Steatosis and intrahepatic hepatitis C virus in chronic hepatitis

✍ Scribed by Fujie, Hajime; Yotsuyanagi, Hiroshi; Moriya, Kyoji; Shintani, Yoshizumi; Tsutsumi, Takeya; Takayama, Tadatoshi; Makuuchi, Masatoshi; Matsuura, Yoshiharu; Miyamura, Tatsuo; Kimura, Satoshi; Koike, Kazuhiko

• Publisher: John Wiley and Sons
• Year: 1999
• Tongue: English
• Weight: 111 KB
• Volume: 59
• Category: Article
• ISSN: 0146-6615
• DOI: 10.1002/(sici)1096-9071(199910)59:2<141::aid-jmv3>3.0.co;2-5

✦ Synopsis

Hepatic steatosis has been reported as one of the characteristics which discriminates hepatitis C from other forms of hepatitis, besides lymphoid follicles and bile duct damage. However, it is unclear whether or not the presence of hepatitis C virus (HCV) itself is associated with the development of steatosis. The possibility that the HCV itself is directly related to the development of steatosis was examined. The intrahepatic core protein levels, as a marker of the HCV load, were correlated with the presence of steatosis in 43 patients with chronic hepatitis C. Among 43 patients studied by Western blotting, the core protein was detected in the liver in 27 (62.8%). On the other hand, hepatic steatosis was observed in 21 (48.8%) of the 43 patients. Importantly, the core protein was detectable in 19 (90.4%) of the 21 patients with steatosis, while it was detected in only 8 (36.4%) of the 22 patients without steatosis (P = 0.008). However, serum HCV-RNA levels as determined by the Amplicor monitor were not significantly different between patients with and without steatosis. Multivariate analysis showed that the serum alanine aminotransferase level (P = 0.013), body mass index (P = 0.038), and intrahepatic HCV core protein positivity (P = 0.038) were the independent parameters best predictive of steatosis. These results indicate a close relationship between intrahepatic HCV and the development of steatosis, and suggest a possible role of the HCV itself or core protein in the pathogenesis of steatosis in human chronic hepatitis C.