NATAP - DDW Liver Conference, San Diego, May 21-24 - Report 3

FAT IN THE LIVER AND ITS CORRELATION WITH VARIOUS FACTORS INCLUDING CHOLESTEROL, TRIGLYCERIDES, AND DIABETES

HEPATOCELLULAR FAT ACCUMULATION IN CHRONIC HEPATITIS C - IMPACT OF HEPATITIS C VIRUS SUBTYPES.

Harald Hofer, Hans-Christian Bankl, Friedrich Wrba, Petra E. Steindl-Munda, Christian Mueller, Alfred Gangl, Peter Ferenci, Univ of Vienna, Vienna, Austria.

Hepatic steatosis (fat in the liver) in chronic hepatitis C may be due to a direct cytopathic effect caused by the virus. Aim: The aim of this study was to investigate the influence of HCV-subtypes on development of liver steatosis. Patients and

Methods: A liver biopsy was obtained in 103 patients with chronic hepatitis C (m=73, f=30; mean age: 39+10.4). A pathologist unaware of clinical data graded/staged (0 to 4) portal and periportal inflammation and fibrosis on HE stained sections according to Ludwig. The degree of steatosis was expressed as percent of liver cells containing fat. Body mass index (BMI), triglycerides and cholesterol levels were determined at baseline and during therapy. HCV subtypes were assessed by a line probe assay (INNO-LiPA II, Innogenetics, Zwigngarde, Belgium).

Results: Steatosis was present in 35 of 41 (85.4%) pts. with subtype-3a and in 31 of 51 (60.8%; p=0.018) with subtype-1. In addition, the degree of steatosis was more extensive in patients with subtype 3a (43.3±29 [% of hepatocytes; mean+SD]) than in patients with subtypes 1 (11.8±13.5; p<0.05). There was no difference in the extent of portal and periportal inflammation, or fibrosis grade. The degree of steatosis did not correlate with BMI (esstentiallt BMI is weight) (subtype 3a: 23.5±3; subtype 1: 24.3±3.5), serum triglycerides, or cholesterol levels, or the presence or absence of diabetes.

Conclusion: Fat accumulation in hepatocytes is more common and more extensive in patients infected with HCV-genotype 3a than in those with genotype 1. Fat storage in hepatocytes appears to be a direct consequence of viral replication and cannot be explained by obesity or altered lipid metabolism.