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

BARCELONA . SPAIN
48 POSTGRADUATE COURSE SYLLABUS ALCOHOLIC LIVER DISEASE 49
APRIL 18 - 19/2012 THE INTERNATIONAL LIVER CONGRESS TM 2012
NOTES
Figure 2
Overview of the pathogenetic pathways leading to fibrosis in alcoholic liver disease. The top part of
the figure summarizes the mechanisms that are more specific to the pathogenesis of alcoholic fibrosis. The
contribution of other pathways, such as obesity and the cannabinoid system, operating also in other chronic
liver diseases is indicated in the bottom part.
CLINICAL CASE : A PATIENT WITH CHRONIC ALD
Alexandre Louvet, Florent Artru, Philippe Mathurin
Lille, France
E-mail: p-mathurin@chru-lille.fr
KEY POINTS
• Despite the fact that liver biopsy is still the gold standard for the diagnosis of alcoholic liver
disease, serum biomarkers and transient elastography are relevant to establish liver fibrosis.
• Tobacco consumption has a moderate negative impact on fibrosis progression in ALD, in
contrary to coffee consumption. Overweight and drinking outside the meals also accelerate
fibrosis progression. Few clinical data are available regarding binge drinking but it may be
speculated that this pattern of consumption worsens the evolution of liver fibrosis.
• Raised GGT and MCV are not good predictors of persistent alcohol consumption, especially in
cirrhotic patients.
• Disulfiram, naltrexone, acamprosate and baclofen are efficient in the prevention of alcohol
relapse but only baclofen has been tested in cirrhotic patients.
INTRODUCTION
A 56-year old man is referred for abnormal liver tests. He has no past medical history. He is married and
lives with his wife and his two children. He is not working but is a former employee in a bank. He recognizes
a daily alcohol consumption of around 50-70 g/day (beer and spirits) that he mentions to have stopped 1
month ago. He stopped his alcohol consumption after his family doctor raises the possibility of alcoholic
cirrhosis. He does not report any sobriety period before. He began to drink alcohol beverages at the age of
18 and was binge drinking during 10 years (from the age of 20 to 30), mainly with friends and colleagues
but almost never during the meals. He does not report any hidden alcohol consumption and was never
drinking alone. His motivation for long-term abstinence seems good, although he mentions to have still
some craving episodes. He has no current symptoms and feels to be in good condition. Clinical examination
does not reveal any spider naevi, swollen legs, hepatomegaly or jaundice. Body mass index is 31 kg/m 2
and he reports to have become overweight at the age of 35. He does not report any marijuana or other drug
consumption but has smoked a lot, from the age of 20 to 50 years (between 20 and 30 cigarettes a day).
His biological tests are as follows:
White cell count 9,200/mm 3 , hemoglobin 14.5 g/dL, MCV (mean corpuscular volume) 101 fl, platelet count
135,000/mm 3 , INR 1.12, serum creatinine 0.8 mg/dL, AST (aspartate aminotransferase) 89 IU/L (upper limit
of normal value: 40 IU/L), ALT (alanine aminotransferase) 56 (upper limit of normal value: 40 IU/L), gammaglutamyltransferase
185 IU/L (upper limit of normal value: 55 IU/L), alkaline phosphatase 157 IU/L (upper
limit of normal value: 240 IU/L), serum bilirubin 0.9 mg/dL, serum albumin 3.4 g/dL. Alpha-fetoprotein,
ferritin and serum iron are within the normal ranges and screening is negative for HIV, HCV and HBV.
Ultrasonography has already been performed and has shown liver brightness related to probable steatosis,
however the examination was hampered by abdominal obesity.
Question 1: If the General Practitioner is correct, give the patient characteristics that are present in this
observation that may have led to the development of cirrhosis.
Answer:
Despite differences related to gender (females are more prone than males to develop hepatic damages at
the same daily alcohol intake), a recent meta-analysis has shown that individuals drinking more than 25 g/
day are at higher risk of morbidity related to cirrhosis than the others (1), even if the risk of cirrhosis was
far higher in patients drinking more than 120 g/day. Between these two cut-offs, many individuals develop