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