%0 Journal Article
%T Central Portalization Correlates with Fibrosis but Not with Risk Factors for Nonalcoholic Steatohepatitis in Steatotic Chronic Hepatitis C
%A Hwajeong Lee
%A Sanaz Ainechi
%A Karen Dresser
%A Elizabeth M. Kurian
%J International Journal of Hepatology
%D 2014
%I Hindawi Publishing Corporation
%R 10.1155/2014/329297
%X Concomitant steatosis in chronic hepatitis C is associated with fibrosis and unfavorable treatment outcome. Central zone injury in nonalcoholic steatohepatitis (NASH) manifests as central portalization, with centrizonal microvessels and ductular reaction. We investigated whether central portalization in steatotic HCV biopsies would identify patients with metabolic risk factors for NASH. Liver biopsies with chronic hepatitis C and >10% steatosis were evaluated for the degree of steatosis, zonation of steatosis, fibrosis, and nonalcoholic fatty liver disease (NAFLD) activity score. The presence of centrizonal microvessels, sinusoidal capillarization, ductular reaction, and CK7 positive intermediate-phenotype hepatocytes were evaluated by CD34 and CK7 immunostain. The degree of steatosis and fibrosis showed a positive correlation. Additional positive correlations were noted between centrizonal angiogenesis and NAFLD activity score and central portalization and fibrosis. However, neither central portalization nor zonation of steatosis identified patients with metabolic risk factors for NASH. Therefore, central portalization cannot be used as a surrogate marker to identify patients with metabolic risk factors for NASH in steatotic HCV biopsies. The mechanism of centrizonal injury in steatotic HCV hepatitis is not solely attributable to the metabolic risk factors for NASH. 1. Introduction In chronic hepatitis C, steatosis is a common histologic finding. Studies have categorized the steatosis of chronic HCV into viral type versus metabolic type. The ※viral§ type of steatosis is well demonstrated in HCV genotype 3; these liver biopsies show a greater amount of steatosis compared to those of non-3 genotypes [1每4]. Experimental studies suggest that the HCV viral core protein impairs lipid oxidation and induces accumulation of triglyceride in the hepatocytes [5每7]. Furthermore, the degree of steatosis is related to the viral load [4每6, 8, 9], and the amount of steatosis decreases following treatment [10每12]. In the setting of liver transplantation, the hepatic steatosis is an early indicator of HCV reinfection [13]. The second type of ※metabolic§ steatosis is usually demonstrated in non-3 genotypes and is associated with risk factors of nonalcoholic fatty liver disease, such as high body mass index (BMI) [1, 4, 14每16]. In these patients, insulin resistance enhances peripheral lipolysis and hepatic lipogenesis [17], while impairing the export of triglycerides from the hepatocytes [6]. Thus, insulin resistance appears to play a key role in the development of
%U http://www.hindawi.com/journals/ijh/2014/329297/