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

BARCELONA . SPAIN
120 POSTGRADUATE COURSE SYLLABUS ALCOHOLIC LIVER DISEASE 121
APRIL 18 - 19/2012 THE INTERNATIONAL LIVER CONGRESS TM 2012
NOTES
CLINICAL CASE: LONG-TERM MANAGEMENT OF ALD
A. De Gottardi
Bern, Switzerland
N. Goossens
Geneva, Switzerland
E-mail: Nicolas.Goossens@hcuge.ch
A 48 year old man with chronic HCV infection, genotype 1b and cirrhosis (Child-Pugh B 7, MELD 14) comes
for a routine visit to your outpatient clinic.
He was treated for alcoholic hepatitis 5 years ago and after this episode he continued to drink excessively.
After an inpatient treatment for alcoholism, he stopped his alcohol intake 6 months ago. Currently he
drinks 3 alcohol-free beers a day. He injected intravenous drugs when he was a teenager and he currently
consumes intranasal cocaine once a month. He smokes 20 cigarettes per day.
His medication includes losartan, sertralin, propranolol, spironolactone and torasemide.
He works as a barkeeper and has a stable family situation.
An ultrasound examination with intravenous contrast shows a 3 cm lesion in the right liver with arterial
enhancement and washout suggesting hepatocellular carcinoma. There is, in addition, a partial thrombosis
of the splenomesenteric confluence. There is no ascites and the spleen is 15 cm in diameter.
Laboratory analyses show albumin 31 g/L, bilirubin 32 umol/L (1.87 mg/dL), creatinine 101 umol/L (1.14
mg/dL), INR 1.5, alpha-fetoprotein 20 ug/L.
ALCOHOL CONSUMPTION AS A CO-FACTOR FOR OTHER LIVER
DISEASES
Helmut K. Seitz
Heidelberg, Germany
E-mail: helmut_karl.seitz@urz.uni-heidelberg.de
KEY POINTS
• Chronic alcohol consumption is a risk factor the deterioration of various types of liver diseases,
such as hepatitis B and C, NAFLD, hereditary haemochromatosis and drugs induced liver
injuries including vitamin E associated liver fibrosis.
• Depending on the underlying liver disease this negative effect of alcohol is time and dose
dependent but may occur already at much lower alcohol intake as compared to an alcohol dose
necessary to initiate alcoholic liver disease itself.
• Alcohol intake should be avoided or at least limited and ... not consumed chronically under
these conditions.
INTRODUCTION
Chronic alcohol consumption is a major risk factor for chronic liver disease. Beside the fact that alcohol by
itself causes chronic liver disease an additional consumption of alcohol in the presence of other types of
liver diseases may result in a progression of the disease. According to the data of the Centre of Disease
Control and Prevention in 2007 24 % of all chronic liver diseases are due to alcohol, 14 % to alcohol and
hepatitis C and 3 % to alcohol and hepatitis B (1). In addition, alcohol may also negatively influence the
course of non-alcoholic fatty liver disease (NAFLD) (2) and of hereditary hemochromatosis (HH) (3). Finally,
alcohol interacts with the metabolism of certain drugs (4) and vitamin A (5) resulting occasionally in an
increased toxicity of these compounds.
ALCOHOL AND HEPATITIS C
Influence of alcohol of the prevalence of HCV infection
It has been shown that the prevalence of hepatitis C virus (HCV) infection increases with the progression
of alcoholic liver disease (ALD) (Fig.1). This increase in hepatitis C infection in alcoholics may be due to
a risky life style of these patients often associated with drug abuse as well as to the immunosuppressive
action of alcohol.
Hepatic interaction of alcohol and HCV virus reduplication, fibrosis and hepatocellular carcinoma (HCC)
The impact of alcohol consumption on serum HCV RNA levels shows clearly that with increasing self
reported alcohol consumption serum HCV RNA increases constantly (6) (Fig.2). On the other hand it has
been shown that serum HCV RNA decreases with alcohol reduction (Fig.3). In this study by Cromie and coworkers
(7), serum HCV RNA copies dropped significantly (p = 0.018) 4 months after alcohol consumption
was reduced. Alcohol consumption also resulted in progression of hepatitis C (8). A great number of studies
have shown that chronic alcohol consumption mostly of more than 50 grams alcohol per day significantly
leads to disease progression (Tabl.1, Fig.4). Fibrogenesis was also found to be faster under alcohol
consumption as compared to non drinking (Fig.5) (9). In a study by Poynard et al., patients with more than
50 grams alcohol per day had an increased fibrosis score regardless of the age at biopsy and regardless
of the duration of infection (10). Also small amounts of daily alcohol consumption on the course of hepatitis
C have been investigated. 78 patients with two liver biopsies, 6.3 years from each other and an alcohol
consumption of less than 40 grams per day (median 5 g/day, 1 - 12 g/day) have been studied (11). The
results showed an increasing progressive fibrosis with an increased total alcohol intake (15.4 kg vs. 3.9
kg; p = 0.007) with an increased daily alcohol consumption (5.7 g/day vs. 2.6 g/day; p = 0.03) and a higher
drinking frequency (35 vs. 8 days/year; p = 0.006).