gual A, et al. Alcoholic liver disease. Nat Rev Dis Prim 2018;4:16.
               6.   Testino G, Leone S, Borro P. Alcohol and hepatocellular carcinoma: a review and a point of view. World J Gastroenterol
                   2014;20:15943-54.
               7.   Matsushita H, Takaki A. Alcohol and hepatocellular carcinoma. BMJ Open Gastro 2019;6:e000260.
               8.   Teschke R. Alcoholic liver disease: current mechanistic aspects with focus on their clinical relevance. Biomedicines 2019;7:68.
               9.   Logan BK. Endogenous ethanol “auto-brewery syndrome” as a drunk-driving defence challenge. Med Sci Law 2000;40:206-15.
               10.   Cordell BJ, Kanodia A, Miller GK. Case-control research study of auto-brewery syndrome. Global Adv Health Med 2019;8:1-7.
               11.   Jolly NP, Augustyn OPH, Pretorius IS. The role and use of the non-Saccharomyces yeasts in wine production. S Afr J Enol Vitic
                   2006;27:15-39.
               12.   Moreno-Arribas MV, Polo MC. Wine Chemistry and Biochemistry. Springer New York; 2009.
               13.   Seitz HK, Egerer G, Simanowski UA, Waldherr R, Eckey R, et al. Human gastric alcohol dehydrogenase activity: effect of age, gender
                   and alcoholism. Gut 1993;34:1433-7.
   14   15   16   17   18   19   20   21   22   23   24