2004, Number S2
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Gac Med Mex 2004; 140 (S2)
HCV infection and hepatic steatosis
Bosques-Padilla F
Language: Spanish
References: 26
Page: 73-76
PDF size: 563.79 Kb.
ABSTRACT
The mechanism by which hepatitis C virus (HCV) causes
chronic, progressive liver damage is unknown. Factors
other than the virus itself have been implicated. The role of
liver steatosis has been recently studied. Hepatic steatosis
is a common histologic finding occurring in › 50% of
patients with chronic hepatitis C. Both host and viral
factors have been demonstrated to play an important role
in its development. In patients infected with genotype 1,
steatosis appears due to co-existence of Non-alchoholic
steatohepatitis (NASH) with HCV and associated with
increased body mass index (BMI). Some recent observations
suggest that steatosis may be of viral origin and related to
genotype 3. This fact raises the possibility of a direct effect
of specific viral sequences on the pathogenesis of lipid
accumulation. Furthermore, hepatic steatosis attributed to
genotype 3 correlates directly with serum and intrahepatic
titers of HCV RNA. Resolution of steatosis after successful
antiviral therapy as well as steatosis being a sign of
recurrent HCV infection in patients with genotype 3 add
convincing evidence that steatosis is viral-related. The
pathogenic mechanism induced by genotype 3 is speculative.
Correlation between steatosis, intrahepatic HCV RNA, and
core protein expression suggest a direct effect. Further
support is provided by the finding that HCV core protein
induces steatosis in transgenic mice. Another possibility
relates to interaction with hepatic triglyceride turnover. In
conclusion, for patients infected with genotype 1 BMI plays
a role in the pathogenesis of steatosis, while in those
infected with genotype 3 steatosis may be due to a virusspecific
cytopathic effect. Regardless of etiology, the
contribution of both to liver fibrosis progression appears to
be accepted.
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