barcelona . spain - European Association for the Study of the Liver

BARCELONA . SPAIN
130 POSTGRADUATE COURSE SYLLABUS ALCOHOLIC LIVER DISEASE 131
APRIL 18 - 19/2012 THE INTERNATIONAL LIVER CONGRESS TM 2012
Table 1
HEPATOCELLULAR CARCINOMA: IS IT DIFFERENT IN PATIENTS
WITH ALCOHOLIC LIVER DISEASE
Thomas Decaens
Creteil, France
Email: thomas.decaens@hmn.aphp.fr
KEY POINTS
• Compared to the incidence of hepatitis B virus (HBV) and hepatitis C virus (HCV), alcohol
consumption is increasing. The incidence of alcohol-related hepatocellular carcinoma (HCC) is
probably under-estimated with regard to worldwide alcohol consumption.
• Alcohol is now well-defined as a liver carcinogen. Although the general mechanisms of alcoholrelated
carcinogenesis are similar to those of viral carcinogenesis, there are many differences
in the fine details. However, only a few studies have been designed to compare alcohol-related
with viral-related HCC.
• The prognoses of patients with HCC who are referred to hepatologists do not seem to vary
significantly. However, liver-transplantation data show that ALD patients have less access to
treatment compared to other patients. There may also be discrimination against other treatments
for HCC in ALD patients, though these comparisons have not been made as yet.
Table 2
INTRODUCTION
Hepatocellular carcinoma (HCC) is the sixth most common cancer worldwide and the third most common
cause of cancer-related death 1 . In 70–90% of cases, HCC develops on underlying liver cirrhosis or
inflammation. Worldwide, 75–80% primary liver cancers are attributable to chronic viral infections of
either HBV (50–55%) or HCV (25–30%). In contrast, the percentage of alcohol-related HCCs is not well
defined. According to a World Health Organization (WHO) report 2 , the percentage of deaths from liver
cancer attributable to alcohol is 30.3%. Thus, we can suppose that 25–30% of HCCs are related to alcohol
consumption. However, the overall 5-year incidence of HCC is 10% for HBV infection, 30% for HCV infection,
20% for hemochromatosis-related liver damage, but only 8% for alcohol-induced cirrhosis.
HOW TO ATTRIBUTE HCC TO ALCOHOL CONSUMPTION
In the setting of cirrhosis, there are no specific biological markers that suggest an alcoholic etiology of HCC
(compared to HBV and HCV infections). Information on alcohol intake must be collected through interviews
with patients, which are open to error regarding methodologies used for acquisition (for example: x beers
per day and not y g/day), as well as the unreliability of patients’ recall and/or reporting. Moreover, data
collection can be prone to mistakes made by physicians as well as underestimations of alcohol consumption
made by patients.
As shown in Figure 1, the geographical distribution of alcohol use is very variable worldwide. Although
global alcohol consumption seems to be stable, according to the WHO 5-year change-in-alcohol use
2001–2005 report 2 , over a longer period of time, alcohol consumption has increased in many countries.
For example, in China, where almost all cases of HCC are supposed to be related to HBV, the rate of
alcohol production increased by nine-fold between 1978 and 1997. In a Chinese survey, annual ethanol
consumption among adults (aged 15+) was 4.5l, and heavy drinkers accounted for 6.7% of the sample 3 .
As the current Chinese population is ~1.3 billion, heavy drinkers represent ~87.1 million people (compared
to 14 million in the USA). Alcohol consumption is also increasing in other countries, such as Japan, South
Korea, USA, Russian Federation, and the UK. These data are worrying because we know that per capita
alcohol consumption is correlated with alcoholic cirrhosis in various populations 4 . Compared to the increase
in alcohol consumption, it is of note that HBV infection 5 and HCV infection 6 are currently decreasing.
Heavy alcohol intake (>50–70 g/day) for prolonged periods (5–10 years) is a well-recognized risk factor
for HCC, and its risk (odds ratio) increases linearly when alcohol intake is >60 g/day for men and women