Thursday, April 7, 2011

DIFFERENT PATTERN OF DECOMPENSATION IN ALCOHOLIC VERSUS NON-ALCOHOLIC LIVER CIRRHOSIS

EASL Session Title: Category 02b: Cirrhosis and its complications: Clinical aspects


Presentation Date: 31 MAR, 2011

DIFFERENT PATTERN OF DECOMPENSATION IN ALCOHOLIC VERSUS NON-ALCOHOLIC LIVER CIRRHOSIS

M. Kuehne1*, J. Wiegand1, P. Pradat2, J. Moessner1, F. Zoulim2, C. Trepo2, H.L. Tillmann1,3

1Gastroenterology and Rheumatology, University of Leipzig, Leipzig, Germany, 2Department of Hepatogastroenterology, Hôtel Dieu Hospital University, Lyon, France, 3Duke Clinical Research Institute, Duke University Medical Center, Durham, NC, USA. *johannes.wiegand@medizin.uni-leipzig.de

Background: The clinical course of alcoholic versus non-alcoholic liver cirrhosis has not been well described yet. However, hepatic decompensation may be differentiated either in consequences of fibrosis (i.e. jaundice, variceal bleeding) or in lack of function (i.e. ascites) resulting in variable morbidity and mortality. We therefore evaluated the pattern of decompensation in relation to the etiology of liver cirrhosis.

Patients and methods: 220 cirrhotic German patients hospitalized between 2002 and 2006 were retrospectively evaluated (cohort A). Results were confirmed in a second cohort of German and French patients (cohort B: n=217) and in an overall analysis. Hepatic decompensation was defined as presence of either ascites, jaundice, encephalopathy, variceal bleeding, hepatorenal syndrome, spontaneous bacterial peritonitis, or hepatocellular carcinoma.

Results: In cohort A and B, alcoholic cirrhosis was present in 76.4% and 73.7% of cases. 8.9% of cases were in Child status A, 30.2% status B, and 44.6% status C (p=n.s.).

Compared to non-alcoholic cirrhosis (cryptogen n=37, HCV n=30, HBV n=11, other n=31), alcoholics (n=328) were significantly younger (55.6y ± 11.5 vs. 62.4y ± 12.8, p=0.000), more often male (75.9% vs. 53.2%; p=0.000) and smokers (60.8% vs. 28.8%; p=0.000).

Alcoholics were significantly more frequently hospitalized for ascites (cohort A: 56.5% vs. 38.5%, p=0,023; cohort B 53.2% vs. 36.8%, p=0.042; total: 54.6% vs. 37.6%; p=0.002) and showed a higher incidence of spontaneous bacterial peritonitis (total: 8.9% vs. 2.8%; p=0.033) compared to non-alcoholics. Non-alcoholics presented with significantly higher rates of hepatocellular carcinoma (31.2% vs. 17.2%; p=0.002). There were no significant differences in jaundice, variceal bleeding, hepatorenal syndrome, or encephalopathy.

A subgroup analysis of alcoholic vs. viral hepatitis confirmed ascites as dominant decompensation in alcoholics (54.6% vs. 36.6%; p=0.03).

In alcoholic cirrhosis, survival did not differ between cases with or without ascites (p=0.957). However, it was significantly impaired once ascites occurred in non-alcoholic disease (p< 0.001).

Conclusions: Ascites is the leading initial pattern of decompensation in alcoholic cirrhosis whereas hepatocellular carcinoma dominates in non-alcoholics. Non-Alcoholics developing ascites show a poor survival.

http://www1.easl.eu/easl2011/program/Posters/Abstract48.htm

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