alcohol consumption is associated with an increased risk of liver cancer for
people with hepatitis C virus (HCV) infection with compensated cirrhosis, investigators from Belgium
report in the Journal of Hepatology.
Five-year incidence of hepatocellular carcinoma (HCC) was twice as high among
people who reported alcohol consumption compared to individuals who did not
drink alcohol. Levels of daily alcohol consumption among people who developed
liver cancer were low, the investigators stressing, “drinking alcohol, not the
amount of alcohol intake, was associated with an increased risk of HCC.” They
therefore caution, “there is no safe threshold for alcohol” for people with HCV infection with cirrhosis.
Patients who drank
alcohol and who did not eradicate their HCV infection during follow-up had
especially poor outcomes, including an increased risk of decompensated liver
disease and death.
consumption is a well-established risk factor for cirrhosis, decompensated
liver disease, HCC and death in people with chronic HCV infection. Whether
light-to-moderate alcohol consumption is similarly associated with poorer
outcomes after cirrhosis has developed is unclear. The interaction between alcohol use and eradication of HCV
with antiviral treatment on outcomes in people with compensated cirrhosis is
- compensated cirrhosis
The earlier stage of
cirrhosis, during which the liver is damaged but still able to perform most of
its functions. See also ‘cirrhosis’ and ‘decompensated cirrhosis’.
- decompensated cirrhosis
The later stage of
cirrhosis, during which the liver cannot perform some vital functions and
complications occur. See also ‘cirrhosis’ and ‘compensated cirrhosis’.
- hepatocellular carcinoma (HCC)
Liver cancer. A long-term complication of chronic inflammation of the liver or cirrhosis.
Belgium therefore designed a prospective study involving people with
compensated HCV-related cirrhosis. Data on alcohol consumption and viral
eradication were collected prospectively at intervals of at most six months.
Study participants were asked to report their typical quantity, frequency and duration of
alcohol consumption. Each alcoholic drink was assumed to contain 10g of pure
ethanol. HCV therapy was provided according to Belgium national guidelines and
after 2011 included direct-acting agents. The study outcomes were development
of HCC, decompensated cirrhosis and death.
place between January 2009 and December 2010. Of the 192 people eligible for
inclusion, 61% were abstinent from alcohol. Median daily alcohol consumption
among the 39% of individuals who reported drinking was 15g/day – approximately 1.5
units. During follow-up, 86% of people underwent antiviral treatment and 41%
had a sustained virological response.
During the course
of the study, 17% of people developed HCC, including 14% of people who
abstained from alcohol and 23% of those who reported alcohol consumption (p =
study participants who reported drinking alcohol showed that median daily intake of
alcohol was 10g for those who developed HCC and 20g for individuals who did not
progress to liver cancer. Therefore, it was alcohol consumption per se, and not
the level of drinking, that was associated with the development of HCC.
The rate of HCC
was significantly lower among people who achieved viral eradication compared
to those with persistent viraemia (10% vs. 20%).
The proportion of people developing decompensated cirrhosis did not differ according to alcohol
use. The rate of this outcome was lower among people with viral eradication
compared to those without viral eradication (15% vs. 35%).
A fifth of study participants died. Mortality rates did not differ according to alcohol consumption
(20% for both groups). Only 3% of people with viral eradication died compared
to 30% of people without viral eradication.
five-year incidence of HCC was 11% among alcohol abstainers and 24% among those
who reported alcohol consumption (p = 0.087). Annual incidence rates among
abstainers and consumers were 2% and 6%, respectively.
five-year incidence of HCC was 2% in people with viral eradication and 22% in those with persistent viraemia; annual rates were 0.4% and 5%, respectively.
In multivariate analysis,
lack of viral eradication (p = 0.04) and alcohol consumption (p = 0.04) were
both associated with an increased risk of HCC.
The lowest risk of
HCC was seen in people who abstained from alcohol and who had viral
eradication (0%), followed by people with alcohol consumption and viral
eradication (6%), people without alcohol consumption but persistent viraemia
(16%) and people with alcohol consumption and no viral eradication (29%).
There was no
evidence that alcohol consumption had a significant association with the risk
of decompensated cirrhosis (18% five-year incidence for abstainers vs. 22% for
consumers). However, incidence was significantly lower among people with
viral eradication compared to those without eradication (4% vs. 27%, p =
0.001). Individuals without alcohol consumption and with viral eradication had the
lowest risk of decompensation (3%; p = 0.012 compared to other groups).
Mortality risk did
not differ according to alcohol use. Five-year incidence of all-cause mortality
and liver-related mortality were similar for people who abstained and
consumed alcohol (20% vs. 18%; 14% vs. 14%). Individuals without alcohol
consumption and viral eradication had the lowest risk of death (0%) and
liver-related death (0%).
consumption was associated with an increased risk of HCC,” comment the authors.
“As the median amount of alcohol intake was low in consumers, we can conclude
that light-to-moderate alcohol intake increases the risk of HCC.”
“patients with HCV-related cirrhosis should be strongly advised against any
alcohol intake. Patient care should include measures to ensure abstinence.”