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Teschke. Hepatoma Res 2019;5:40 I http://dx.doi.org/10.20517/2394-5079.2019.0017 Page 13 of 16

transferrin (CDT; 63%), gamma-glutamyltransferase (GGT; 58%), mean corpuscular volume of erythrocytes
(MCV; 45%), aspartate aminotransferase (AST; 47%), alanine aminotransferase (ALT; 50%), and GGT +
[15]
CDT (90%) .
Under the aspect of prevention and associated diagnosis, a liver biopsy to establish the diagnosis of any
ALD stage is certainly not recommended under routine conditions, although it was previously considered
as diagnostic gold standard. Exemptions now are pretransplantation evaluations or RCTs to test efficacy of
drugs for instance in patients with AH, but in most other cases the patient will have no benefit from this
[5]
invasive procedure. This is also confronted with a fatality rate, though rather low .

Pharmacotherapy option
If AHCC is diagnosed, the patient should abstain from further alcohol use to prevent destruction of the
remaining, still functioning liver. While some pharmacotherapy measures are partially effective in patients
with severe AH , respective options with proven efficacy are not available for AHCC. Instead, palliative
[53]
measures for pain and symptom relief is the only choice.

Segment resection, liver transplantation, and tumor ablation
[66]
A stringent algorithm for management of AHCC has been presented that should be used as a guideline .
Options must consider specific criteria and may include segment resection, disputed liver transplantation,
locoregional ablation using Sorafenib, transarterial chemoembolization, and radiotherapy. Investigational
studies should be performed in the frame of RCTs.

Prognosis
Presenting mostly as an end stage of the tumor disease, patients with AHCC have a poor prognosis,
because overall survival was in a range of 15 to 32 months, which compared to 16 to 47 months in patients
[59]
who received a curative treatment . This again calls for an early recognition of potential individuals with
[79]
an alcohol problem and associated early stages of ALD. Vague estimates based on four studies allow the
tentative conclusion that abstinence from alcohol use may reduce AHCC development perhaps by 6% to 7%
per year, but a wash out period of 23 years being necessary to achieve the same incidence of AHCC seen in
abstinent individuals [59,79] . In other words, early abstinence is better than late abstinence.

EPIDEMIOLOGY AHCC
Worldwide epidemiology data of AHCC suggests that alcohol accounts for around one third of global
incident cases of primary liver cancer, with a substantial variability of results among different countries
and regions, ranging from 6% in Iran to 61% in Estonia and Moldova [59,80] . Details can be derived from a
recent large study of the Global Burden of Disease Liver Cancer Collaboration, which considers the burden
of primary liver cancer and underlying etiologies from 1990 to 2015 at the global, regional, and national
level . Accordingly, for virtually all countries data of AHCC and liver cancer due to HBV, HCV, and other
[80]
[80]
causes (OC) are available, for example : Australia (AHCC 38%, HBV 9%, HCV 40%, OC 13%), Austria
(AHCC 49%, HBV 15%, HCV 30%, OC 6%), Belgium (AHCC 48%, HBV 16%, HCV 28%, OC 8%), China
(AHCC 33%, HBV 41%, HCV 8%, OC 18%), France (AHCC 37%, HBV 17%, HCV 36%, OC 9%), Germany
(AHCC 44%, HBV 8%, HCV 33%, OC 14%), India (AHCC 21%, HBV 42%, HCV 20%, OC 18%), Japan (AHCC
17%, HBV 8%, HCV 69%, OC 6%), Russia (AHCC 53%, HBV 15%, HCV 24%, OC 8%), United Kingdom
[80]
(AHCC 36%, HBV 17%, HCV 38%, OC 9%), and United States (AHCC 37%, HBV 9%, HCV 31%, OC 22%) .
In countries with a high AHCC percentage, a high alcohol consumption is likely. In other countries, HBV
and HCV infections are causative for HCC.

CONCLUSIONS
Ethanol per se is not carcinogenic but has to be viewed as a procarcinogen involved in the development
of AHCC. This process is triggered by ROS including activated molecules derived from ethanol or