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

BARCELONA . SPAIN
150 POSTGRADUATE COURSE SYLLABUS ALCOHOLIC LIVER DISEASE 151
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.
Figure 3: The mechanisms underlying the hepatoprotective and antimicrobial effects of IL-22.
Treatment of hepatocytes with IL-22 results in upregulation of many genes that prevent hepatocyte apoptosis
and stimulate hepatocyte proliferation. IL-22 also downregulates lipogenic genes such as SREBP-1 in the
liver, thereby ameliorating fatty liver disease. Finally, IL-22 stimulates hepatocytes to produce lipocalin-2,
which may contribute to IL-22 inhibition of bacterial infection.
In summary, IL-22 treatment appears to have multiple beneficial effects on alcoholic hepatitis, such as
preventing hepatocellular damage, promoting hepatocyte proliferation, and inhibiting bacterial infection.
In addition, the side effect of clinical treatment with IL-22 may be minimal because IL-22 only targets
epithelial cells such as hepatocytes. Clinical trials examining combination therapy with IL-22 or IL-22 plus
corticosteroids for patients with severe alcoholic hepatitis are warranted.
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.
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