icon_folder.gif   Conference Reports for NATAP  
  AASLD ( American Association for the Study of Liver Diseases)
November 9-13, 2001, Dallas
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  Nathalie Ganne-Carrie, Hosp Jean Verdier, Bondy France; Sylvie Chevret, Hosp Saint-Louis, Paris France; Catherine Guettier, Marianne Ziol, Christos Christidis, Jean-Claude Trinchet, Michel Beaugrand, Hosp Jean Verdier, Bondy France
editorial note: Steatosis can be defined as the accumulation of fat globules within the cells of the liver resulting in deterioration of tissue and diminshed functioning of the liver. In HIV/HCV coinfection fat can increase in the blood for patients taking HIV therapy. Steatosis in coinfected patients may be associated with the accelerated HCV progression seen in HIV-infected patients. More research is needed on this subject. As well, a recent study presented at Retrovirus 2001 showed that HCV/HIV coinfected patients may be more likely to have lipodystrophy than patients with only HIV.
Steatosis is a frequent feature of HCV chronic hepatitis and may contribute to hepatocyte apoptosis and liver fibrogenesis. The aim of this study was to assess the influence of macrovesicular steatosis in the outcome of HCV-related cirrhosis without HBV or HIV co-infection. Patients and Methods: all consecutive patients hospitalized in our unit for compensated HCV-related cirrhosis (Child-Pugh A) from 1990 to 1995 and who were then prospectively followed for hepatocellular carcinoma (HCC) screnning until death or june 2000 were enrolled. Liver steatosis was scored and its predictive value for death and the occurrence of HCC was assessed by Kaplan-Meier method, Log-Rank test and Cox model.
Results: 164 patients were enrolled (91 men, mean age 64). Forty-three of them had daily alcohol consumption > 40 g, 36 had mellitus diabetes and 62 had BMI > 25 Kg/m2. Mediane and mean values of hepatocyte steatosis were 5 and 11% (0-80); 71 had < 5% steatosis and 93 > or equal to 5% (including 22 with steatosis > or equal to 30%). At the reference date, (mean follow-up: 109 months), 41 have developed HCC and 78 have died (including 16 with HCC). The Cox model selected 3 predictive parameters for death : age (p=0.04, RR 1.8), prothrombin time (p=0.04, RR 2.2) and steatosis > or equal to 30% (p=0.04, RR 2.3), and 4 predictive parameters for the occurrence of HCC : steatosis < 5% (p=0.05, RR 3.3), age > or equal to 50 years (p=0.03, RR 9.3), male sex (p=0.04, RR 2.3) and presence of esophageal varices (p=0.003, RR 3.3).
Conclusions: in HCV-related cirrhosis, macrovesicular steatosis is predictive for death and is inversely correlated with the occurrence of HCC. These results could suggest a pro-apoptotic role of steatosis.